Standardizednomenclaturefor Inbred Strainsof Mice

[CANCER RESEARCH 45, 945-977, March 1985]

StandardizedNomenclaturefor InbredStrainsof Mice: EighthListing1

Joan Staats

The Jackson Laboratory, Bar Harbor, Maine 04609 For the International Committee on Standardized Genetic Nomenclature for Mice

ABSTRACT to be extinct or because they were not reported. Appendix 2 is a list of standard abbreviations for the names of persons or This paper presents a list of inbred strains of mice with their institutions maintaining inbred strains. The principal use of the origins and characteristics, and a list of standard subline desig symbols is in designating sublines. For example, strain AU/Ss nations. upon transfer from Silvers to The Jackson Laboratory becomes AU/SsJ or AU/J. INTRODUCTION The Committee stresses the importance of using full strain or substrain designations in publications, and also of spelling out Previous listings of Standardized Nomenclature for Inbred the source of the animals. The brief symbol C57, for example, Strains of Mice appeared in Cancer Research in 1952, 1960, could stand for seven or eight different strains. The many differ 1964,1968,1972,1976, and 1980 (5). Between issues, additions ences among substrains emphasize the importance of using full and deletions to strain holdings appear in Mouse News Letter (4) designations. For example, CBA/J carries the gene for retinal and Inbred Strains of Mice (3). degeneration whereas CBA/Ca has the normal alÃele;the two Most fostered and otherwise manipulated lines, named genes differ in radiosensitivity, they are not histocompatible, and they on inbred backgrounds, and congenie histocompatibility strains vary in at least five polymorphic loci. We also stress the impor have been omitted, to keep the list to a manageable size. Lists tance of identifying the sex of the parents when listing hybrids. of congenie and segregating inbred strains and recombinant It is customary to list the female first. Thus, C57BL/6J 9 x DBA/ inbred strains can be found in two new publications (1,2). Since 2J a is B6D2F,, and DBA/2J 9 x C57BL/6J a is D2B6F,. comprehensive revised rules for nomenclature of strains, genes, and chromosome anomalies are presented in both these books, REFERENCES they are not included here. Appendix 1 is the list of inbred strains and some clearly defined 1. Foster, H. L, Small, J. D., and Fox, J. G. (eds ) The Mouse in BiomÃ©dical Research, Vol. 1. New York: Academic Press, Inc., 1981. substrains. It contains 233 entries, compared with 299 in the 2. Green, M. C. (ed.). Genetic Variants and Strains of the Laboratory Mouse. seventh listing and 124 in the first. Several strains have been Stuttgart: Gustav Fischer Verlag, 1981. dropped since the seventh listing, either because they are known 3. Inbred Strains of Mice: an informal biennial document listing laboratories maintaining inbred strains of mice; the companion document to Mouse News Letter. ISM No. 13 appeared in July 1983. 4. Mouse News Letter: an informal semiannual document carrying information on 1 Preparation of this paper was supported in part by Grant DEB 79-26708 from mutant genes, research stocks of mice, and research news. MNL is currently the National Science Foundation. Address requests for reprints to: Library, The edited by Dr. J. Peters; No. 71 appeared in July 1984. Jackson Laboratory. Bar Harbor, ME 04609. 5. Staats, J. Standardized nomenclature for inbred strains of mice: seventh listing. Received October 30,1984; accepted November 8,1984. Cancer Res., 40: 2083-2128,1980.

APPENDIX BLM-2 Green, E. L. (ed.) Biology of the Laboratory List of inbred strains of mice and their clearly defined sub- Mouse, Ed. 2. New York: McGraw-Hill, strains. 1966. Abbreviations Charac characteristics. In some cases journal ref Inbr = number of generations of brother x sister erences are given. Letters in parentheses inbreeding. The substrain on which the fig indicate specific contributions to Inbred ure is based is indicated in parentheses. If Strains of Mice. The key to the letters will a line has been produced by appropriate be found in Appendix 2. In a few cases crosses to an inbred strain, the number of information has been obtained by corre generations is preceded by N. spondence or personal communication. Genet = genetic constitution, mainly mutant coat and eye colors. Maintained by persons or laboratories maintaining each strain, insofar as information is available, Origin origin. In some cases references are given. are indicated by substrain symbols. A table in Chap. 1 of BLM-2 gives more extensive information. b x s brother x sister inbreeding.

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SNISM-7 Staats, J. Standardized nomenclature for than other sublines (E. S. Russell et al., inbred strains of mice: seventh listing. Can Proc. Soc. Exp. Biol. Med., 78: 761,1951) cer Res., 40: 2083-2128,1980. hematocrit 48%, systolic blood pressure 81 mm Hg (G. Schlager and R. S. Weibust, J. SPF specific-pathogen-free. Hered., 67: 295, 1976); cleft lip with or without cleft palate occurs sporadically (H. A/He Inbr: 195. Genet: abc. Origin: Strong, Kalter, Teratology, 20:213,1979); cleft pal 1921, from cross of Cold Spring Harbor ate is easily induced with a variety of albino and Bagg albino. Majority of sublines agents; very sensitive to X-irradiation (BLM- trace to a stock that Bittner obtained from 2); some heart disease in old breeders Strong in 1927. Charac: mammary tumor (BLM-2); moderately susceptible to audi- incidence varies with colony and breeding ogenic seizures over a long period up to status, from 0 to 80% (SNISM-7); some 245 days (E. Vicari, J. Psycho!., 43: 111, reticular tissue neoplasms; few skeletal var 1957); low alcohol preference (C. L. Good- iants (Gr); 40% of ?9 have positive LE cells rick, J. Stud. Alcohol, 39:19,1978); lowest or antinuclear antibodies (Umc); 84% neo- activity level of liver arylsulfatase C of 24 natally thymectomized develop runting syn Jax strains tested [K. Nelson and W. D. drome; high incidence of hyperplastic alveo Daniel, Experientia (Basel), 35: 309,1979]; lar nodules correlated with pregnancy (Ki); protein kinase C activity one-half that found cleft lip with or without deft palate occurs in 7 other strains (A. M. Malkinson et al., sporadically, cleft palate is easily induced Biochem. Biophys. Res. Commun., 722: with a variety of agents (H. Kalter, Teratol 492, 1984); resistant to Salmonella typhi- ogy, 20: 213, 1979); highly susceptible to murium C5 (V. Hormaeche, Immunology, measles virus (B. Rager-Zisman, Fed. 37: 311, 1979); intermediate susceptibility Proc., 35: 391, 1976); susceptible to Plas- to rabies virus (D. L. Lodmell, Fed. Proc., modium chabaudi (M. M. Stevenson ef al., 41:566,1982); susceptible to Ustoria mon- Infect. Immun., 3d: 80, 1982); resistant to ocytogenes (E. Skamene and P. A. L. Kong- Leishmania infection (D. J. Bradley, Clin. shaven, J. Reticuloendothel. Soc. 24 Exp. Immunol., 30:130, 1977). Maintained (Suppl.): 32a, 1978); resistant to Bacillus by: Crc, Cv, Dv, Fre, Icrf, Imr, Ki, Man, Ok, Calmette-Guerin (A. Forget et al., Fed. Ola, Ph, Ros, Ss, Sy, Tru, Tu, Y, Zgr. Proc., 41: 730,1982); most susceptible to Pseudomonas aeruginosa of 16 strains A/He Inbr (N): 215. Strong to Heston 1938, He to tested (J. E. Pennington and R. M. Williams, J 1948. Charac: low incidence of mammary J. Infect. Dis., Ã•39:396,1979); sensitive to and lung tumors (SNISM-7); high incidence Cryptococcus neoformans due to the He" of renal disease in older animals, some cleft alÃele(J. C. Rhodes er a/., Infect. Immun., lip observed in young (J); cleft palate is 29:494,1980); for other susceptibilities see easily induced with a variety of agents; lung N. N. Nesbitt and E. Skamene. J. Leuk. tissue very susceptible to methylcholan- Biol., 36: 357, 1984. resistant to induction threne (J); most susceptible to ectromelia of amyloid (M. A. Scheinberg and E. S. virus of 8 strains tested (S. M. Ermolaeva Cathcart, Immunology, 37: 443, 1976). et al., Sov. Genet. (Eng. TransÃ.Genetika), Maintained by: Ao, Cr, Gh, Han, Ibg, J, Odn, 8: 681,1972); relatively susceptible to Op- Ola, Ori, Pt, Scr, Sg, Sx, Ucsd, Univ. Hel isthorchis felineus (A. G. Zelentsov, Med. sinki (O. MÃ¤kelÃ¤),Yok Parazitol. Parazitamye Bolezni, 43: 95, 1974); susceptible to rabies virus infection AB/Jena Inbr (Jena): 70. Genet: AB DC Hbb". Origin: (D. L. Lodmell, Fed. Proc., 41: 566, 1982); from Agnes Bluhm to P. Hertwig in 1934, hematocrit 48%, systolic blood pressure 82 to J. Fortner in 1945, to H. RÃ¶hrerin 1949, mm Hg (G. Schlager and R. S. Weibust, J. to Jena in 1952; 1945-1959 random bred, Hered., 67: 295, 1976); serum Â«t-antitryp- new start of b x s in Jena in 1959 (Z. sin lowest of 34 strains tested (S. K. Chan, Versuchstierk Nd., 11: 241,1969). Charac: Arch. Environ. Health, 27:271,1973). Main av. litter size at birth 7.3 Â±0.15 (S.D.), av. tained by: Cr, Cum, Gh, Hok, Han, 1er, J, litter size at weaning 6.5 Â±0.10; sex ratio Kun, Mob, N, Novosibirsk, Rl, Ros, Sf, Sv. 49.2% do at weaning; body weight at wean ing (21 days) 10.2 Â±0.28 g ?$, 10.9 Â±0.30 A/J Inbr (J): 196. Origin: Strong to Cloudman g <5(Ã®;meanlife span in Jena 18.1 mo $$; 1928; survivors of Bar Harbor fire to Jax fetal retentions and accompanying purulent 1947 at F73. Charac: mammary tumors panmetritis in a small number of breeding moderate (J); renal disease in older animals 9$; in animals older than 1 year more than (Umc); lower percentage of granulocytes 80% amyloidosis mostly affecting, in de-

CANCER RESEARCH VOL. 45 MARCH 1985 946

scending order of frequency, the liver, kid Immunol., 36: 251, 1978). Oslo subline neys, spleen, adrenals, and intestine; in vir source of adrenocortical lipid depletion gene gins 25% lymphomas, less than 10% lung (K. Amesen, Acta Pathol. Microbiol. Scand., tumors, 6% uterine leiomyosarcomas, few 58:212,1963); low concentration of lipid in sarcomas of soft tissue, but no mammary adrenals (BLM-2); hematocrit of AKR/J tumors; susceptible to chronic interstitial 47.6%, systolic blood pressure 80 mm Hg nephritis; highly susceptible to mousepox, (G. Schlager and R. S. Weibust, J. Hered, Sindbis-, MM, Mengo, encephalomyocardi- 67: 295,1976); resistant to Leishmania in tis, and Columbia S. K. viruses, epidemic fection (D. J. Bradley, Clin. Exp. Immunol., diarrhea of infant mice, and Plasmodium 30:130,1977). Maintained by: A, Bkl, Bog, berghei, moderately susceptible to mouse Cr, Crc, Cri, Cri, Cum, Dp, Fhc, Fib, Han, pneumonia virus; strong antibody response Hok, 1er,Icrf, J, Ki, N, Novosibirsk, Ok, Ola, to sheep RBC; males are aggressive. Main Ori, Ph, Pp, Pt, Rij, Ros, Ser, Sy, W, Wn, tained by: Jena. Y.

ABP Inbr (Le):64. Genet:abbtpse wa-1. Origin: AL Inbr (N): 195. Genet: a b c. Origin: believed A. B. Griffen to Lane 1968, sib-mated since to have originated from strain A outcrossed then. Charac: useful for linkage testing. to unknown strain followed by b x s mating. Maintained by: Le, R. Should not be considered a strain A subline. Charac: mammary tumor incidence 20% at 15 months (N); high incidence of amyloi- AE Inbr (Nctr): 70. Genet: a" o ofp se. Origin: Hollander, Iowa, 1962. Charac: mean litter dosis (J. S. Ram ef al., Proc. Soc. Exp. Biol. size at weaning more than 9. Maintained Med., 730: 462, 1969); expression of by: Nctr. XenCSA is low on thymic and high on splenic lymphocytes (H. C. Morse III ef al., AEJ/Gn Inbr (Rk): 70. Genet: a". Origin: Hollander J. Exp. Med., 122: 443, 1979); susceptible (Schaible), Iowa State, Ames waltzer stock to rabies fixed virus and Lansing strain polio virus, young animals susceptible to toxo- with miscellaneous markers to M. C. Green in 1963. Crossed once to C57BL/10Gn fol plasmosis infection (N). Maintained by: la, lowed by cross to C57BL/6J->TJ, then b x N, Pt. s. F28 to Roderick in 1972. Charac: high AU Inbr (J): ? + 69. Genet: a U. Origin: R. A. fertility, mean litter size 9. Maintained by: Fisher,about 1937.50% GrÃ¼neberg'sCBA, Le, Rk. 28.5% Fisher's color stocks, and 21.5% GrÃ¼neberg'swavystock, the latter 2 being AG/Cam Inbr (Cam): about 155. Genet: A*/a" x A*/ a", with Aâ„¢,A,A", a', a, and p, continually unrelated to stocks of American origin (J. backcrossed to Ay/a" line. Origin: R. A. R. Morton, personal communication). To Fisher, "A" from GrÃ¼nebergin1945 [a CBA Medawar 1947, to Silvers at F23 in 1957, to Jax 1967. Charac: 9$ do not reject d subline (J. R. Morton, personal communi isografts; unusual induction of kidney ÃŸ- cation)]. Various a-locus alÃelesintroduced glucuronidase by testosterone (Cv). Main by backcrosses, stock maintained mainly by sib-mated sublines until 1959. Back- tained by: Cv, J. crossing to one Ay/a x Ay/a line started AX/Pa Inbr (Pa); 27. Genet: a*. Origin: L. B. Rus 1959; central line now replaced by Ay/a" x sell's balanced lethal stock Ay/a" 6PB; to Ay/a". Charac: high penetrance of Nil, 0% M. H. L. Snow in 1969 who separated the penetrance of chylous ascites in Ra (B. M. alÃelesbya cross to C57BL/6 and back- Herbertson and M. E. Wallace, J. Med. Ge crossed a* mice to C57BL/6 for 4 gen. net., 1: 10, 1964). Maintained by: Cam, Snow to Papaioannou in 1973; sib-mated Odn. with forced heterozygosity. Charac: embry onic lethal at the agouti locus (V. E. Pa AKR Inbr (N): 181. Genet: a Be. Origin: a dealer paioannou and H. Mardon, Dev. Genet., 4: named Detwiler in Norristown, PA; carried 21,1983). Maintained by: Pa. by Furth as a high-leukemia strain from 1928 to 1936, then random-bred at Rock BA Inbr (Nmg): 64. Genet: b. Origin: Falconer, efeller Inst. for several generations, b x s noninbred obese stock. Charac: good re mated 9 gen. by Mrs. Rhoades and 21 by productive performance; no known tumors. C. Lynch. Charac: lymphatic leukemia in Poor retention in black-white discrimination various colonies from 68 to 91% (SNISM- learning (J. van Abeelen ef al., Physiol. & 7). AKR/J and AKR/Cum reject each other's Behav., 10: 751, 1973). Maintained by: spontaneous lymphomas (M. M. Zatz, Cell. Nmg.

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BALB/C Inbr (Hok): 186. Genet: b c. Origin: albino soma mansoni (M. M. Fanning, Parasite Im stock acquired by H. Bagg in 1913. Prior munol. (Oxf.), 6: 95,1984). Maintained by: inbreeding uncertain (E. C. MacDowell, J. A, Ani, Ao, Be, Bkl, By, Cox, Cr, Crc, Crgl, Gen. Phystol., 11: 57,1927). MacDowell to Cri, Cri, Cum, Dp, Dub, Dv, Dy, Ei, Ess, Snell (who added the /c) in 1932 at F26; Fhc, Fib, Fnn, Ga, Gy, Han, Hf, Hok, Hsd, subsequently widely distributed, especially Ico, 1er, Imr, J, Ki, Kun, Lac, Ul, Man, Mcd, by Andervont. Charac: susceptible to Mel, N, Nii, Odn, Ok, Ola, Ori, Pas, Ph, Pp, chronic pneumonia, extremely sensitive to Pt, Rij, Rk, Rl, Ros, Saf, Ser, Sed, Sg, Sid, radiation (J. Vacha ef al., Z. Versuchs- Sim, Stutman, Sx, Sy, Tac, Tbr, Tru, Tu, tierkd., 26: 157, 1984); long breeding life. Uct, Urne, Univ. Helsinki (O. MakelÃ¡), W, Some heart lesions in old breeders, arter Wm, Wn, Wrm, Y, Yok. iosclerosis common in both sexes (BLM-2). Relatively nonaggressive. Very large retic- BBT/Ha Inbr (Cv): 65. Genet: a of GUS". Origin: cross uloendothelial organs relative to body of noninbred hr/hr Ã¶f/of x C57BL/Ha. To weight (T. Gotjamanos, J. Reticuloendothel. Chapman 1974. Charac: belted. Maintained Soc., 8: 421, 1970). Mammary and lung by: Cv. tumor incidence varies with colony and breeding status (SNISM-7). Susceptible to BDP Inbr (J): 124. Genet: a b d p rd se. Origin: the induction of plasma cell tumors with W. H. Gates, inbred since 1926; dilute mineral oil. Cd subline develops sponta brown ? from Uttte x pink-eyed d from neous bilateral adenocarcinoma of the kid Strong (W. H. Gates, Genetics, 12: 295, ney, 60-70% in both sexes at 9-15 mo; 1927). Charac: frequent mammary tumors; adenocarcinoma cells inhibit body growth hemorrhagic ovaries; polycystic kidneys; when grafted into the same or other strains hematocrit 52.2%, systolic blood pressure (Cd). Almost all <5dsnow spleen amyloidosis 84 mm Hg (G. Schlager and W. S. Weibust, by 20 mo (P. Ebbesen, J. Nati. Cancer Inst., J. Hered., 67:295,1976). Maintained by: J. 47:1241,1971); high level of a-fetoprotein in BALB/cJ (D. R. Pollard ef al., Can. J. BLN Inbr (Nmg): 58. Genet: a B. Origin: Cpb, Genet. Cytol., 24: 343, 1982); 38% of noninbred yellow stock. Charac: very good BALB/cJ have dorsoventral vaginal septa reproductive performance. Maintained by: versus 0-8% in other sublines (T. Cunliffe- Nmg. Beamerand D. B. Feldman, Lab. Anim. Sci., 26:895,1976); highest wheel-running activ- BN/a Inbr (W): 90. Genet: A B c D H-2*1. Origin: ity of 18 strains tested (M. F. W. Festing, Anna Dux, Gliwice, September 1950, from Lab. Anim., 11: 257, 1977); hematocrit unknown parents. F13 taken to Warsaw 52.2%, systolic blood pressure 128 mm Hg, June 1956, where it was split into 2 sub- highest of 21 Jax strains tested (G. Schla strains, inbreeding continued (A. Dux, No ger and R. S. Weibust, J. Hered., 67: 295, wotwory, 7: 67, 1957). Charac: 35% lung 1976). BALB/cJ has twice the level of 3- tumors at 662 days; 7.1% leukemia at 647 catecholamine-synthesizing enzymes in the days; 23% chronic nephritis at 562 days. adrenals as do BALB/cN; they also differ in Used for carrying transplantable vaginal ep- fighting behavior (R. Ciaranello ef a/., Proc. ithelioma G93. Maintained by: W. (Bog Nati. Acad. Sci. USA, 71:3006,1974); 35% maintains the unsplit BN strain at F91.) of BALB/cAnN develop spontaneous mon oclonal B-cell tumors at 20-21 mo (R. Keller BN/b Inbr (W): 96. Genet, and Origin: as BN/a. ef a/., Blood, 58: 161 a, 1981); relatively Charac: lung tumors 25% at 629 days; resistant to Candida albicans (H. F. Hector 1.8% leukemia at 512 days in $9, 13% ef al., Infect. Immun., 38: 1020, 1982); re chronic nephritis at 493 days; used for car sistant to Eimeria vermlformis (M. E. Rose rying transplantable vaginal epitelioma et al., Parasitology, 88: 45,1984); resistant G94. Maintained by: W. to Cryptococcus neoformans due to He1 alÃele(J. C. Rhodes ef al.. Infect. Immun., BNT Inbr (Le): 73. Genet: a Bn/+. Origin: muta 29: 484, 1980). Susceptible to: Salmonella tion to bent tail arose in Navy Med. Res. typhimurium C5 (C. E. Hormaeche, Immu Unit stock, discovered by E. D. Garber. nology, 37: 311, 1979); measles virus (in From A. B. Griffen to Lane 1960. Inbred to termediate) (B. Rager-Zisman, Fed. Proc., F27 followed by one outcross to C57BL/6J 35: 391, 1976); Leishmania (D. J. Bradley, x CBA/Ca F,, then b x s. Charac: tails of Clin. Exp. Immunol., 30: 130, 1977); spot hemizygous males are more kinked and ted fever group rickettsiae (L. Sammons, shorter than tails of heterozygous females. Lab. Anim. Sci., 27: 229, 1977); ScWsfo- Penetrance is complete. Maintained by: Le.

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BRSUNT Inbr (N): 158. Genet: abC. Origin: Strong, sence of lower third molars in about 18%, a branch of BRS (from strain NH) continued few skeletal variants (Gr); some mammary without further methylcholanthrene treat tumors in breeders. Do not develop antinu ment. Charac: gastric lesions; adiposity; clear antibodies or LE cells with aging 100% incidence of periodontal disease. (Urne). Birmingham strain Â¿Â¿over 120 Maintained by: N, Y. weeks all have hepatomas (J. G. Sharp ef al., J. Pathd., T19:211.1976). Resistant to BRVR Genet: c. Origin: Webster 1930, at Rocke S. typhimurium C5 (C. E. Hormaeche, Im feller Inst. (L. T. Webster, J. Exp. Med., 57: munology, 37: 311, 1979); resistant to 793,1933). Charac: resistant to salmonella, Leishmania infection (D. J. Bradley, Clin. some encephalitic viruses, and experimen Exp. Immunol., 30:130,1977). Maintained tal allergic encephalomyelitis. Normal im by: Ao, Bkl, Cam, Cnb, Cr, Crc, Cum, Gy, mune response (D. Briles et al., Eur. J. H, Hb, J, Kw, Lac, N, Nii, Novosibirsk, Ola, Immunol., 9:255,1979). Maintained by: Dv. Ori. Pt, Scr, Stutman, Tu, Uct, Univ. Helsinki (0. MakelÃ¤),W, Y, Zal, Zbr. BSVR Gent: c. Origin: as above and L. T. Webster (J. Exp. Med., 65:261,1937). Charac: sus- CBA/H-T6 Inbr (J): N13 F88. Genet: T6/T6. Origin: ceptible to salmonella, resistant to some T(14;15)6Ca translocation homozygotes encephalitic viruses. Maintained by: Db. were backcrossed to CBA/H by M. F. Lyon, eventually sib-mated. Charac: homozygous BSVS Genet: c. Origin: as above. Charac: suscep for small marker chromosome of T6 trans- tible to salmonella, some encephalitic vi location. Congenie with CBA/H. Maintained ruses, and experimental allergic encephali by: Bkl, Cam, Crc, H, Hok, J, Lac, Pt, Rij, tis. Immune response deficient. Maintained W, Y, Zgm. by: Db, Dv, Pt. CBA/J Inbr (J): 194. Genet: rd. Origin: see C3H/St; BUB Inbr (J): 122. Genet: a c rd. Origin: from Strong to Andervont 1947, to Jax 1948. albinos of unknown origin at Brown Univ.; Charac: 65% hepatomas in Â¿6(J.B. Storer, maintained by random breeding until 1945. J. Gerontol., 21: 404, 1966); 24% hepato Charac: selected for good growth and re mas in da, 15% lymphomas in $9 and 33% productive performance; no known tumors; mammary tumors in 9$ (G. S. Smith ef al., relatively resistant to Schistosoma mansoni J. Nati. Cancer Inst., 50:1195,1973). Mid- (M. M. Fanning ef al.. Parasite Immunol. range of radiation resistance (BLM-2); renal (Oxf.). 6:95,1984). Maintained by: J. tubulointerstitial lesions in 78% of mice 3- 22 mo (U. H. Rudofsky, Am. J. Pathol., 92: BXSB Inbr (Mp): 49. Origin: C57BL/6J x SB/Le- 333,1978); hematocrit 46.3%, lowest of 21 sa bg/sa bg (E. D. Murphy); selection of the Jax strains tested, systolic blood pressure satin, non-beige recombinant followed by b 78 mm Hg (G. Schlager and R. S. Weibust, x s mating with forced heterozygosis at the J. Hered., 67: 295, 1976). Susceptible to sa locus (Mouse News Lett., 58:52,1978). amyloid induction by casein (M. A. Schein- Charac: a new recombinant inbred strain. berg and E. S. Cathead, Immunology, 37: All animals develop spontaneous autoim 443, 1976); highly susceptible to measles mune disease characterized by moderate virus (P. A. Neighbour ef al.. Infect. Immun., lymphadenopathy with hypergammaglobu- 21:764,1978); resistant to rabies virus (D. linemia, splenomegaly, Coombs-positive L. Lodmell, Fed. Proc., 41: 566,1982); de hemolytic anemia, and immune complex ficient in a kidney metalloendoproteinase glomerulonephritis with nephrotic syn [R. J. Beynon and J. S. Bond, Science drome. 9? survive an average 63 weeks,

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tained by: Ao, Cr, Dub, Dv, Hsd, 1er,N, Nil, started in 1964. Maintained by: Jic. NOTE: Rij, Scr. There are several other inbred CFW lines. They should not be assumed to be identical CBA/St Inbr (Man): 173. Genet: +. Origin: see C3H/ because of heterozygosity of the original St. Strong to Mann 1962. Charac: mam stock. mary tumor incidence high in both virgin and breeding $$; long lived. Ki has 2 sub- CHI Inbr (Man): 160. Genet: +. Origin: see C3H/ lines, one with less than 1% mammary tu St. Charac: similar to C3H. Maintained by: mors and carrying rd, the other with 40% Man. mammary tumors and normal eyes; skin grafts between them not accepted. Main- CL/Fr Inbr (Fr): 70. Genet: b c. Origin: stock from Morgan carrying "msl" (migratory spot le tained by: Ao, Ki, Man, Ok. sion, a variable white spot on the retina), CC57BR Inbr (Y): 115. Genet: a b. Origin: Medvedev, crossed with A/J and inbred b x s with 1943, BALB/cN ? x C57BL/N a. Charac: selection for high spontaneous deft lip fre no spontaneous mammary tumors but quency. Msl now has low penetrance. about 60% when milk agent is introduced; Charac: cleft lip in 25% of viable 17-day primary lung tumors 22%. Incidence of all fetuses (D. M. Juriloff, Prog. Clin. Biol. Res., other tumors less than 1%. Maintained by: 46: 39, 1980). Maintained by: Fr, Ksb, M. Igg, Novosibirsk, Sto, Y. C. Johnston (Univ. North Carolina), Nem.

CC57W Inbr (Y): 107. Genet: abc. Origin and CS Inbr (Nga): 94. Genet: a b c D s. Origin: Charac: see CC57BR. Relatively resistant established in 1956 from hybrids between to Opisthorchis felineus (A. G. Zelentsov, NBC and SII, both now extinct. Unrelated Med. Parazitol. Parazitarnyes Bolezni., 43: to IVCS. Charac: good reproductive per 95,1974). Maintained by: Sto, Y. formance; quick moving; Japanese crooked tail 16%. Maintained by: Nga. Inbr (J): 97. Genet: A c" rd*. Origin: wild CE mutant trapped in Illinois by J. E. Knight. CWD Inbr (Agi): 37. Genet: a b cw. Origin: CBA/ Color genetics studied by Detlefsen. Inbred CtH-sw (from Cbi) x B6C3Fi. Offspring by Eaton at least 15 gen., some sent to crossed to DBA/2 J, then inbred. Charac: Woolley. Speirs (2 gen. from Woolley) to strongly curled whiskers in cw/cw. High Wy and Jax in 1948. Charac: mammary incidence of spontaneous B-cell lympho- tumors 3% in breeding ?$, ovarian tumors mas. Maintained by: Agi. less than 10%, reticular tissue neoplasms less than 4% (Ki); high incidence of hepa- CXBD Inbr (By): 91. Genet: +. Origin: D. W. Bailey, tomas (M. Festing and D. K. Blackmore, cross of BALB/cAnN $ x C57BL/6J a, then Lab. Anim., 5: 179, 1971); high adrenocor- b x s inbred. Charac: carries histocompati- tical carcinoma incidence in both sexes after bility mutation which has arisen and become neonatal gonadectomy (J). Large amount of fixed since F10. Maintained by: By. The lipid in adrenals (BLM-2); hematocrit 54.8%, recombinant inbred strains CXBD, CXBE, systolic blood pressure 86 mm Hg (G. CXBG, CXBH, CXBI, CXBJ, and CXBK Schlager and R. S. Weibust, J. Hered., 67: were each derived from the above cross 295, 1976); serum Â«t-antitrypsin second and thereafter independently sib-mated for lowest of 34 strains tested (S. K. Chan, 54 gen. or more. For each strain it has been Arch. Environ. Health, 27: 272,1973); sus determined whether the BALB/c or the ceptible to Leishmania infection (D. J. Brad C57BL/6 alÃelehas been fixed at each of ley, Clin. Exp. Immunol., 30: 130, 1977); 47 loci. These strains are useful in linkage highest activity level of liver arylsulfatase C and pleiotropism studies [D. W. Bailey, of 24 Jax strains tested [K. Nelson and Transplantation (Baltimore) 11: 325,1971]. W. L. Daniel, Experientia (Basel) 35:309, Maintained by: By, Pt, Ty. 1979]. Maintained by: A, J, Univ. Coll. Lon don, Univ. Helsinki (O. MÃ¤kelÃ¤). C3H/BI Inbr (Ki): 160. Genet: +. Origin: see C3H/ St. Strong to Bittner 1931, Bi to Kirschbaum CFCW Inbr (Rl): 100+. Genet: c Ca. Origin: Car- 1952. Charac: mammary cancer more than worth Farms 1/3/48 to Rl, b x s inbreeding 99% in breeders and virgins (V. Likhite, by Rl. Maintained by: Rl. personal communication, 1981); high inci dence of hyperplastic alveolar nodules. Leu CFW/Jic Inbr (Jic): 58. Genet: c. Origin: from non- kemia less than 0.5% in breeders, 14% in inbred Carworth Farms mice, inbreeding 66. Hepatomas 0% in ?$, 10% in dd (Ki).

CANCER RESEARCH VOL. 45 MARCH 1985 950

Very susceptible to hepatic carcinogens; 1920, from cross of Bagg albino $ x DBA 98% neonatally thymectomized develop <3.Strains C, CBA, CHI, and C12I also orig runting syndrome (Urne). Maintained by: Ao, inated from this cross. Charac: high mam Icrf, Ki, Urne. NOTE: There are major differ mary tumor incidence in both breeders and ences between sublines of C3H mice (L. M. virgins. Maintained by: Ao, Hf, Kun, Man, Glode and D. L. Rosenstreich, J. Immunol., N, Nmg, Ros, Scr. J.117:2061,1976; Hered., 69: 66,1978). H-H. Krog ~ and R. Moutier, C3Hf Inbr (N): 141. Origin: Heston, 1945, from a litter of C3H bom by cesarean section and CSH/He Inbr (N): 160. Genet: rd. Origin: see C3H/ foster nursed on C57BL/6. There are sev St; Strong to Andervont 1930, An to Heston eral other fostered C3H lines, not all fos 1941 after 35 b x s gen. Charac: 85% tered on C57BL/6 and not all from the same hepatomas at 14 mo, 97% mammary tu C3H subline. All C3Hf lines lack the mam mors in breeders at av. age 7.8 mo (Lac); mary tumor milk factor and hence are low 100% in virgins at 10.6 mo (He); 90% in tumor but highly susceptible to its introduc both breeders and virgins (Crgl); 84% in tion. Maintained by: Bd, Cr, Cum, Dp, Ga, breeders at 272 days (Y). C3H/HeN have Gh, Hf, 1er, Imr, Kam, Kun, Nctr, Lac, N, 41 % primary hepatocellular carcinomas (F. Ok, Rl, Ros, Sed. F. Becker, Cancer Res., 41: 3320, 1981); high complement activity (S. Goto ef al., C3HA Inbr (Y). 102. Genet: +. Origin: Pogosianz, Jpn. J. Exp. Med., 41: 311, 1971). Highly C3H 9 x A a, subsquent inbreeding. susceptible to cardiac calcinosis (89%) in Charac: originally 30% mammary tumors, mated ?$ (G. L. Eaton ef al., Am. J. Pathol., gradually decreased [V. I. Gelshtein, Probi. 790: 173, 1978); resistant to Leishmania Oncol. (Engl. TransÃ.Vapr. Onkol.), 7(10): infection (D. J. Bradley, Clin. Exp. Immunol., 45, 1961]; susceptible to hepatic carcino 30: 130, 1977); the B6C3F, hybrid is the gens. Maintained by: Y. designated Nati. Toxico!. Program strain (M. F. Reilly ef al.. Infect. Immun., 42: 645, C3HeB/De Inbr (Dt): 125. Origin: Deringer, fertilized ova 1983). Maintained by: A, Ao, Bkl, Bog, Cox, of C3H transferred to C57BL. Charac: lacks Cr, Crgl, Cri, Cv, Dp, Dub, Dy, Ei, El, Gy, H, milk agent; hepatomas 58% in virgin 99 after Han, Hsd, 1er,Imr, N, Nctr, Nii, Novosibirsk, 24 mo, 30% in breeders, 38% in force-bred, Odn, Ok, Ola, Ph, Pt, Rl, Scr, Sim, Sy, Tac, 90% in breeding dd; mammary tumor 4% in Tru, Uct, W, Wn, Wrm, Y. virgins, 55% in breeders, 74% in force-bred; many ovarian tumors (M. K. Deringer, J. C3H/HeJ Inbr (J): 180. Genet: rd. Origin: see CSH/St. Nati. Cancer Inst, 77: 533, 1956). Main Heston to Jax 1947. Charac: some mam tained by: Dt. mary tumors in breeding 9$, fewer in virgins; high mortality in <Ã®<Ã®exposedto chloroform C3HeB/FeJ Inbr (J): 123. Genet: rd. Origin: Fekete, or turpentine fumes; hepatomas in

CANCER RESEARCH VOL. 45 MARCH 1985 951

in 9?, 4% in

CANCER RESEARCH VOL. 45 MARCH 1985 952

C57BL/1OJ Inbr (J): 158. Origin: see C57BL/6J. Charac: C57L Inbr (J): 162. Genet:a o In. Origin: J. Murray, incidence of eye defects 20% in $9, 3% in 1933, mutation to In in F20 of a C57BR Â¿Â¿,malocclusionsand hydrocepnalus rarer subline which is now extinct. Maintained by than in C57BL/6J (J); occasional vaginal Cloudman, to Heston 1938, to Jax 1947 at septa, some fusion of bones in feet (Fo). F45. Charac: low mammary tumor inci Hematocrit 50.7%, systolic blood pressure dence; some pulmonary tumors in old ani 68 mm Hg, second lowest of 21 Jax strains mals, congenital cystic ovaries frequent (J); tested (G. Schlager and R. S. Weibust, J. type B reticular cell tumors 54.5% in breed Hered., 67: 295, 1976); susceptible to S. ers (T. B. Dunn and M. K. Deringer, J. Nati. typhimurium C5 (J. Plant and A. A. Glynn, Cancer Inst., 40:771,1968); uniformly sus J. Infect. Dis., 733: ;72, 1976); androgen ceptible to Plasmodiumberghei infection (H. deficient (A. Bartke et al., J. Endocrino!.,75: Most ef al., Mil. Med., 737: 915, 1966); 441,1977); 30% lymphomas in both sexes resistant to Leishmania infection (D. J. (G. S. Smith ef al., J. Nati. Cancer Inst., 50; Bradley, Clin. Exp. Immunol., 30: 130, 1195,1973). Maintained by: Bg, J, Mod, Nii, 1977); hypersusceptible to infection with on, RI. Echinococcus multilocularis (Z. Ali-Khan, J. ParÃ¡sito!.,60:231,1974); resistant to Plas modium chabaudi (M. M. Stevenson ef al., C57BL/10ScSn Inbr (J): 7 + 136. Origin: see C57BL; Little Infect. Immun., 38: 80, 1982); hematocrit to W. L. Russell, to J. P. Scott at F26 as a separate subline, to Snell at F35-36. 54.1%, systolic Wood pressure 97 mm Hg Charac: behavior traits differ from C7BL/ (G. Schlager and R. S. Weibust, J. Hered., 67: 295,1976). Maintained by: J, N, Pt, Rl, 10J [V. H. Denenberg, Science (Wash. DC), 730:451,1959]; susceptible to Lelshmania Scr.Y. infection (D.J. Bradley, Clin. Exp. Immunol., 30: 130, 1977); intermediate susceptibility C57P/A Inbr (A): 115+. Origin: R. Korteweg, 1934; to rabies virus (D. L. Lodmell, Fed. Proc., DBA 9 X C57BL a, then N20 to C57BL, 41: 566, 1982); susceptible to S. typhimu then b x s inbred. Maintained by: A (for rium C5 (C. E. Hormaeche, Immunology, merly listed as P/A). 37: 311, 1979); resistant to Cryptococcus neoformans due to the He1 Ã¡ltete(J. C. C58 Inbr (J): 198. Genet: a. Origin: MacDowell, Rhodes et al., Infect. Immun., 29: 494, 1921, from mating of littermates 9 58 and Â¿ 1980). Has been used for the production of 52 of Miss Lathrop's stock; d 52 mated to congenie resistant lines differing from 9 57 gave rise to C57 strains. Charac: high C57BL/10ScSn by single histocompatibility incidence of leukemia before 1 year; fre loci (G. D. Snell and L. C. Stevens, Immu quent polyovular follicles; aplasia of kidney nology, 4:366,1961 ). Maintainedby: A, Ao, about 10% (J); 95% lymphatic leukemia in Cr, Crc, Dv, Dy, Eg, Fre, Grf, Gy, Hsd, 1er, both sexes (Urne);relatively resistant to P. Icrf, J, Kun, Lac, Ul, Mob, N, Ola, Ph, Pp, berghei infection (H. Most, Mil. Med., 737: Rl, Scr, Sf, Sg, Sx, Tu, W, Y. 915,1966); resistant to Cryptococcus neo formans due to the We1alÃele(J.C. Rhodes C57BR/cd Inbr (J): 178. Genet: a b. Origin: Ã¼ttte,from ef al., Infect. Immun., 29: 494, 1980); sex cross that gave rise to C57BL, C57BR/a, ratio 0.552 Â¿Â¿,highestof 30 Jax strains (J. and C57L. Black and brown lines were sep A. Weir, Genetics, 84: 755, 1976). Main arated in the first generation. Subline cd tained by: A, Dv, J, N, Ok, Ola, Ori, Scr, was established in gen. 13 from a cross of Wm, Y. 2 brown lines, one of which had previously given rise to C57BR/a. To Heston 1938, to DA/Hu Inbr (Mob): 125. Gent: c rd. Origin: Hummel, Jax 1947 at F66. Charac: low mammary brother and sister bom 12/48 to a noninbred "Swiss" with a mammary gland tu tumor, some hepatomas in &o (J); very re sistant to X-irradiation but sensitive to in mor. Charac: low mammary tumor; parti sulin (Lac); resistant to Leishmaniainfection tioned vaginas. Maintained by: Mob. (D. J. Bradley, Clin. Exp. Immunol.,30:130, 1977); resistant to Cryptococcus neofor- DBA Inbr (A): 7 + 126. Origin: Little, 1909, from mans due to the He1 Ã¡ltele(J.C. Rhodes ef color stocks. The oldest inbred strain. In al. Infect. Immun., 29: 494, 1980). Hema 1929-1930 crosses were made between tocrit 55.1%, systolic blood pressure 73 mm sublines and several new sublines were Hg (G. Schlager and R. E. Weibust, J. He- established. Two of these were 12 (now red., 67:295,1976). Maintained by: Han, J, called 1) and 212 (now called 2). Maintained Rl. by A, Cv, Rl.

CANCER RESEARCH VOL. 45 MARCH 1985 953

DBA/1 Inbr (J): 7 + 117. Genet: a b d. Origin: see the animals develop liver granulomas that DBA. Charac: resistant to most DBA/2 tu consist mainly of macrophages accumulat mors; P1534 grows in 50% of DBA/1; S91 ing ceroid-like lipopigment (Jena). High RBC grows in both strains; mammary tumors in count, low concentration of lipid in adrenals, about % of breeders over 1 year and in calcareous heart deposits (BLM-2). Main some virgins after 18 mo, susceptible to tained by: Ao, Bg, Bkl, Bog, Cox, Cr, Cri, inoculated TB (J); high RBC count, calcar Cum, Dub, El, Fhc, Fib, Fnn, H, Han, Hsd, eous heart deposits in almost all retired Ibg, Ico, 1er, Icrf, Imr, J, Jena, Ki, Lac, N, breeders (BLM-2); 61.5% mammary tumors Nii, Nmg, Novosibirsk, Ola, Ori, Pp, R, Rij, in breeders at 460 days, 8.4% leukemias, Ros, Saf, Ser, Sg, Sid, Sim, Smn, Sx, Sy, 3.8% primary lung tumors in 99 (Y). Uni Tac, Tru, Tu, Uct, Urne, Univ. Coll. London, formly resistant to Plasmodium berghei in We, Wn, Y, Yok. fection (H. Most, Mil. Med., 131:915,1966); susceptible to Lelshmania infection (D. J. DBAf Several lines. Not all are the same DBA Bradley, Clin. Exp. Immunol., 30: 130, subline or fostered on the same strain. 1977); highly susceptible to Schistosoma Charac: low tumor incidence, no mammary mansoni [M. M. Fanning, Parasite Immun. tumor agent. (Oxf.), 6: 95,1984]; resistant to Cryptococ- cus neoformans due to the He' alÃele(J. C. DC/Le Inbr (Le): 100. Genet: Dc/+. Origin: muta Rhodes ef al., Infect. Immun., 29: 494, tion to dancer arose in an obese stock 1980); susceptible toS. typhimurium C5 (C. outcrossed to a BALB/cHu x C3H/HeDi E. Hormaeche, Immunology, 37: 311, hybrid in 1956. One cross to C3H/HeJ, then 1979); susceptible to Coxiella bumetil infec inbred. Charac: semidominant mutation lo tion (G. H. Scott ef al., Lab. Anim. Sci., 28: cated on chromosome 19. HÃ©tÃ©rozygotes 673,1978). Maintained by: Bg, Glw, J, Lac, exhibit circling and head tossing behavior N, Novosibirsk, Ola, OrÃ,Ph, Ros, Ser, Tu, and are not deaf. Homozygotes die at birth Y. with cleft lip and cleft palate. Penetrance is incomplete. Maintained by: Le. DBA/2 Inbr (J): 150. Genet: a b d rd+. Origin: see DBA. Charac: tumor incidence varies be- DD Inbr (A): 91. Genet: A B c S. Origin: from tween colonies (SNISM-7); blood pressure noninbred ddN of Central Lab. Exp. Anim. relatively low [G. Schlager, Nature (Lond.), to Osaka Univ., 1956, to Heston 1957, to 272: 519, 1966]; audiogenic seizures in Nara 1959. Charac: mammary tumors 77% 100% at 35 days, 5% after 55 days; high in breeders; both sexes transmit mammary mortality in Ã´Ã´exposed to chloroform and tumor virus (Tbr). Maintained by: A, Novo oxidation products of ethylene oxide, and sibirsk, Tbr. to vitamin K deficiency (J); relatively resist ant to Plasmodium berghei infection (H. DDD Inbr (Hok): 81. Genet: A B c D S. Origin: dd- Most et al., Mil. Med., 737: 915, 1966); stock mice taken by Dr. S. Hata from Ger resistant to Leishmania infection (D. J. many to Kitasato Inst. before 1920 (dd = Bradley, Clin. Exp. Immunol., 30: 130, Deutschland-Densenbyo Kenkyosho). To 1977); susceptible toS. typhimurium C5 (C. Manchuria (K. Ando) and back to Japan; E. Hormaeche, Immunology, 37: 311, inbreeding begun by Suzuki in 1962 at Univ. 1979); most susceptible to Opisthorchis fel- Tokyo (A. Matsuzawa ef al., Jpn. J. Exp. ineus of 6 strains tested (A. G. Zelentsov, Med., 40:159,1970). Charac: carries mam Med. Parazitol. Parazitarnye Bolezni, 43: mary tumor virus; tumor incidence has de 95, 1974); resistant to Plasmodium cha- clined. Maintained by: Hok. baudi (M. M. Stevenson ef al.. Infect. Im mun., 38:80,1982); susceptible to Candida DDI Inbr: 83. Genet: a B c D S Hbb'. Origin: albicans (R. F. Hector ef al., Infect. Immun., animals from Lab. Infect. Dis., Tohoku Univ. 38:1020,1982); intermediate susceptibility in 1948 and 1953. Maintained by D. Taka- to Schistosoma mansoni [M. M. Fanning, suka (1948-1963), by H. Nikaido (1960- Parasite Immunol. (Oxf.), 6: 95,1984]; sus 1965), and by Sadao Ishigaki since 1965. b ceptible to Cryptococcus neoformans due x s inbreeding started April 1960 by Ni to He" alÃele(J. C. Rhodes ef al., Infect. kaido; F20 achieved March 1968. Selected Immun., 29: 494, 1980). Low alcohol pref only for good growth and reproductive per erence (C. W. Schneider ef a/., J. Comp. formance. Charac: pregnancy rate 82.7%, Physiol. Psychol., 82: 466, 1973); low mor av. litter size 8.2; survival rate at 20 days phine preference (G. P. Horowitz, Psycho- 97.8%; av. body wt. at 20 days 9.7 g pharmacology, 52: 119, 1977). About half (JEARA, 1973); induced the highest inter-

CANCER RESEARCH VOL. 45 MARCH 1985 954

feron titer as compared with ddy, ICR, C3H/ EBT/Ha Inbr (Cv): 63. Genet: a of e Gusa. Origin: He, C57BL/6J, BALB/c, and DBA/2 (S. cross of noninbred bt/bt x C57BL/Ha-e/e. Matsubara ef a/., Cell. Immuno!., 43: 214, To Chapman 1974. Charac: of/of. Main 1979. Maintained by: Tohi. tained by: Cv.

DDK Inbr: 105. Genet: A B c D S. Origin: K. EL Inbr (Yok): 84. Genet: El/El. Origin: K. Imai- Kondo, from so-called German mice (dd zumi, mutation in noninbred albino mice in stock) from Inst. Infect. Dis., Tokyo, in 1954. Charac: epilepsy-like behavior; brief, 1944. Charac: fertility is reduced when Ã‡Ã‡ violent convulsion after being tossed up are outcrossed, caused by embryonic death gently 10-15 cm several times; susceptibil at the morula-blastocyst stage (N. Waka- ity begins at about 7 weeks (K. Imaizumi ef sugi, J. Reprod. FÃ©rtil.,33:283,1973). Skel al., Bull. Exp. Anim., 8:6,1959). Maintained etal characters: fusion of frontal and perietal by: Yok. bones 94%, predominantly 26 presacrai vertebrae. RBC 8.5 Â± 0.22/10" cu mm, F/St Inbr: 140 +. Genet: a b c01 d s. Origin: hematocrit 48.9 Â±0.9%; WBC 5.81 Â±1.05/ Strong, from a group of unpedigreed Bus- 103 cu mm. Maintained by: Lac, Nga. sey Inst. mice. Charac: high leukemia in older animals regardless of breeding con DHS Inbr (Hok) 98. Genet: c. Origin: Germany to ditions; white head markings; resistant to Inst. Kitasato Med. Res. in 1910 to 1920, Leishmania infection (D. J. Bradley, Clin. to Inst. Infect. Dis. (Univ. Tokyo) in 1944, to Exp. Immunol., 30: 130, 1977). Maintained Hok July 1957; b x s inbreeding started in by: Hm, Lac, N, Pt. 1957. Charac: high incidence of polydactyly (R. Shoji and E. Ohzu, Zool. Mag. (Tokyo), FB/Ki Inbr (Ki): 58. Origin: Kirschbaum, 1942- 74:115,1965). Maintained by: Hok. 1952. Multiple crosses between A, F, and NH. Charac: reticular tissue neoplasms DKI Inbr: 92. Genet: a Be S. Origin: noninbred about 50%; some myeloid leukemia. Main ddN of Central Lab. Exp. Anim.; inbreeding tained by: Ki. started by B. Kitasato, 1953. Charac: uni form sensitivity to Salmonella enteritidis (D. FL/1 Re Inbr (Brk): 93 since establishment of f/f line, Ushiba et al., Jpn. J. Exp. Med., 32: 519, 1956. Genet: afrd Lv". Origin: flexed gene 1962). Maintained by: Jko. originally obtained from George Jay from Snell's WA linkage testing stock; 7 rounds DKI-R Inbr (Jko): N11 F36. Genet and Origin: see of cross-intercross to C3H by Jay and E. S. DKI. Offspring of DKI/Jko x C3H/He were Russell; outcross to WB/Re by Re; b x s backcrossed to DKI. Gene for relative re matings of f/f progeny started 1956. sistance to S. enteritidis was introduced Charac: homozygous W+/W+ f/f stock, with from C3H (D. Ushiba, Med. Biol., 83: 341, diffuse hemoglobin, both Â«-chain and fi- 1971). Charac: congenie with DKI but re chain hemoglobins characterized. FL/4, a sistant to S. enteritidis. Maintained by: Jko. line congenie to FL/1, is maintained, seg regating for W/+ and f/+. Fetuses and new- Inbr (Ra): 105. Genet: a se +/+ d1. Origin: DL bom of FL/1 show microcytic siderocytic balanced se +/+ d1 from Truslove to E. S. anemia, completely cured by 14 days. Var Russell, to Kelton 1958. Inbred by Kelton. iable belly spotting and tail flexure. Good Maintained by: Ra. breeding when young, later impaired by obesity. Maintained by: Brk, Mob. DLS Inbr (Le): 85. Genet: a se +/+ d1. Origin: mutation to d1 occurred in C57BL/Gr in FL/4Re Inbr (Mob): N30 F46. Origin: separated from 1950. Truslove to E. S. Russell 1957 as FL/1Re-f/+ W/+ at N30 in 1968; in 1980 to balanced stock. To Le 1968 at F32. Charac: barrier facility by hysterectomy derivation d'/d' die before weaning. Maintained by: Le. and fostering on C57BI/6J at N30 F28. Maintained by: Mob. DRC/Hok Inbr (Hok): ? + 48. Origin: DDD mated to C57BL/6; Fi offspring backcrossed 8 times FRG Inbr (Tbr): 35. Origin: non-inbred dd mice; to DDD, then b x s; to Hok in December Chugai Lab. to Tbr 1981 at F26. Charac: 1972 from Univ. Tokyo. Maintained by: Hok. resistant to Friend leukemia virus. Main tained by: Tbr. DW/J Inbr (J): 110. Genet: dw/+ In. Origin: Le to J 1966. Charac: dwarf, useful for endocrine FS Inbr (Dn): 77. Genet: b c01 frpsh-1. Origin: studies. Maintained by: Dt, J. Snell, linkage testing stock, to M. C. Green,

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to Eicher 1971, to Davisson 1983. Main Heston, to Chase, to E. L Green 1952, to tained by: Dn. Les 1956, to M. C. Green 1959, to Jax 1964. Mating pattern +/hr ? x hr/hr S. FSB Inbr (Dn): 98. Genet: a fr/+. Origin: furtess Charac: permanent near-hairlessness after mutation arose in unpedigreed stock at first moult; tylotrichs may persist up to 1.5 Ohio State Univ. in 1951; mutant $$ mated years (S. J. Mann, Anat. Ree., 770: 485, with C57BL/10<Ã•Â¿.Charac: low fecundity 1971). Some +//v tose most of their fur and viability; fs/fs have periodic partial hair- after 4 mo. Leukemia in hr/hr 45% at 8-10 lessness; all types of hairs are shorter than mo, 71% at 18 mo (H. Meier ef a/., Proc. normal (E. L. Green, J. Hered., 45: 115, Nati. Acad. Sci. USA, 63:759,1969). Hem- 1954). Maintained by: Dn. atocrit 50%, systolic blood pressure 63 mm Hg, lowest of 21 Jax strains tested (G. Inbr (Le): 50. Genet: gl +/+ dlj. Origin: GL/Le Schlager and R. S. Weibust, J. Hered, 67: mutation to gray-lethal discovered in a 195,1976); show premature decline in im stock segregating for c* by H. GrÃ¼neberg mune competence (H-J. Heiniger et al., Can in 1935. From G. Jay to M. Dickie to P. cer Res., 34: 201,1974); absolute and rel Lane. Inbred to F25. One outcross to dljÂ¡ ative kidney weight greatest of 21 strains dlj from heterogeneous stock and main surveyed [G. Schlager, Nature (Lond.), 272: tained b x s as balanced stock. Charac: 519,1968]). The Charles River "hairless" is recessive lethal mutation on chromosome not the same gene (S. J. Mann, J. Invest. 10. Homozygotes die at about 20 days of Dermatol., 56: 170, 1971). Maintained by: age. They lack the power of secondary J, Kun, Y. bone rÃ©sorption.Coat lacks yellow pigment. Maintained by: Le. HTG Inbr (Mob): 51. Formerly called H-2G. Main tained by: Ao, Mob. GLF Inbr (Y): 65. Genet: +. Origin: from Jax as bearers of gray-lethal mutation; selected for HTH Inbr (Ao): ? + 53. Formerly called H-2H. the normal genotype by progeny testing. Maintained by Ao. Maintained by: Y. HTI Inbr (Ao) ? + 54. Formerly called H-2I. Main GRS/A Inbr (A): 101. Genet: a c. Origin: MÃ¼hlbock tained by: Ao, Fre. obtained breeding pairs of "Grunder" mice from A. Grumbach, Zurich, in 1955 and HYIII Inbr (Le): 83. Genet: hy-3/+. Origin: muta inbred (0. MÃ¼hlbock,Eur. J. Cancer, 1:123, tion to hydrocephalus-3 discovered in a het 1965). Charac: breeding ?$ have nearly erogeneous stock by H. GrÃ¼neberg.To M. 100% mammary tumors, latent period 3 mo C. Green in 1963 and b x s inbred. To Lane (R. van Nie and J. Hilgers, J. Nati. Cancer 1975. Charac: recessive lethal mutation on Inst., 56:27,1976), highly hormone respon chromosome 8. Homozygotes die with sive, carries a mammary tumor agent differ frank hydrocephalus by 4-5 weeks. Main ent from MTI, transmitted both by milk and tained by: Le. gametes (G. Vlahakis, J. Nati. Cancer Inst., 59: 447, 1977). This strain was never se Inbr (N): 143. Genet: a b d p s; some lines lected for high mammary tumor incidence carry In and/or e0" and some do not. Origin: in contrast to many others. The host range Strong, 1926, from a group of unpedigreed of GRS mammary tumor virus is different mice. Charac: resistant to chemical induc from that of C3H mammary tumor virus. tion of tumors; complement is not detecta Very similar genetically to MAS/A: both ble (Urne); sex-linked phosphorylase kinase carry Hbb3 and Â»-2a*.15% leukemia in 63, deficiency (J. B. Lyon, Jr., Biochem. Genet., 38% lung tumor in <5<3.Maintained by: A 4: 169, 1970). Maintained by: Crgl, Cv, J, Bom, Fib, Imr, Js, N, Rij, Tbr. N, Ph, Y.

HLC/Ckc Inbr: 47. Origin: see LLC. Selected for high IC/Le Inbr (Le): 59. Genet: /c/+. Origin: Carter to leukocyte count. Charac: mean total leu Snell 1950, to M. C. Green 1970, to Lane kocyte count 36,000 (<Ã®<Ã®)to38,000 (??). 1975. Ic/ic from heterogeneous stock Thymus and spleen weights much higher crossed to CBA and nonsib followed by than in strain LLC (Ckc). Maintained by: sibmatings. A +/+ line was derived at F22. Harrison (JaxLab). Charac: homozygous ic/ic show abnormal clumping of chromatin in nuclei, most se HRS/J Inbr (J): 79. Genet: bed hr/+. Origin: hr verely in leukocytes. Useful as cell marker. stock originally from Crew to Camochan, to Maintained by: Le.

CANCER RESEARCH VOL. 45 MARCH 1985 956

Inbr (A): 70. Genet: a'. Origin: G. Bonser IF congenital malformations, except for fre (Leeds) in 1932-1936; selection for early quent tail kinks; suffers from minor inbreed papilloma development after treatment with ing depression: about 15% mortality of carcinogens. Charac: no mammary tumor newboms up to 3rd postnatal week (Jd). agent or spontaneous mammary tumors, Used for testing teratogenic effects of psy- but highly susceptible to induction by chem chotropic drugs (Jd). Maintained by: Cv, Jd. icals or the agent; susceptible to chemical ovarian tumor development; high incidence jE/Le Inbr (Le): 47. Genet: a f ru Â¡e/ru+. Origin: of pseudopregnancy. Maintained by: A. Fisher to Snell 1948, to Lane 1969, b x s since 1972. Charac: female/e/y'e are poor

IITES Inbr (Nga): 76 [ll-tester]. Genet: a b d s. mothers. Useful for linkage testing. Main Origin: crossbred among CS, DBA/2, NBC, tained by: Le. and ITES. Charac: useful for testing for color genes. Maintained by: Nga. JGBF Inbr (Ty): 55. Genet: a jg +/+ bf. Origin: mutation to jagged tail occurred in C3H/HeJ IS/Cam Inbr (Dn): 42+46. Genet: +. Origin: Mus in 1960. Crossed once to C57BL/10 and b musculus praetextus caught in Israeli port x s; crossed once to C57BL/6J-te and b x x M. m. musculus composite stock carrying s to F5; crossed once to C57BL/6J-bf and bf/bf, m/m, b/b, and a/a. Inbred by M. Wal inbred as balanced stock. Charac: homo- lace; to Roderick and Eicher 1971 at F42, zygous jg/jg usually bom dead in inbred to Dn 1983. Maintained by: Dn, H, Univ. strain; if they survive 66 are sterile and 9$ Coll. London. are poor breeders. Maintained by: Le, Ty.

ITES Inbr (Nga); 87 [l-tester]. Genet: a b d/+ s. ju Inbr (Ct): 99. Genet: a c. Origin: Falconer, Origin: Crossbred among CS, DBA/2, and 1952, from crosses involving Goodale's and SII in 1962. Charac: useful for testing for MacArthur's large strains, Bateman's high- color genes; radiation resistant, LD50/3ois lactation strain, and various mutant stocks 790 R. Maintained by: Nga. with about 50% of C57BL/Fa ancestry (D. S. Falconer, Mouse News Lett., 18: 5, IVCE Inbr (Csk): 73. Origin: separated during in 1958). Charac: av. first litter size 9 (Cam); breeding and selection of IVCS. Charac: high prenatal mortality (50%) in second lit docile; regular 4-day estrus cycle; littler size ters when gestation is concurrent with 9; mean body wt. at 70 days, 99 25.1 g, 66 suckling first littler (Fa); low penetrarle of 29.9 g (T. Nobunaga, Lab. Anim. Sci., 23: Nil (Cam). Maintained by: Ct, Fa. 803,1973). Maintained by: Csk. KE Inbr (Kw): 94. Genet: abc P. Origin: Krza- IVCS Inbr (Csk): 73. Genet: a B c S. Origin: from nowska, 1952, from mice of unknown ori ddN stock of Central Lab. Exp. Anim., se gin; cross also produced KP (H. Krza- lected for regular estrus cycling 1960. nowska, Mouse News Lett., 32: 54,1965). Named 4CS for "4-day cycle of vaginal Charac: mean litter size 6.1 ; tow percentage smear"; designation changed to conform of fertilized ova (H. Krzanowska, Folia Biol., with nomenclature rules. Charac: docile; 8: 269,1960); 17.6% of spermatozoa have regular 4-day estrus cycle established by abnormal heads, the inheritance of this vaginal smear; appearance of 3-day estrus characteristic being associated with the Y cycle by the proximity of males or by estra chromosome. Maintained by: Kw. dici injection (K. Takahashi, Bull. Nippon Vet. Zootech. Coll., 26: 109, 1977). Highly Â«F Inbr (Tbr): 48. Genet: a Be S. Origin: non- susceptible to toxoplasma (K. Kamei et al., inbred ddN stock of Central Lab. Exp. Anim. J. Parasitol., 62:714,1976). Maintained by: to Nara in 1964. Charac: recipient for Leydig Csk, Jic. cell tumor. Maintained by: Tbr.

J/Glw Inbr (Glw): 92. Genet: A b. Origin: Falconer. Kl Inbr (Glw): 141. Genet: c FuM/+. Origin: Charac: high frequency of cleft palate (M. Dunn and Gluecksohn-Waelsch. Charac: Vekemans and F. C. Fraser, Teratology, 75: kinky incomplete dominant; hÃ©tÃ©rozygotes 18A, 1977). Maintained by: Glw. show tail abnormalities; homozygotes die before birth. Maintained by: Glw. JBT Inbr (Jd): 86. Genet: a b bt. Origin: from Falconer's outbred JC stock [D. S. Fai- KK Inbr: 90 +. Genet: a B c D S. Origin: K. coner, J. Cell. Comp. Physiol., 56(SupplV Kondo, 1944, from Japanese dealer stock 153, 1960]. Charac: very low incidence of (Kasukabe group). Charac: small litters, 5.6.

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Frequent diabetes mellitus, occasional obe Charac: 55% late-occurring tumors of var sity in old animals (H. Iwatsuka et al., En ious types in 99,19% in dd (J. B. Storer, J. docrino!. Jpn., 17: 23,1970); skeletal char Gerontol., 21: 404, 1966); hematocrit acters: cervical rib 66%, predominantly 25 52.4%, systolic blood pressure 109 mm Hg presacrai vertebrae; liver and kidney ester (G. Schlager and R. S. Weibust, J. Hered., ase different from C57BL/6J and DBA/2; 67: 295, 1976); large amount of lipid in erythrocyte count 9.35 x 106, hematocrit adrenal glands in both sexes (BLM-2). Main 51.6%, hemoglobin 18.62, leukocyte count tained by: J, Univ. Helsinki (O. MakelÃ¤). 5.23 x 103. Maintained by: Jic, NY Med. Coll., Univ. Toronto. LPT/Le Inbr (Le): 89. Genet: Lp/+. Origin: mutation to loop-tail arose in A strain in 1949. From KP Inbr (Kw): 91. Genet: ab p. Origin: see KE. W. Hollander to G. Snell 1950. Crossed 7 Charac: mean litter size 5.0; high embryonal times to C57BL/6J, once to C3H/He, then and postembryonal mortality; frequent ster b x s. To Lane 1969. Charac: semidominant ile matings; low sperm production and low on chromsome 1. HÃ©tÃ©rozygoteshave libido of d<5;testis abnormalities; degenera looped or crooked tails and often show tion of some tubules and cells, large amount head wobbling. 99 have high incidence of of interstitial tissue (B. Godowicz, Folia imperforate vagina. Homozygotes die at Biol., 73:297,1965). Maintained by: Kw. birth. Maintained by: Le.

KR Inbr (Nga): 102. Genet: A B c D S. Origin: LS/Le Inbr (Le): 80. Genet: a* /s/++. Origin: mu as KK, 1952. Charac: good reproductive tation to Is occurred in C57BL-a'at Harwell. performance; liver and kidney esterase like Phillips to Lane as balanced stock 1961. DBA/2; imperforate vagina 2%. Maintained Charac: homozygous /s//s develop mega- by: Nga. colon but some live and breed. Maintained by: Le. KSB Inbr (Nga): 80. Genet: a B D s. Origin: as KK, 1944-1948. Charac: resembles KK. LT Inbr (Sv): 121. Genet: a fl*. Origin: Mac- Maintained by: Nem, Nga. Dowell, 1950, mutation at the brown locus in strain C58, outcrossed to BALB/c. To LG Inbr (J): 104. Genet: a c. Origin: developed Chase, to Re in 1957 at F28. Charac: hair by Goodale through selection for large size, almost white except for blackish tip. Spon beginning in 1931; inbred by Runner. taneous ovarian teratomas in about one- Charac: birth wt. 1.8 g, 28-day wt. 20.1 g, half of females (L. C. Stevens and D. 60-day wt. 47.4 g. Av. litter size 6, sex ratio Vamum, Dev. Biol., 37: 369, 1974). Main 56% dd, mean life span 491 days; docile, tained by: Cv, Hok, Lac, Ph, Sv. thyroid activity low. Maintained by: J. LTS/A Inbr (A): 98. Genet: c. Origin: MÃ¼hlbock, LIS/A Inbr (A): 101. Genet: c. Origin: MÃ¼hlbock, from P. Loustalot, Ciba, Basel, in 1954. from Hyg. Inst. ZÃ¼richin 1955; closely re Charac: high mammary tumor incidence in lated to STS/A and LTS/A (J. Hilgers, per both virgins and breeders; closely related sonal communication). Charac: low mam to LIS/A and STS/A, as deduced from iso- mary tumor incidence in 99, lung tumors in zyme pattern. A fostered low tumor line, both sexes. Maintained by: A. LTSv/A, is also kept. Maintained by: A.

Inbr (J): 132. Genet: c. Origin: Marsh's LLC/Ckc Inbr: 46. Origin: from a hybrid stock derived MA by cross-breeding C57BL/6J, C57BR/cdJ, strain 3; started from a pair of mice from A/J, BALB/cJ, LG/Ckc, and SM/Ckc. Se the Lathrop-Loeb colony; 32 gen. of cousin lected for low and high leukocyte count (see matings by Marsh, to W. S. Murray who also HLC). Charac: mean total leukocyte inbred b x s. Charac: 5% gross tumor inci count 4000-5000/cu mm. All mice 10-18 dence in virgin 99, 0% in dd; polydipsia- mo old have amyloid deposition in spleen polyuria 79% in virgin 99, 12% in dd; 25% and kidney; most exhibit reticular cell hy- gross kidney disease in dd (J. B. Storer, J. perplasia (C. K. Chai, Am. J. Patriot., 85: Gerontol., 21: 404, 1966). High resistance 49, 1976). Thymus and spleen weights to chronic whole-body X-irradiation; pitui much lower than in strain HLC. Maintained tary cysts in over 50% (J); reduction in size by: Gorevic (SUNY Stony Brook), D. Harri of lateral septal nucleus (R. E. Wimer). Hem son (JaxLab). atocrit 49%, systolic blood pressure 128 mm Hg, highest of 21 Jax strains tested (G. LP/J Inbr (J): 125. Genet: A" s. Origin: Dunn. Schlager and R. S. Weibust, J. Hered., 67:

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295, 1976). Serum ai-antitrypsin at mid ing (H. U. Aeschbacher ef a/., MutÃ¢t.Res., point of 34 strains tested (S. K. Chan, Arch 59: 301, 1973). Charac: more susceptible Environ. Health, 27:272,1973). Maintained than other strains to several mutagens/car- by: J, Wim. cinogens. Maintained by: Ae.

MAS/A Inbr (A): 98. Genet: c. Origin: MÃ¼hlbock,as MWT Inbr (Le): 59. Genet: a'Mf" W T. Origin: M. GRS/A. Charac: low mammary tumor inci C. Green,from heterogeneous background, dence in 99, high lung tumor in both sexes. about 1959. Charac: has been character As in BALB/c, this strain is susceptible to ized for many polymorphic loci. Useful for both C3H mammary tumor virus and GRS linkage testing. Maintained by: Le. mammary tumor virus. Very similar to GRS/ A; of over 50 genetic markers, only 2 are MYD/Le and Inbr (Le): MYD N7 F11, MYD-+/+ 65. Ge different. Maintained by: A. MYD/Le-+/+ net: Os +/+ myd. Origin: mutation to myd occurred in 1963 in te stock received from MK/Re Inbr (Ty): 78. Genet: mk/+. Origin: Jax mu R. Phillips in 1961. Crossed to C57BL/6J- tant 63-36, B6D2F,-mfr from M. M. Dickie A^/A^and sib-mated; a +/+ line was de to Re, 1963. Charac: segregates for com rived at F35. Charac: homozygous myd/ pensating microcytic anemia. All mk/mk are myd show a progressive and diffuse my- bom alive; Vs to Vz die before 3 weeks, opathy in all skeletal muscles and die be developing skin lesions and tail amputation, tween 5 weeks and 5 mo. Maintained by: but surviving mk/mk are fertile and appear Le. normal except for supernormal numbers of very small erythrocytes. Hematology well N/St Inbr (Ao): 119. Genet: a b d s. Origin: characterized (BLM-2). Maintained by: Bn, Strong, about 1926, from a group of un- Ty. pedigreed mice; ancestral to PBR strain. Charac: low tumor incidence, resistant to MOR/Cv Inbr (Cv): 44. Genet: a Mor-1". Origin: wild chemical carcinogenesis. Maintained by: trapped in Ohio by Bruell; to T. Shows, Yale Ao. Univ., to Chapman, 1972. Charac: mito chondria! malate dehydrogenase varient NBR Inbr (Nga): 90. Genet: a b. Origin: from MOR-1B (T. B. Shows ef al., Biochem. Ge mongrels of Japanese fancy mice (Nishiki- net., 4: 707,1970). Maintained by: Cv. Nezumi group) between 1944 and 1949 (K. Kondo ef a/., Bull. Exp. Anim., 6:107,1957). MRL Inbr (J): 65. Genet: a c lpr/+. Oirgin: E. D. Charac: poor reproductive performance; Murphy, from a series of crosses involving liver and kidney esterase like DBA/2. Main C57BL/6J, C3H/DÃŒ,AKR/J,and LG/J fol tained by: Nga. lowed by b x s inbreeding; matings are made to produce /pr//pr, /pr/+, and +/+. NC Inbr (Nga): 112. Genet: A b. Origin: K. Charac: Ipr/lpr mice have massive general Kondo, from Japanese fancy mice (Nishiki- ized lymph node enlargement beginning by Nezumi). Charac: leukocyte count 2.95 x 8 weeks of age and progressing to over 103/ml, erythrocyte count 9.06 x 106/rnl, 100 times control lymph node weight by 16 hematocrit 50, hemoglobin 19 g/100 ml. weeks. $9 die at approx. 17 weeks and

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with BÃ³rdeteIla pertussis. Charac: no eco- NZO. Charac: autoimmune hemolytic ane tropic murine leukemia virus inducibility [C. mia; extramedullary erythropoiesis (Ori); lu A. Kozak and W. P. Rowe, Science (Wash. pus-like nephritis (Scr); high incidence of DC), 204:69,1979]. Maintained by: Cr, Fib, chronic gastroduodenal ulcÃ©ration (J. B. Ul, N. Howie, Proc. Univ. Otago Med. Sch., 62: 7, 1984); spontaneous hypertension and hy NGP/N Inbr (N): 69. Genet: a c. Origin: a randomly pertensive vascular disease (U. G. Svend- selected litter from the NIH General Purpose son, Acta Pathol. Microbio!. Scand., 85A- outbred stock N:GP(S). Maintained by: N. 548, 1977); susceptible to Cryptococcus neoformans due to the He" alÃele(J. C. NH Inbr (Ao): 109. Genet: a d p s. Origin: Rhodes ef al., Infect. Immun., 29: 494, Strong, from crosses involving CBA, N, and 1980); resistant to Leishmania infection (D. JK. Charac: low tumor incidence; nodular J. Bradley, Clin. Exp. Immunol., 30: 130, hyperplasia and adrenal adenomas in at 1977). Maintained by: A, Cr, Hok, Hsd, J, least 10% of old mice; gonadectomy at 6 Lac, N, Ola, Ori, Scr, Urne, A. Gabrielson weeks enhances adenomas; some obesity; (Albany). breeding ceases at approx. 9 mo. Main tained by: Ao, Ki, N, Pt. NZBR Genet: a b. Origin: from NZB/BI at F73, brother-sister pairs with brown coat color. NIH/Ola Inbr (Ola): ? + 27. Genet: a herd. Origin: Charac: spontaneous autoimmune hemo Pitman at NIH, from N:NIH(S) stock, to Nati. lytic anemia, like NZB. About 20% of

CANCER RESEARCH VOL. 45 MARCH 1985 960

tion's foundation stock. Charac: glomeru- PAA Inbr: 45. Origin: live-trapped pair from a lonephritis beginning at 13 mo (J); hybrids Philadelphia factory (J. L. Connor, J. Comp. between NZB and NZW develop lupus ne Physiol. Psychol., 89:118; 1975). See also phritis with positive LE cell tests (Lac) and next 4 strains. Charac: reasonably fertile, antinuclear antibodies (Umc); susceptible to no obvious abnormalities. Maintained by: N. Leishmania infection (D. J. FVadley, Clin. Henderson (Oberlin Coll.). Exp. Immunol., 30:130,1977). Maintained by: Cr, Hsd, J, Mcd, N, Ola, Ser, Umc, Y, PAB Inbr: 42. Origin: see PAA. Charac: small A. Gabrielsen (Albany). The subline main litters, otherwise fertile; white spot on fore tained by Univ. Otago has been designated head of 91 % of breeders. Maintained by: as OUW. PAA.

NZX Inbr (Wehi): 90. Origin: see NZO. From an PAC Inbr: 42. Origin: see PAA. Charac: relatively NZC 9 (F33) and an NZY 6 (F27), offspring infertile unless maintained on vitamin A and b x s mated. Charac: from F13, some 99 D supplements. Deterioration of skin and have shown imperforate vagina, and both epithelium starts at about 3 days, producing sexes have a low incidence of megacolon. eventual baldness and skin lesions. Main Maintained by: Wehi. tained by: Cv, N. Henderson (Oberlin Coll.).

NZY Inbr (Wehi): 120. Genet: b s. Origin: see PAD Inbr: 45. Origin: see PAA. Charac: relatively NZO; a piebald a which appeared at F2 was infertile even with vitamin A and D supple mated with a tan sister; at F4 a piebald ments; slow breeder. Maintained by: as brother-sister appeared; b x s mating with PAA. selection for s led to fixation of the coat pattern at F7. Charac: high mammary can- PE Inbr (RI): 90+. Genet: pe/+. Origin: The cer incidence associated with pituitary en mutation pe arose in C3H/HeRI. b x s mated largement in breeders; heritable megacolon (pe/+ x pe/pe). Maintained by: Rl. (Bl); highly susceptible to ovarian tumor in duction by chemicals (Ber). Maintained by: PET Inbr (Wmr): 91. Origin: mixed stock of C3H Wehi. and black pet shop mice, Med. Coll. Va. 1956, to Wmr 1958. Charac: Pigmented O20 Inbr (A): 194. Genet: a c. Origin: R. Kor- Extraepidermal Tissues; occasional mam teweg, 1931, from an Amsterdam petshop mary tumors in older 99. Maintained by: (P. I. Van Gulik and R. Korteweg, Am. J. Wmr. Cancer, 38: 506,1940). Charac: Mammary tumor 0% in virgins, 5% in breeders, 13% PF Inbr (Fo): 35. Genet: a s tef/+. Origin: selec in force-bred; believed not to carry the milk tion for high expression of hindfoot polydac- agent, but susceptible to it and can transmit tyly. Charac: high expression of forefoot it to offspring (0. MÃ¼hlbockand T. G. van and hindfoot polydactyly and occasional Rijssel, J. Nati. Cancer Inst., 15: 73,1954). moderate tibial hemimelia in hÃ©tÃ©rozygotes, Maintained by: A, Cv, Sid. great reduction of radius and tibia in homo zygotes. Maintained by: Fo. P/J Inbr (J): 153. Genet: a b d se p rd. Origin: Snell, extracted following outcross of similar PHH Inbr (We): 95. Genet: a In. Origin: Weir, from stock (BDP) developed by W. Gates. MacArthur outbred stock obtained from Charac: high resistance to chronic whole- Butler 1949; b x s inbreeding with selection body irradiation. Tumor incidence: 23% var for high blood pH. Charac: blood pH 7.48 ious kinds in virgin 99, 6% in 66; some Â±0.004, blood lactic acid 3.6 Â±0.2 mol/ml. polycystic or granular kidneys, both sexes; CO2 output 5.90 Â± 0.01 mg/hr/g body mean life span 510 days in virgin 99, 384 weight, sex ratio 0.535 66 (J. A. Weir. Ge days in 66 (J. B. Storer, J. Gerontol., 21: netics, 84: 755, 1976). Overall fertility low. 404,1966). Sex ratio 47% 66, lowest of 30 Maintained by: We. Jax strains (J. A. Weir, Genetics, 84: 755, 1976). Hematocrit 54.5%, systolic Wood PHL Inbr (We): 97. Genet: a* b In. Origin: same pressure 94 mm Hg (G. Schlager and R. S. as PHH, selected for low blood pH. Charac: Weibust, J. Hered., 67: 295,1976). Serum Wood pH 7.43 Â±0.004, blood lactic acid ai-antitrypsin highest of 34 strains tested 5.4 Â±0.3 mol/ml, CO2 output 5.90 Â±0.03 (S. K. Chan, Arch. Environ. Health, 27:272, mg/hr/g body weight, sex ratio 0.435 66 (J. 1973). Maintained by: Cr, Glw, J, N, Univ. A. Weir, Genetics, 84: 755, 1976). Overall Coll. London. fertility high. Maintained by: We.

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PL Inbr (J): 130. Genet: c. Origin: from non- Kanwar ef al., Biomedicine (Paris), 22:209, inbred "Princeton" mice started in 1922 1975]. Maintained by: Brk. from 200 mice purchased from a dealer (J. B. Nelson, J. Infect. Dis., 82: 169, 1948). PUH/Cam Inbr (Cam): 50. Origin: wild Peru-Harland x Inbred by Lynch, giving rise to a high leu CBA. Wild mouse from Rimach Valley in kemia line B (PL) and a second line (PLA) Peru (Mouse News Lett., 67: 28, 1979). with lower incidence. Maintained by: J, Pt. Charac: many mutations in this strain. Main Sf. tained by: Cam.

RBA/Dn PM/Se Inbr: 80. Origin: C. Biancifiori, Perugia; Inbr (Dn): ? + 25. Genet: A. Origin: derived C3Hb ? x BALB/cfC3H a, descendants sib- from wild mice captured near Mutten, Albula mated with selection for high incidence of Valley, Grisons, S. E. Switzerland [A. Gropp mammary tumors. Charac: high mammary and H. Winking, Chromosoma (Beri.), 39: tumor incidence; polycystic kidney trait 265,1972]. Gropp to Davisson and Roder ick 1977, to Davisson 1981. Charac: homo- arose in the 49th inbred generation, trans mitted as an autosomal recessive charac zygous for Robertsonian translocation Rb(4.12)9Bnr; males are aggressive; has teristic (R. Ribacchi, Lav. Ist. Anat. Istol. Patol. Univ. Studi Perugia, 37: 27, 1977): never been outcrossed to a laboratory Maintained by: Perugia. strain. Maintained by: Dn.

RBB/Dn Inbr (Dn): ? + 35. Genet: A. Origin: derived PN Inbr: 52. Genet: c. Origin: albino mice from from wild mice captured near Bondo, Val a pet shop in New Zealand in 1948. Off spring were named "TW outbred" and Bregaglia, Grisons, S. E. Switzerland [A. Gropp and H. Winking, Chromosoma raised at Palmerston North Hosp. Some (Beri.), 39: 265, 1972]. Gropp to Davisson were taken to Massey Univ. where they were renamed "NOS outbred." NOS were and Roderick 1977, to Davisson 1981. Charac: homozygous for Robertsonian sent to Glaxo Labs of New Zealand and named "GW ourbred." Breeding pairs were translocation Rb(1.10)1 OBnr; probably have never been outcrossed to a laboratory returned to Palmerston North Hosp. where they were renamed "PN mice" and main strain, but not as wild as RbOBnr. Main tained by: Dn. tained in the Med. Res. Dept. under Dr. Wigley. Inbreeding started 1964, with selec- RBC/Dn Inbr (Dn): ? + 33. Genet: c. Origin: the tion for positive ANA tests in the first 3 Robertsonian translocation Rb(8.17)1lem generations. The primary breeding line was arose in "a colony of nonlinear white mice" named PN/nA. At F9, a subline (PN/nB) was at the Inst. Exp. Med. In Leningrad (V. S. started by cousin-cousin mating and contin Baranov and A. P. Dyban, Ontogenez, 2: ued with b x s. Subline A mice were dis 164,1971 ), originally from Rappolovo Nurs carded in 1975. Cesarean-derived mice ery of the Academy of Medical Sciences of were raised on pathogen-free CD-1 fe the USSR; to Gropp, to Davisson and Rod males. Charac: animal model of systemic erick 1977, to Davisson 1981. Maintained lupus erythematosus; positive tests for an- by: Dn. tinuclear antibodies appear at 5 mo; 80% are ANA positive by 10 mo. Glomerular Inbr (Dn): 60. Genet: c F*. Origin: derived deposits of IgG, IgM, IgA, and complement from crosses of Swiss mice (probably appear at 2-4 weeks. Neoplasms in 14% NMRI/Han; Gropp, personal comunication (S. E. Walker ef al., J. Lab. Clin. Med., 97: to Dn) to wild mice captured in the Valle di 932,1978). Maintained by: Hm, Mac. Poschiavo in S. E. Switzerland. The wild population was originally published as the Inbr (Brk): 61. Genet: ac0" p Pro-f. Origin: "tobacco" mouse because of their coat PRO E. S. Russell, 129/ReJ x C57BL/6J, prog color. They also appear in the literature as eny tested for a, e0", and p; b x s inbred. Mus poschiavinus Patio and more recently Charac: hyperprolinemia and prolinuria, in Mus musculus poschiavinus [A. Gropp ef a/., Cytogenetics (Basel), 9: 9, 1970]. F1's creased taurine excretion (R. L. Blake ef a/., Life Sci., 14:1285,1974); altered polyamine from Alfred Gropp (probably via F. Ruddle) metabolism (C-A. Manen ef a/., Biochem. to Roderick in 1970, b x s ever since; to J., 758: 529, 1976); aminonucleoside ne- Davisson 1981. Charac: homozygous for phrosis (Y. S. Kanwaref al., Proc. Soc. Exp. Robertsonian translocations Rb(1.3)1Bnr, Bid. Med., 755:339,1977); sluggish move Rb(8.12)5Bnr, and Rb(9.14)6Bnr. Main ments, 50% generalized hair loss [Y. S. tained by: Dn.

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RF Inbr (J): 113. Genet: a c. Origin: Furth, 1928, Rill Inbr: 80+. Genet: c. Origin: Dobrovolskaia- from Rockefeller Inst. General-purpose Zavadskaia, Inst, du Radium, Paris, 1928 stock of domestic origin, transferred to Oak (N. Dobrovdaskaia-Zavadskaia, C. R. Soc. Ridge. History somewhat questionable. Biol., 704: 1191, 1930). Charac: have milk Charac: up to 50% leukemia (Ms); skin agent; non-mammary tumors rare; urethan painting with methylcholanthrene markedly causes hepatic angiomatosis; susceptible enhances leukemia incidence (M. L. Duran- to Graffi virus; resistant to gold thioglucose Reynals ef al., J. Exp. Med., 147: 459, obesity (Rd). Mammary tumor incidence 1978); glomerulosclerosis progressive with 65-95%. Maintained by: A, Imr, Rho, Sy, age (W. D. Gude and A. C. Upton, J. Ger- Univ. Helsinki (O. MÃ¤kelÃ¤). ontol., 15:373,1960); midrange of radiation resistance (BLM-2); resistant to infection Rill/An Inbr (N): 105. Genet: A c. Origin: see Rill. with Sendai virus (J. C. Parker ef a/., Infect. Charac: 45% mammary tumors in virgin $$, Immun., 19: 123, 1978). Maintained by: J, 10% various tumors in dd; mammary tumor Ok, Univ. Helsinki (O. MÃ¤kelÃ¤). incidence in one line declined from 100% in breeders and virgins in 1954 to less than RFM/Un Inbr: 120+. Genet: a c. Origin: Furth, to Oak 3% in 1961 (H. B. Andervont and T. B. Ridge 1949. Charac: 78% leukoses, 26% Dunn, J. Nati. Cancer Inst., 28:159,1962). lung tumors (G. E. Cosgrove ef al., J. Ger- Have audiogenic seizures at sufficiently ontol., 33:178,1978); ovarian tumors 3.8% loud sounds (Up); hematocrit 50.1%, sys (N. K. Clapp, RadiÃ¢t.Res., 74: 405,1978); tolic blood pressure 79 mm Hg (G. Schlager leukemia higher after X-irradiation. Main and R. S. Weibust, J. Hered., 67: 295, tained by: Cr, Bd, Rij. 1976). Maintained by: Ki, N, Ok.

Inbr (Le): 72. Genet: hr^l+a b c. Origin: RIIIS/J RHJ/Le Inbr (J): 59 since reconstitution. Genet: c mutation to rhino-J arose in a Carworth rd. Origin: in 1967, both RIII/AnJ (at F66) Farms stock received by E. P. Nagler. Na- and RIII/J (at F58) stopped producing viable gler returned the mutation to C. F. and C. young. The following crosses were made: F. sent it to M. M. Dickie, 1951. To Lane RIII/AnJ x SEC/1 Re, 9 progeny mated to a 1960. Crossed to BALB/cHu 6 times, b x s RIII/AnJ. ? progeny of that cross-mated to to F16. One outcross to c/c Hk/+ stock a RIII/J d- Charac: as Rill/An except that and b x s. Charac: mutation on chromo RIIIS/J mice can be expected to have Vaof some 14. Homozygotes begin to lose hair their genes derived from SEC/1 Re (L. E. at about 10 days; skin becomes thicker and Mobraaten, Mouse News Lett., 57: 20, more wrinkled than in hr/hr. Females do not 1977, and Mouse News Lett., 60:49,1979). nurse young. Maintained by: Le. Maintained by: J.

RNC Inbr: 50+. Genet: nu Re/++. Origin: 3 pairs SB/Le Inbr (Le): 101. Genet: sa bg Aw rd. Origin: of mice from R. C. Roberts, Edinburgh, in mutations to sa and bg, possibly radiation Oct. 1968. $9 were heterozygous nu and induced, occurred independently in stocks Tr, So were heterozygous nu and Re. Tr used for mutation rate studies at Oak was lost. Recombinant Re nu/+ + were Ridge; nonsib pair from Rl to Le 1961; sib- mated and b x s continued for 16 gen. (B. mated since. Charac: high susceptibility to A. Croy and D. Osoba, J. Immunol., 773: chronic respiratory disease. Maintained by: 1626, 1974). Maintained by: B. A. Croy, Le. Brock Univ. (St. Catherines, Ontario, Can ada). SD Inbr(Glw): 122. Genet: cSd/+. Origin: Dunn and Gleucksohn-Waelsch. Charac: Sd in ROP Inbr (Le): 67. Genet: Ra/+ Os/+ Pf/+. Ori complete dominant affecting axial skeleton gin: M. C. Green from very heterogeneous and urogenital systems; homozygote lethal background in 1960; to Lane 1975. Charac: after birth. Maintained by: Glw. useful for linkage testing. Maintained by: Le, Ori. SEA Inbr (J): 142. Genet: b d +/d se. Origin: E. L. and M. C. Green, from BALB/c x P. RSV Inbr (Le): 66. Genet: Re/Re Sd/+ Va/+. Charac: host for transplantable rhabdomy- Origin: Carter's Stock 1 (Edinburgh linkage osarcoma T811. Maintained by: J, Rl. testing stock E1) to Woodworth 1950. Out- crossed to C57BL/6, CBA, and C3H and SEC/RI Inbr (RI): 100+. Genet: a b cc" of se/++. non-sib-mated. To Lane 1967, b x s there Origin: from E. L. Green 5/19/48 at F20 and after. Maintained by: Le. F21. Maintained by: Pp, Rl.

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SEC/1 Gn Inbr (Le): 149. Genet: a b cch se/+. Origin: of virgin 9$ at av. age 13.3 mo, 88% of Green, from cross of NB x BALB/c. Charac: breeders at 13.5 mo, 91% of Ã¢Ã¢at12.5 mo; multiple lung cysts, especially in se/se. high resistance to chronic whole-body X- Maintained by: Le. irradiation; relatively large litter size. Fastest heart rate of 7 strains tested (D. A. Blizard SEC/1 Re Inbr (J): 138. Genet: a b e0". Origin: from and R. Welty, J. Comp. Physiol. Psychol., SEC/1 Gn, short-ear eliminated by E. S. 77:337,1971); susceptible to experimental Russell. Charac: excellent breeder (Re); autoimmune thyroiditis [A. O. Vladutiu and serum ai-antitrypsin second highest of 34 N. R. Rose, Science (Wash. DC), 174:1137, strains tested (S. K. Chan, Arch. Environ. 1971]; 71 and y2 paraproteinemia [H. J. Health, 27: 272, 1973). Maintained by: El, Wanebo ef al., Science (Wash. DC), 754: J. 901,1966]; plaque-forming cell response to SHI begins to decline by age 42 weeks (A. SF/Cam Inbr (Dn): 42 + 32. Genet: +. Origin: wild M. Smith, J. Immunol.. 776:469,1976); <Ã®:9 mice trapped in a coal mine and sib-mated sex ratio at weaning 46:54; dd have low to F10 by M. Bamawell (Berkeley, CA) as erythrocyte count (C. G. Crispens, Lab. "Corte Madera," to Cambridge 1959. Anim. Sci., 23: 408, 1973); hepatosplenic Charac: adrenal X-zone relatively and ab amyloidosis after 6 mo (Rd); highly resistant solutely large in 99; very poorly developed to measles virus (P. A. Neighbour ef a/., zona glomerulosa (M. E. Wallace, Environ. Infect. Immun., 27: 764, 1978); least sus Pollut., 1: 175, 1971). Maintained by: Dn, ceptible to Sendai virus of 19 strains tested Rk. (J. C. Parker ef al.. Infect. Immun., 79:123, 1978). Maintained by: A, Cr, Crc, Han, Hok, SH1/Le Inbr (Le): 78. Genet: c^ sh-1/tÃa<+.Origin: J, N, Ola, Ort, Pt, Scr, Wn, Y. Snell's FS stock to M. C. Green. Out- crossed to C57BL/1 OGn and b x s. To Lane SK/Cam Inbr (Dn): ? + 38. Origin: from 3 mice trap 1975. Charac: homozygotes show circling, ped on Skokholm Island off Pembrokeshire head tossing, deafness, and hyperactivity. in 1962 (R. J. Berry); inbred by M. Wallace. Maintained by: Le. Charac: fairly large litters, the size of which dropped little on inbreeding. Maintained by: SHN Inbr (Mei): 51. Genet: Abe. Origin: SWM/ Dn, Rk. Ms from Nati. Inst. Genet., Misima, Dec. 1963. Lines were selected for high early SL/Ms Inbr (A): ? + 90. Genet: A B c. Origin: mammary tumor incidence and for high late derived from SMA as high-leukemia strain incidence; SHN is early tumor line, see a/so by K. Tutikawa; in Misima, leukemia inci SLN; b x s started April 1964; F20 attained dence is low. Maintained by: A, Ms, Wn. in June 1972. Charac: have mammary tu mor incidence, tumor incidence 90-100% SLN Inbr (Mei): 45. Origin: see SHN; SLN is the in breeders at 6.6 mo, slightly tower in vir high-late-tumor incidence line. Charac: gins (H. Nagasawa, Exp. Anim., 28: 561, mammary tumor incidence 50-60% in 1979); litter size 7.6, weaning rate 89%. breeders, 9-10% in virgins at 10 mo, litter Maintained by: Mei, Tbr. size 5.8, weaning rate 60%. Maintained by: Mei, Tbr. SHR Inbr (Dn): 59. Genet: fÃe+/+ shm. Origin: E. L. Green, shm mutation arose in random- SM Inbr (J): 112. Genet: Aw/a or a/a. Origin: bred stock in March 1960. Crossed on suc MacArthur, 1939, by crossing 7 stocks (in cessive occasions to C57BL/6J, C3HeB/ cluding DBA) and selecting for small body FeJ, and finally to rex linkage testing stock. size; to Runner in 1948, who began b x s Antecedent strains SHM and SHM/2 were mating. Charac: small body size at birth and discontinued in 1970 and 1977. Charac: at weaning; relatively small size tends to homozygotes have abnormal gait, small disappear as the animals mature; very low body size, phospholipidosis, sterility, low tumor incidence of any kind; both sexes live viability (Gn). Maintained by: Dn. for 570-600 days (J); amyloidosis at 1 year or older (Ml). Maintained by: A, Cv, H, J, SJL/J Inbr (J): 104. Genet: c p rd. Origin: Swiss Sid, Univ. Coll. London, Univ. Helsinki (0. Webster stock of 3 sources that were MÃ¤kelÃ¤). brought to Jax between 1938 and 1943. Pen-bred until 1955 when b x s was started. SRH Inbr (Nmg): 50. Origin: van Abeelen, C57BL/ Charac: multicellular reticulum cell sarco 6J x DBA/2J, backcrossed to DBA/2 4 mas resembling Hodgkin's disease in 91% gen., followed by b x s with selection for

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behavioral traits. Charac: high frequency of STU Inbr: 90. Origin: Swiss; GÃ¶nnert,Bayer-Lev exploratory rearing responses and high lo- erkusen, to Max-Planck-lnst. FÃ¼rVirus comoter activity [J. H. F. van Abeelen, Na forsch. (TÃ¼bingen)in 1950. Charac: used ture (Lond.), 254: 239, 1975]. Maintained for passage of Ehrlich asertes tumor and by: Nmg. Rous sarcoma virus-induced fibrosarco- mas, and for transplantation experiments SRL Inbr., Genet., and Origin as SRH. Charac: with Rous sarcomas. Maintained by: Tu, low frequency of exploratory rearing and Tumor Bid. Unit (Univ. Florida, Gainesville). low locomoter activity. Significant develop mental age-dependent differences between STX/Le Inbr (Le): 59. Genet: E^/F0 Tw/+ Xfy/+. SRH and SRL in behavioral components (J. Origin: M. C. Green, from F" on C3H from H. F. van Abeelen and A. H. Schoones, N. Bateman to M. Foster to M. C. Green Dev. Psychobiol., 10:17,1977). Maintained 1966; Tw from M. Lyon to M. C. Green in by: Nmg. 1967 and b x s inbred. Charac: has been characterized for many polymorphic loci; Genet: H-2". Subline separated after con ST/a useful for linkage testing. Maintained by: siderably more than 8 gen., differs from ST/ Le. b at the H-2 locus. Maintained by: Fib, Si.

Swiss Various lines from mainly commercial ST/b Inbr (J): 143. Genet: abcrd H-2*. Origin: a sources, inbred in different laboratories, as Mrs. Street started breeding Danish white mice in 1932 as a closed colony; Engel- ICR/Bc, SW/Fr, SWJ/Mk, SWM/Ms, etc. breth-Holm started b x s mating about SWR Inbr (J): 148. Genet: c rd. Origin: 1926, 1940. Eh to Heston 1947 at F23, He to J "Swiss" mice from Albert de Coulon of Lau 1948 at F25. Charac: uniformly sensitive to Plasmodium berghei infection (H. Most et sanne, inbred by C. Lynch (C. J. Lynch, al., Mil. Med., 131: 915, 1966). 1-2% leu- Lab. Anim. Care, 79: 214, 1969). Charac: kemias including some plasma cell types; low incidence of mammary tumors in breed other tumors including pulmonary adeno ers and virgins; about half primary lung mas and mammary carcinomas, about 3% tumors; high mortality in 66 exposed to (J); hematocrit 47.2%, systolic Wood pres ethylene oxide products and to vitamin K sure 80 mm Hg (G. Schlager and R. S. deficiency (J). Midrange of radiation resist Weibust, J. Hered., 67: 295, 1976). Main ance, arteriosclerosis common in both sexes (BLM-2); hematocrit 52.9%, systolic tained by: J, N, Univ. Helsinki (O. MÃ¤kelÃ¤). blood pressure 118 mm Hg (G. Schlager STAR/N Inbr (N): 83. Genet: c. Origin: from Brown and R. S. Weibust, J. Hered., 67: 295, at F46. Charac: homozygous for dominant 1976). Maintained by: Bkl, Dt, Fnn, Fo, J, cataract. Maintained by: N. Ola, Pp, Scr, Y.

STR Inbr (N): 145. Genet: a b. Origin: Strong; SWV Inbr (Be): 73. Genet: A c and unknown coat between F4 and F27, mice were given in color dilution gene. Origin: from Central An jections of methylcholanthrene. Charac: imal Depot, Univ. British Columbia, which susceptible to periodontal disease (P. N. had obtained stock from Defense Res. Bd., Baer ef al., J. Dent. Res., 40: 23, 1961). Suffield, Alberta, Canada, in 1949 and main Maintained by: N. tained as a closed colony; inbreeding started in 1959. Charac: 9$ over 8 mo have STR/1 Inbr (N): 138. Genet: a b s. Origin: piebald a hereditary polydipsia-polyuria defect with branch of STR/N, 1961. Charac: osteoar- a severe increase in water turnover and with thropathy of the knee joints [M, Silberberg hypotonie urine that contains no glucose, and R. Silberberg, Gerontologia (Basel), 6: blood, or protein; i.e., nephrogenic diabetes 91,1962]; obstructive uropathy in 66 before insipidus. They are vasopressin resistant; 16 mo (L. Sokoloff and M. F. Barile, Am. J. $? also have a progressive kidney defect Pathol., 41: 233, 1962). Maintained by: N, which, although it resembles nephronophth- Ort. isis in some aspects and hypokalemia in others, is unique. 66 have a milder form of STS/A Inbr (A): 100. Genet: c. Origin: MÃ¼hlbock, the defect at an older age and show no from Hyg. Inst. ZÃ¼richin 1955. Charac: no signs of histopathology (N. S. Virgo and J. mammary tumors; lung tumors in both R. Miller, Can. J. Genet. Cytol., 19: 667. sexes; closely related to LIS/A and LTS/A. 1977). Maintained by: Be, Fnn, Fr, W. Lay- Maintained by: A, Nii, Pt. ton (Dartmouth). Ucsd.

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TA1 Inbr: 90. Genet: abc Akp-1", Amy-1", Es- TM Inbr: 90+. Origin: Casas, b x s inbred from T, Es-20, Gdc-1", Got-r, Got-?, Gpd-1b, 2 unpedigreed Swiss albinos since 1948. Gpi-T, Hbtf, Id-r, Ldr-1", Mod-1", Mup-1", Charac: no mammary tumors, some adren- Pep-3Â°,Pgm-r, Pgm-2", Sep-7a, Tam-1", ocortical tumors; unusually large postcas- Trt". Origin: noninbred strain obtained from trational accumulation of body fat; no liver Tianjin in June 1956: inbred since then. tumors. Maintained by: Szepsenwol (Univ. Charac: mammary tumors about 1% in Puerto Rico). breeders, 0 in virgins and males; ovarian tumors 9.5%; pulmonary tumors 2.4%; lym- TP Inbr (Rl): 68+. Genet: a fp/+. Origin: Jax; phocytic leukemia 1% [Y. Li and B. S. Un, taupe mutation arose in C57BL/10J in Dec. Shanghai Bull. Anim. Vet. Sci., 3 (2V 1948; after 6 gen. of backcross-intercross 1983]. Sensitive to 20-methylcholanthrene, to C57BL/10, b x s inbred. Charac: tp/tp particularly /V-phenyl-0-napththylamine in are poor mothers. Maintained by: Rl. male kidney; susceptible to chronic pneu monia, extremely sensitive to radiation. Av. TPS/Y Inbr (Y): 34. Genet: a. Origin: from hetero life span: 99 673 days, 66 555 days; av. wt. geneous background through selection for at 43 days, 5$ 20 g, 66 21 g. Maintained high sensitivity to cytogenetic effect of thi- by: Lab. Exp. Oncol. of Tianjin Med. Coll. in otepa. Maintained by: Y. China (Y. U). TR Inbr (Dn): 81. Genet: McfÂ°.Origin: Dickie; Inbr: 66. Genet: a B c d Akp'1", Amy-1", TA2 tortoise mutation arose in noninbred obese Es-1", Es-26, Gdc-1", Gof-i", Gof-2", Gpd- stock in 1952. Charac: maintained by trio 1", Gpi-1", Hbb", Id-r, Ldr-r, Mod-1", matings for 23 years, now by pair matings Mup-1", Pgm-1", Pgm-2*, Pep-3", Sep-1", Mo'Â°/+9 x +/Y 6. Mo'Â°/+99 with much Tam-1", Trf". Origin: noninbred strain mat white in coat usually do not mature; darker ing, Kun Ming mice, obtained from Bioprod- ones survive well. In this line no McfÂ°[ihave uct Institute in Peking in 1962; inbred since appeared. Maintained by: Dn. then. Charac: mammary tumors 81.4% in breeders, 41.4% in virgins, 3.2% in males. TSI Inbr (A): ? + 72. Genet: a c. Origin: MÃ¼hl Ovarian tumors 4.4%; pulmonary tumors bock, from P. SchÃ¤fer(TÃ¼bingen)in1958. 2.7%; lymphocytic leukemia 1.3% [B. S. Charac: no mammary tumors; high inci Lin, Shanghai Bull. Anim. Vet. Sci. 2 (iy dence of leukosis in both sexes; polyuric. 1982]. Sensitive to radiation. Av. Life Span: Maintained by: A. 9$ 416 days, 66 479 days; av. wt. at 56 days 66 22 g, 99 21 g. Maintained by: Lab TSJ Inbr (Le): 64. Genet: b Ts/+. Origin: muta Exp. Oncol. of Tianjin Med. Coll. in China tion to 7s arose at NCI in 1946 (W. C. (Y. Li). Morgan, J. Hered., 41: 208, 1950). From Morgan to G. D. Snell in 1950. Crossed to TF Inbr (Le): 77. Genet: T tf/+ tf. Origin: M. C. C57BL/6, C57BR/cd, and BALB/cSn, then Green, from T tf/t6 stock received from M. sib-mated. Charac: 7s behaves as dominant F. Lyon in 1961, outcrossed to C57BL/ on this background, with short kinky tail. 10Gn to obtain +tf chromosome in 1962, Maintained by: Le. thereafter b x s. To Lane 1975. Charac: good chromosome 17 markers. Maintained TTR/I e Inbr (Le): 54. Genet: 7 tf/t6 + AÂ¡A.Origin: by: Le. TR" stock of M. F. Lyon to M. C. Green in 1961, to Le 1970. One cross to jittery- TH Inbr (Wl): 93. Genet: a*. Origin: mass se grizzled stock, b x s to F7, one cross to lected for high blood pH (H. G. Wolfe, Ge BÃ´CBAFr/r^/A in 1972, b x s thereafter. netics, 46: 55, 1961). Charac: good repro Charac: small litters, some sterility, useful ductive performance; arterial heart blood pH for testing 7 alÃeles.Maintainedby: Le. 7.34, sex ratio at birth 57.1% 66 (H. G. Wolfe and J. A. Weir, J. Hered., 63: 109, v/Le Inbr (Le): 49. Genet: a fz In/fz In s v/+. 1972). Maintained by: Wl. Origin: G. D. Snell, v, s, In from Ludwin 1947. Crossed to C57BL/10, crossed to fz TL Inbr (Wl): 96. Genet: Awb. Origin: see TH. 1960 and non-sib-mated. To Lane 1969 and Mass selected for low blood pH. Charac: sib-mated. Charac: original Japanese good reproductive performance; arterial waltzer mutation, v/v are poor mothers. heart blood pH 7.30, sex ratio at birth Useful for linkage testing. Maintained by: 50.6% 66. Maintained by: Wl. Le.

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VY Inbr (Nctr): 74. Genet: A^/a. Origin: C57BL/ feder, Br. J. Cancer, 20: 361, 1966). 6J-XÂ»""from M. M. Dickie, 1962. Charac: Charac: no tumors of any kind; does not prolific and vigorous; frequency of agouti- carry milk agent but produces antibodies colored /r/a offspring about 10%. 24% against it; gives immune responses to hepatoma in A"*/a Ã¡Ã¡at 12-16 mo; 13% in sheep RBC and possesses high phagocytic a/a. Maintained by: Granholm (S. Dakota activity; newborn are moderately suscepti St. Univ.), L, Nctr. ble to Friend leukemia virus, adults are re sistant; resistant to polyoma and FBJ vi WB Inbr (J): 119. Genet: a W rd/+ rd. Origin: IV ruses; resistant to liver carcinogenesis with hÃ©tÃ©rozygotesfromS. J. Holman and S. G. 2-acetylaminofluorene; partially resistant to Waelsch; b x s inbreeding started in 1948. leukemogenesis by dimethylbenzanthra- Charac: W/W homozygotes are anemic, cene; irradiation not carcinogenic. Main sterile, lack pigmentation in coat; hÃ©tÃ©rozy tained by: Gf. gotes have normal blood picture and fertil ity, but white ventral spotting; anÃ©miesdie YBR Inbr (Ki): 132. Genet: A"/a b. Origin: Little to Andervont 1936, to Heston 1946 at An's a approximately 11 days. Many other ane mia-producing mutant alÃeles are main F30. Charac: amyloid at least 50% in both tained congenie with this strain. Maintained sexes with A*/a or a/a; obesity in hybrids by: Bn, J, Pp. between A"Â¡aand other strains; low tumor; lacks microsomal /3-glucuronidase. Main WC Inbr (J): N58 F37. Genet and Origin: as WB. tained by: Ki. Charac: as WB, except that anÃ©miesdie at approximately 14 days. Maintained by: 1er, YS Inbr (Nctr): 84. Genet: A*/a s. Origin: Chase, J. 1959. Charac: hepatoma incidence in ?$ at 12-16 mo: 11% in A"/a, 4% in a/a. Main WHT Inbr (Gy) 125+. Genet: c. Origin: Hewitt, tained by: Nctr. Westminster Hosp., London, 1958. Charac: hardy, breeds well; origin of several spon- YT Inbr (Y): 42. Genet: abcchpd goY In H-2". taneous squamous carcinomas (J. Dene- Origin: from crosses of C57L, DBA/2, kamp ef a/., Br. J. Cancer, 41:1,1980); 12 C57BL-go, 129/J. Charac: multiply reces transplantable nonimmunogenic tumors of sive. Maintained by: Y. spontaneous origin maintained in this strain. Maintained by: Cbi, Gy, Uct. YX Inbr: 50. Genet: A*/a*. Origin: /Â»"/a*from L. B. Russell crossed with AÂ»/a 6 in 1968. WLHR Inbr (Le): 97. Genet: a b wl +/+ hr. Origin: Maintained by: Roger Pederson (San Fran mutation to wl occurred in pirouette stock cisco). in 1948. Crossed to hr from K. P. Hummel in 1949. Dickie to Lane in 1958 and inbred 101 Inbr (El): 93. Genet: A". Origin: Dunn (L C. as balanced stock. Charac: homozygous Dunn, J. Genet., 33: 443, 1936). Charac: wl/wl die before weaning. Maintained by: low mammary tumor incidence; slow to Le. breed, fertility moderate (H); high suscepti bility to skin and lung tumor induction. Main WLL Inbr (A): 7 + 112. Genet: c. Origin: Krey- tained by: Cum, El, H, Rl, Y. berg, 1929, from a commercial dealer in Oslo (L Kreyberg, Br. J. Cancer, 6: 140, 129/Re Inbr (J): 89. Genet: A" cch p/cc/>p. Origin: 1952). In 1934 "White Label" mice were see 129/RrJ; b x s dystrophic-normal sub- sent to Leeds, becoming WLL, and some line, descended from the 129/Re-dy sub- stayed in Oslo, becoming WLO (that strain line, from tested dy+/dy+ offspring. Main not recently reported). Maintained by: A. tained by: J, Y.

WN Inbr (Nga): 60. Genet: a W/+. Origin: new 129/RrJ Inbr (J): 97. Genet: A" cc/1p/c p. Origin: mutant at W locus. W"IW die at 16-18 days Dunn, a derivative of strain 101 (W. L. Rus gestation with anemic syndrome, occasion sell and J. G. Hurst, Proc. Nati. Acad. ally survive birth but die in a few days. Sci., 37: 267, 1945, and correspondence). HÃ©tÃ©rozygotehasnormal blood and is via Charac: 5% spontaneous testicular tera- ble and fertile. Amount of white spotting is toma (Sv); not susceptible to mammary tu greater than in W/+. Maintained by: Nga. mor agent; useful for ovary transplant and ova transfer studies; highly sensitive to es X/Gf Inbr (GÃ¬):89. Genet: a B/b c. Origin: un trogen at all ages (J); very resistant to X- known; inbred by Gf since 1953 (A. Gold irradiation, high incidence of urinary calculi

CANCER RESEARCH VOL.45 MARCH 1985 967

(BLM-2); slowest heart rate of 7 strains Gpd-7", Gp/-7", Hbtf, Id-T, Ldr-r, Mod-1- tested (D. A. Blizard and R. Welty, J. Comp. ", Mup-1", Pep-y, Pgm-1", Pgm-2", Sep-1", Physiol. Psychol., 77:337,1971). Resistant Tam-1c, Trf". Charac: 40XX, 40XY, G-band- to Leishmania infection (D. J. Bradley, Clin. ing pattern standard. Av. litter is 6.7; av. Exp. Immunol., 30: 130, 1977); most sus number of weaners is 6.3. Mammary tumor ceptible to Sendai virus of 19 strains tested incidence in multiparous mice is 14.3%; pul (J. C. Parker er a/., Infect. Immun., 19:123, monary adenoma and leukemia within 18 1978). 129/J is this subline. Maintained by: months are 36.7% and 5.8%, respectively; Dt, J, Kun, Ola, Ori, Rk, Rl, Sv, Y. 22 transplantable tumor lines have been established from this strain. These tumor Inbr (Sv): N8 F45. Genet: Aw c+ p+. Origin: strains can be used for screening of anti- 129/terSv derived from 129/Sv-lV C P, which was cancer drugs, studying tumor immunology, developed to determine the effect that the and mechanism of tumor formation. Main gene W+ might have on teratocarcinogene- tained by: Lab. Exp. Anim., Inst. Hematol- sis (none detectable). Wf+ animals were ogy, Tianjin, China. repeatedly backcrossed to 129. A W/+ 9 of Recommended abbreviations for widely used strains; in all gen. N8 produced 38 male offspring of cases the full strain designations should always be given in either which 8 had testicular teratomas. All 129/ the Introduction or the Materials and Methods section of any ter mice are descended from that mating. paper; e.g., ". ..C57BL/6J x DBA/2JF, (hereafter called Charac: about 30% incidence of sponta B6D2F,)..." In hybrid designations, the female parent should be neous congenital testicular teratomas, ap listed first. pearing between the 12th and 13th day of STRAIN ABBREVIATION gestation. Tumors may occur on either side or both and may contain tissues derived AKR AK from all germ layers; rarely metastasize (L. BALB/c C C. Stevens, J. Nati. Cancer Inst., 50: 235, CBA CB 1973). Maintained by: A, Cam, H, Hok, J, C3H C3 Ph, Scr, Sv. C57BL B C57BL/KS BKs 201/R1 Inbr (R1): 75+. Genet: A*/a pe. Origin: Rus C57BL/6 B6 sell, from PE/RI and noninbred Ay/a stock. C57BL/10 B10 Mating is always Ay/a pe/pe $ x a/a pe/pe C57BR BR 6. Charac: occasional somatic reverse mu C57L L tations pe to +. Maintained by: Rl. DBA/1 D1 DBA/2 D2 615 Inbr: 64. Genet: a bC H-2", Akp-1', Amy- HRS/J HR 1a, Es-1", Es-2", Gdc-1", Got-1", Gof-2", Rill R3

APPENDIX 2 University of South Carolina, Charleston, SC 29401 Alt University of Alberta, Edmonton, Alberta, Canada Abbreviations for use in symbolizing substrains of mice and rats Am Dr. J. L. Ambrus, Roswell Park Memorial Institute, and for designating holders of strains. Buffalo, NY 14203 An Dr. H. S. Andervont (deceased) A Antoni van Leeuwenhoekhuis, Amsterdam C, Sarpha- Ani Argonne National Laboratory, Division of Biological and tistraat 108, The Netherlands (Dr. A. Dux) Medical Research, Argonne, IL 60439 (Dr. T. E. Fritz) Aa Cancer Research Institute, Aarhus, Denmark Ao Dr. D. B. Amos, Duke University School of Medicine, Aai Ace Animals, Inc., P. O. Box 122, Boyertown, PA Department of Immunology, Durham, NC 27710 19512 (Ms. Ruth Cinaglia) Ar A.R.S.A.L., Via di Valle Caia, 00040 Pomezia (Roma), Abg SUNY Albany, Department of Psychology, 1400 Wash Casella Postale 39 Pomezia (dott. Renata Nobili Cas ington Ave., Albany, NY 12222 (Dr. Bruce Dudek) telli), Italy Adr Animal Disease Research Association, Moredun Insti As University of Aarhus, Department of Genetics, Institute tute, Gilmerton, Edinburgh, Scotland of Ecology and Genetics, DK-8000 Aarhus, Denmark Ae Dr. H. J. Aeschbacher, NestlÃ©Department de Re (Drs. J. Peter Hjorth and J. Tonnes Nielsen) cherche, Case postale 88, CH-1814 La Tour de Peilz, Asl Animal Suppliers (London), Ltd., 685 High Road, North Switzerland Finchley, London N 12, England Agi Dr. Joe M. Angel, The Jackson Laboratory, Bar Harbor, Au Dr. Robert Auerbach, University of Wisconsin, Depart ME 04609 ment of Zoology, Madison, Wl 53706 Ags C.S.I.R.O., Division of Animal Genetics, P. O. Box 90, Ba Instituto de Medicina Experimental, Laboratorio de Epping, N. S. W., Australia Genetica, Avda. San MartÃn5481, Buenos Aires, Ar Al Dr. R. C. Allen, Department of Pathology, Medical gentina

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Baf Battelle-lnstitut e.V., Postfach 900160, D-6000 Frank ME 04609 furt am Main 90, BRD (Dr. Anita Schwaier) Bsc Birmingham-Southern College, Department of Biology, Baz Centro per lo Studio e la Cura dei Tumori, Busto Birmingham, AL 35204 Arsizio, Italy (Dr. G. Ceriotti) Bsp BÃoterioCentral of the University of Sao Paulo, Medical Be University of British Columbia, Department of Medical School, Av. Dr. Arnaldo, 455,01246 SÃ¢oPaulo, Brazil Genetics, Vancouver, British Colombia V6T1W5, Can (Dr. Fernando Sogorb Sanchis) ada (Muriel J. Harris and Diana M. Juriloff) Bt Dr. N. Bateman, Field Laboratory, Animal Breeding Ber University of Birmingham, Department of Cancer Stud Research Organization, Roslin, Midlothian, Scotland ies, The Medical School, Birmingham, England (Miss Bts Radiobiology Department, Medical College of St. Bar tholomew's Hospital, London EC1M 6BQ, England V. G. Nash) Bd Biology Division, Oak Ridge National Laboratory, Bldg. (Prof. P. J. Lindop) 9207, P. O. Box Y, Oak Ridge, TN 37830 Bu Dr. Walter J. Burdette, M. D. Anderson Hospital and Be Dr. R. A. Beatty, Institute of Animal Genetics, West Tumor Insitute, University of Texas, Houston, TX Mains Road, Edinburgh, Scotland 77025 Ben Dr. Dorothea Bennett, Sloan-Kettering Institute, Lab- Bua Birmingham University, Department of Anatomy, The oratory of Developmental Genetics, New York, NY Medical School, Birmingham, England 10021 Bw Dr. Russell V. Brown, Department of Biology, Virginia Bg Behavior Genetics Laboratory, University of Connecti Commonwealth University, Richmond, VA 23220 cut, Storrs, CT 06268 (Dr. B. E. Ginsburg or Dr. Steven By Dr. Donald W. Bailey, The Jackson Laboratory, Bar Maxson) Harbor, ME 04609 Bi Dr. J. J. Bittner (deceased) Ca Dr. T. C. Carter, University of Edinburgh, Edinburgh, Bim Martin-Luther UniversitÃ¤t, Biologisches Institut der Scotland Medizinische, Halle-Wittenberg, DDR Gag University of Cambridge, School of Agriculture, Down Bk Dr. Sidney L. Beck, Wheaton College, Norton, MA ing Street, Cambridge, England (Dr. J. R. Morton) 02766 Cam University of Cambridge, Genetics Department, Milton Bkl Bantin and Kingman, Ltd., The Field Station, Grimston, Road, Cambridge, England Aldbrough, Hull 4QE, England (Mr. G. C. Bantin) and Cbi Chester Beatty Research Institute, Institute of Cancer 3403/3421 Yale Way, Fremont, CA 94538 (Mr. Robert Research, Fulham Road, London SW3 6JB, England Schultz) Cd Dr. Albert Claude (deceased). Contact Prof. Paul Ga- Bkr Mrs. Helen Bunker, The Jackson Laboratory, Bar Har land, UniversitÃ©Libre de Bruxelles, Laboratoire de bor, ME 04609 Cytologie et de CancÃ©rologieExperimental, Brussels, BI Dr. M. Bielschowsky (deceased) Belgium Bin Akademie der Wissenschaften der DDR, Abt. Ver- Cds Centers for Disease Control, Lawrenceville Facility, P. suchstiere, Berlin-Buch, DDR 0. Box 363, Lawrenceville, GA 30245 (Dr. James R. Bis Beatrice L. Snow, Suffolk University, Department of Hegner) Biology, Beacon Hill, Boston, MA 02114 Cft Central Food Technological Research Institute, Animal Bm Dr. Wesley G. Beamer, The Jackson Laboratory, Bar House, Mysore, India Harbor, ME 04609 Cg Mrs. A. Cohen, Experimental Oncology Laboratory, Bn Dr. S. E. Bernstein, The Jackson Laboratory, Bar Radiation Therapy Department, Johannesburg General Harbor, ME 04609 Hospital, Johannesburg, South Africa Bnr Abt. Pathologie, UniversitÃ¤tBonn/Rhein, BRD Ch Dr. Herman B. Chase (retired) Bo Biochemical Department of Cancer Institute, Zluty ko- Chi Dr. Jiri Chlumecky, University of Alberta, Health Sci pec 7, Brno, Czechoslovakia ences Small Animal Program, Edmonton, Alberta, Can Bog Jerzy Bogajewski, The Breeding Center for Experi ada T6G 2H7 mental Animals, ul. Poznanska 10, 62081 Przezmi- Chp Mrs. Dorothy R. Chapman, The Jackson Laboratory, erowo near Poznan, Poland Bar Harbor, ME 04609 Bom Laboratory Animals Breeding and Research Center, Ci Dr. Ernst Caspari (retired) GÃ¬.Bomholtgard, 8680 Ry, Denmark Cib Ciba Research Centre, P. 0. Bag 9002, Aarey Road, Boo Boots Pure Drug Co., Ltd., Research Department, Goregaon East, Bombay 63NB, India Biological Sciences, Nottingham NG2 3AA, England Ciu Unidad de Investigaciones Cancerologicas, Avda. Boy Dr. E. A. Boyse, Sloan-Kettering Institute, Division of Cuauhtemoc 240, Ciudad de MÃ©xico,MÃ©xico Immunology, New York, NY 10021 Ckc Dr. C. K. Chai (retired) Br Dr. G. M. Bonser (deceased) CI Mrs. Ruth Clayton, Institute of Animal Genetics, West Brc Brighton Polytechnic, Department of Pharmacology, Mains Road, Edinburgh, Scotland School of Pharmacy, Brighton BN2 4GJ, England Clb Central Laboratory of the Blood Transfusion Service, Bre Dr. E. J. Breyere, Department of Biology, American Netherlands Red Cross, Plesmanlaan 129, Amster University, Washington, DC 20016 dam, The Netherlands (Dr. Paul de Greve) Brii Prof. P. L. Broadhurst, Department of Psychology, Cm Dr. R. B. Cumming, Biology Division, Oak Ridge Na University of Birmingham, England tional Laboratory, Oak Ridge, TN 37830 Brk Dr. Jane Barker, The Jackson Laboratory, Bar Harbor, Cn A. L. Chapman, Ph.D., University of Kansas Medical

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Center, Kansas City, KS 66103 Wycombe, Buckinghamshire HP12 4HL, England Cnb Centre d'Etude de l'Energie NuclÃ©aire,B-2400 Mol, Db Dr. David E. Briles, Cellular Immunobiology Unit, Tumor Belgium (Dr. A. LÃ©onard) Institute, University of Alabama, Birmingham, AL Cne Comitato Nazionale per l'Energia Nucleare, Stabulario 35294 C. S. N., Gasacela, C. P. 2400, Rome, Italy De Dr. Margaret K. Deringer (retired) Co Dr. George A. Carlson, The Jackson Laboratory, Bar Dem Dr. Peter Demant, Netherlands Cancer Institute, Sar- Harbor, ME 04609 phatistraat 108, Amsterdam-C, The Netherlands Col Dr. Robert L. Collins, The Jackson Laboratory, Bar Dg Dr. C. P. Dagg, University of Alabama, College of Harbor, ME 04609 General Studies, Department of Biology, Birmingham, Com ARC Institute for Research on Animal Diseases, Comp- AL 35233 ton, Nr. Newbury, Berkshire, England Di Dr. Margaret M. Dickie (deceased) Cox Laboratory Supply Co., Inc., 3750 Kentucky Ave., Dk Dr. A. G. Dickinson, ARC Animal Breeding Research Indianapolis, IN 46241 (Mr. Eldon J. Cox) Organisation, West Mains Road, Edinburgh, Scotland Cp Dr. A. B. Chapman, Department of Genetics, University Dm Dr. L. Dmochowski (deceased) of Wisconsin, Madison, Wl 53706 Dn Dr. Muriel T. Davisson, The Jackson Laboratory, Bar Cpb Centraal Proefdierenbedrijf T.N.O., P. O. B. 167, Zeist, Harbor, ME 04609 The Netherlands (Dr. J. C. J. van Vliet) Do University of Utah, Radiobiology Division, Salt Lake Cr Division of Cancer Treatment, Animal Genetics and City, Utah 84132 (Dr. Charles W. Mays) Production Branch, National Cancer Institute, Freder- Dp Dr. Giuseppe Della Porta, Section of Experimental ick, MD 21701 (Dr. Joseph Mayo or Mr. Clarence Carcinogenesis, Istituto Nazionale per lo Studio e la Reeder) Cura dei Tumori, Milan, Italy Crc Clinical Research Centre, Harrow, Middlesex, England Dr Prof. Dr. Med. Herman Druckrey, Laboratorium D. (Dr. C. Hetherington) Chirurg. UniversitÃ¤tKlinik, Freiburg im Breisgau, BRD Crgl Cancer Research Genetics Laboratory, University of Dt Dr. Donald P. Doolittle, Purdue University, Population California, Berkeley, CA 94720 (Mrs. Kay Yoshiura) Genetics Institute, Lafayette, IN 47907 Cri Cancer Research Institute, Tata Memorial Centre, Du Dr. Wilhelmina F. Dunning, Papanicolaou Cancer Re Parel, Bombay 400 012, India (Dr. H. P. Randelia) search Institute, 1445 N. W. 14th St., Miami, FL 33136 Crj Charles River Japan, Inc., 795 Shimofurusawa, Atsugi- Dv Dr. Chella S. David, Mayo Clinic, Department of Im shi, Kanagawa 243-02, Japan munology, Rochester, MN 55901 Crl Charles River Breeding Laboratories, Inc., Wilmington, Dy Dr. Raymond Daynes, University of Utah College of MA 01887. And also SociÃ©tÃ©desElevages Charles Medicine, Department of Pathology, Salt Lake City, UT River France S.A., B. P. 29, St. Aubin-les-Elbeuf, S.- 84132 M., France E Dr. Martin Evans, Department of Genetics, University Cs R. T. Charles, "Pencincoed," Glynbrochan Rd., Llan- of Cambridge, Downing Street, Cambridge CB2 3EH, idloes, Montgomery, Wales England Csk Research Laboratories, Chugai Pharmaceutical Co., Ed Centre for Laboratory Animals, University of Edin Ltd., 8-41-3, Takada, Toshima-ku, Tokyo, Japan (Dr. burgh, Milton Bridge, Penicuik, Midlothian EH26 OPL, Toshima Nobunaga) Scotland (T. Graham-Marr) Csl Commonwealth Serum Laboratories, Poplar Road, Eg Dr. I. K. Egorov, The Jackson Laboratory, Bar Harbor, Parkville 3052, Victoria, Australia ME 04609 Csr Charles Salt Research Centre, Orthopaedic Hospital, Eh Dr. J. Engelbreth-Holm (deceased) Oswestry, Shropshire, England Ehs National Institute of Environmental Health Sciences, P. Ct Dr. Bruce M. Cattanach, M.R.C. Radiobiology Unit, O. Box 12233, Research Triangle Park, NC 27709 (Dr. Harwell, Didcot, OXON OX 11 ORD, England Conrad B. Richter) Cu Dr. R. L. Curtis, Department of Anatomy, Medical Ei Dr. Eva M. Eicher, The Jackson Laboratory, Bar Har College of Wisconsin, Wauwatosa, Wl 53226 bor, ME 04609 Cub Charles University, Faculty of General Medicine, De- El Dr. U. H. Ehling, Gesellschaft fÃ¼rStrahlen- und Um partment of Biology, Albertov 4, Prague 2, Czechoslo weltforschung, 8042 Neuherberg bei MÃ¼nchen,BRD vakia Ep Dr. Garios Epper, Radiobiology Laboratory, Atomic Cum Cumberland View Farms, Route 3, Clinton, TN 37716 Energy National Commission, Avda. del Libertador (Mr. Kenneth E. Kile, Sr.) Gen. San Martin 8250, Buenos Aires, Argentina Cv Dr. Verne M. Chapman, Roswell Park Memorial Insti- Er Dr. Robert P. Erickson, Department of Human Ge tute, Department of Molelcular Biology, 666 Elm netics, University of Michigan Medical School, Ann Street, Buffalo, NY 14203 Arbor, Ml 48109 Cvl Richard H. Civil, Division of Geographic Medicine, Uni- Eru Experimental Radiopathology Unit, Hammersmith Hos versity Hospitals, Cleveland, OH 44106 pital, Ducane Road, London, W12 OHS, England Cwr Case Western Reserve University, Animal Facilities, Eup Edinburgh University, Department of Pharmacology, 1 Cleveland, OH 44106 George Square, Edinburgh EH8 9JZ, Scotland Cy Dr. Marianna Cherry (retired) Eus Edinburgh University, Department of Surgical Science, Da Dr. D. A. Davies, Searle Research Laboratories, High Medical School, Teviot Place, Edinburgh EH8 9AG,

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Scotland Gliwice 1, Poland Fa Dr. D. S. Falconer, Institute of Animal Genetics, West Glw Dr. S. G. Waelsch, Albert Einstein College of Medicine, Maine Road, Edinburgh, Scotland Department of Genetics, Eastchester Road and Morris Fe Dr. Elizabeth Fekete (deceased) Park, New York, NY 10461 Ffm UniversitÃ¤tFrankfurt, Institut fÃ¼rHumangenetik, 6 Gm J. P. W. Gilman, DVM, Ontario Veterinary College, Frankfurt/Main, BRD (Dr. K.-H. Degenhardt) Guelph, Ontario, Canada N1G 2W1 Fg Prof. Frank H. J. Figge (deceased) Gn Drs. E. L. and M. C. Green (retired) Fhc Fred Hutchinson Cancer Research Center, Animal Go Dr. Peter Gorer (deceased) Health Resources, 1124 Columbia Street, Seattle, WA Gr Dr. H. GrÃ¼neberg(deceased).Contact Dr. G. M. Trus- 98104 (Ms. Carol Shelmerdine) love, University College London, Department of Zool Fib The Fibiger-Laboratory, Ndr. Frihavnsgade 70, DK- ogy, Gower Street, London, England 2100 Copenhagen (3,Denmark Grf Dr. Ralph J. Graff, Jewish Hospital of St. Louis, De Fis Fisons Agrochemical Division, Chesterford Park Re partment of Surgery, 216 South Kingshighway, St. search Station, Nr. Saffron Waiden, Essex, England Louis, MO 63110 Fia Dr. Lorraine Flaherty, New York State Department of GrÃ² Genetica! Institute, University of Groningen, Kerklaan Health, Albany, NY 12201 30, HÃ¤ren(Gr.),The Netherlands (Dr. G. A. van Oort- Fn Dr. Paul F. Fenton, Brown University, Biology Depart merssen) ment, Providence, Rl 02912 Gs Dr. Ludwik Gross (retired) Fnn Dr. R. H. Finnell, Washington State University, Depart- Gvp Glasgow University Veterinary School, Department of ment of Veterinary Anatomy, Pullman, WA 99163 Veterinary Pathology, Bearsden, Glasgow, Scotland Fo Dr. P. Forsthoefel (retired) Gw Dr. John W. Gowen (deceased) Fp Istituto di Patologia Generate della UniversitÃ di Fer- Gy Gray Laboratory, Mount Vemon Hospital, Northwood, rara, Via Fossato di Mortara, 64/a, 44100 Ferrara, Italy Middlesex HA6 2RN, England (Dr. J. F. Fowler, Dir.) (Dr. Giorgio Benassi) H MRC Radiobiology Unit, Harwell, Didcot, OXON OX11 Fr McGill University, Department of Biology, Montreal, ORD, England (Dr. M. F. Lyon) Quebec, Canada H3A 1B1 (Dr. Daphne G. Trasler) Ha Dr. T. S. Hauschka (retired) Fre Dr. Jeffrey A. Frelinger, Department of Microbiology Hab Tumor and Experimental Animals Laboratory, Depart and Immunology, University of North Carolina, Chapel ment of Biology, Instituto Nacional de OncologÃay Hill, NC 27514 RadiobiologÃa,Habana-4,Cuba (Dr. Raul Castillo) Fs Dr. Morris Foster (deceased) Han Zentralinstitut fÃ¼rVersuchstierzucht, Lettrow-Vor- Fu Dr. Jacob Furth (deceased) beck-Allee 57, Hannover-Linden, BRD (Dr. W. Heine) Fx Dr. Thomas O. Fox, Department of Neuroscience, Har University of Northern Iowa, Department of Psychol Children's Hospital Medical Center, Boston, MA 02115 ogy, Cedar Falls, lA 50613 (Dr. G. M. Harrington) G Glaxo Laboratories, Ltd., Greenford, Middlesex, Eng- Hb Dr. H. Everett Hrubant, California State University, land Department of Biology, Long Beach, CA 90804 Ga Dr. Allen H. Gates, Department of Radiation Biology He Dr. W. E. Heston (retired) and Biophysics, University of Rochester Medical Cen- Hf Dr. Harold A. Hoffman, Animal Genetic Systems, Inc., ter, Rochester, NY 14642 11 Taft Court, Rockville, MD 20850 Gb Dr. Donald B. Galbraith, Trinity College, Biology De- Hg Prof. Dr. Paula Hertwig (retired) partment, Hartford, CT 06106 Hi Dr. Jo Hilgers, Antoni van Leeuwenhoekhuis, Nether Gbi Glasgow University, Department of Bacteriology and lands Cancer Institute, Plesmanlaan 121, 1066 CX Immunology, Western Infirmary, Glasgow W.1, Scot Amsterdam, The Netherlands land HI Dr. Liselotte Herberg, Diabetes Forschungsinstitut Gd Dr. C. M. Goodall, National Cancer Research Labora aufm Hennekamp 65, 4000 DÃ¼sseldorf,BRD tories, University of Otago, Dunedin, New Zealand Hlr Hoffman-LaRoche, Bldg. 34, Room 525, 340 Kings Gda Medical Academy Gdansk, Department of Biochemis land Street, Nutley, NJ 07116 (Dr. Felix Garcia) try, Al. Zwycigstwa 42, Gdansk, Poland Hm Dr. Herbert Morse III, Bldg. 7, Room 304, National Gen Istituto di Farmacologia, UniversitÃ di Genova, Viale Institutes of Health, Washington, DC 20205 Benedetto XV, N.2, Genova, Italy (Dr. Silvio Parodi) Hn Dr. F. K. Hoombeek, University of New Hampshire, Gf Anna Goldfeder, D.Sc. M.U.C., Department of Biology, Zoology Department, Spaulding Bldg., Durham, NH New York University, 952 Brown Bldg., Room 754, 03824 Washington Square, New York, NY 10003 Ho Prof. W. F. Hollander, Department of Genetics, Iowa Gg Institute of Genetics, University of Glasgow, Glasgow State University, Ames, lA 50010 G11 5JS, Scotland (Dr. J. G. M. Shire) Hok Experimental Animal Laboratory, Faculty of Science, Gh Dr. Douglas Grahn, Argonne National Laboratory, Di Hokkaido University, North 10, West 8, Sapporo 060, vision of Biological and Medical Research, 9700 Cass Japan (Dr. M. Sasaki) Avenue, Argonne, IL 60439 How Dr. Alma Howard, Paterson Laboratories, Christie Hos Gif see Ori pital and Holt Radium Institute, Manchester 20, Eng GÃ¬ Dr. A. GlÃ¼cksmann(retired) land Gli Institute of Oncology, Department of Tumor Biology, Hr Dr. G. Hoecker, CÃ¡tedradeBiologia,Av. Zanartu 1042,

CANCER RESEARCH VOL. 45 MARCH 1985 971

Santiago de Chile der Deutschen Akademie der Wissenschaften zu Ber Hsd Hartan/Sprague-Dawley, Box 29176, Indianapolis, IN lin, Beuthenbergstrasse 11, DDR 69 Jena, DDR (Dr. 46229 H. HÃŸinGCKG) Ht Dr. H. B. Hewitt (retired) Jfc Department of Genetics and Breeding, Central Institute Hu Dr. Katharine P. Hummel (retired) for Experimental Animals, 17-2, Aobadi-2, Meguro, Hul Hull University,Department of Zoology, Hull, Yorkshire, Tokyo, Japan England Jko Keio University School of Medicine, Department of Hz Dr. L. A. Herzenberg, Department of Genetics, Stan Microbiology, Shinanomachi, Shinjuku-ku, Tokyo, Ja ford University School of Medicine, Palo Alto, CA pan (Dr. Daizo Ushiba) 94304 Jms Animal Breeding Unit, Institute of Medical Science, Ibg Institute for Behavioral Genetics, University of Colo University of Tokyo, Shiba Shirokane-Daimachi, Min- rado, Boulder, CO 80302 (Dr. G. E. McCleam) ato-ku, Tokyo, Japan (Dr. Yoshio Tajima) Ibm Institute for Bio-Medical Research, Ltd., CH-4402 Ful- Js Dr. Judy M. Strum, University of Maryland School of linsdorf, Switzerland Medicine, Department of Anatomy, John Eager How Ibr Israel Institute for Biological Research, P.O. Box 19, ard Hall, 655 W. Baltimore St., Baltimore, MD 21201 Ness-Ziona, Israel Ka Dr. H. S. Kaplan (deceased) loo Iffa Credo, les Oncins, 69/Saint Germain-sur-l'Arbre- Kam Kathryn A. Mason, Department of Radiation Oncology, sie, France (Dr. Vet. A. Perrot) UCLA School of Medicine, Los Angeles, CA 90024 1er Institute for Cancer Research, 7701 Burholme Ave., Kb Dr. Berenice Kindred, German Cancer Research Cen Fox Chase, Philadelphia,PA 19111 (Dr. Timothy Poote) ter, Institute for Immunology and Genetics, D-6900 Icrc Indian Cancer Research Centre, Parel, Bombay 12, Heidelberg, BRD India (Dr. B. K. Batra) Kch Dr. Walter Kocher, Freie UniversitÃ¤t Berlin, Institut Icrf Imperial Cancer Research Fund, Burtonhde Lane, fÃ¼rToxicologie und Embryonalpharmakologie, Gary- London WC2A 3PX, England strasse 1-9,1000 Berlin 33, BRD lei Institute for Experimental Immunology, University of Kd Dr. J. F. Kidwell, Division of Biology and Medical Sci Copenhagen, Norre Allee 71, DK 2100 Copenhagen ence, Brown University, Providence, Rl 02912 0, Denmark Kfm Kleintierfarm MadÃ¶rin AG, WÃ¶lferweg 34, CH 4414 Ig Dr. Rigoberto Iglesias, Instituto de Medicina Experi FÃ¼llinsdorf,Switzerland mental, Avda. Irarrazaval 849, Casilla 3401, Santiago Kga Kagashim University, Laboratory of Animal Breeding, de Chile Faculty of Agriculture, Kagoshima, Japan (Dr. Manjiro Igg Institute of General Genetics, Division of Histocompa- Taketomi) tibility Genetics, USSRAcademy of Sciences, Moscow Kh Dr. Henry I. Kohn (retired) 117333, USSR (L. E. Pospelov) Ki Kirschbaum Memorial Colony, Kagawa Medical Imr Institute for Medical Research, Copewood Street, School, Ikenobe, Miki, Kagawa 761-07, Japan (Dr. Camden, NJ 08103 (Ms. Jane A. Holben) Masaki Ohmori) Inns Institut de Recherches sur les Maladies du Sang, La- Kl Drs. G. and E. Klein, Department of Cell Research, boratoire d'ExpÃ©rimentationanimale,HÃ´pitalSt.Louis, Karolinska Institute!, Stockholm 60, Sweden 2 place du Dr. Foumier, 75010 Paris, France (Dr. G. Klj Dr. Jan Klein, Department of Immunogenetics, Max Mahouy) Planck Institute for Biology, Corrensstr. 42,7400 TÃ¼b Irr Institute for Research in Reproduction, Jehangir Mer- ingen 1, BRD wanji Street, Parel, Bombay 12, India Km Dr. Robert F. Kallman, Department of Radiology, Stan Itx INTOX Laboratory, 914 Barber Street, Little Rock, AR ford University School of Medicine, Palo Alta, CA 72202 (Dr. Lloyd Jeck) 94304 Iw Institut fÃ¼rVersuchstierkunde und Versuchstierkran- Kn Dr. Fr. KrÃ¶ning,Medizinische Forschungsanstalt, Phar- kheiten der Freien UniversitÃ¤t Berlin, Tietzenweg 85/ makologische Abteilung, Bunsenstr. 10, GÃ¶ttingen, 87,1 Berlin 45, BRD BRD JorJax The Jackson Laboratory, Bar Harbor, ME 04609 KO Dr. N. Kobozieff (retired) JÃ¤h National Institute of Animal Health, Kodaira, Tokyo-to, Kon UniversitÃ¤tKonstanz. Fachbereich Biologie, 775 Kon Japan (Dr. Takayoshi Ino) stanz, Postfach 7733, BRD (Dr. Eberhard! Weiler) Jb Dr. Jan Bruell, Psychology Department, Case Western Â«p Dr. Hilary Koprowski, The Wistar Institute, 36th at Reserve University, Cleveland, OH 44106 Spruce, Philadelphia, PA 19104 Jd A. Jurand, University of Edinburgh, Department of KS Dr. N. Kaliss (retired) Genetics, West Mains Road, Edinburgh 9, Scotland Ksb Dr. Kenneth S. Brown, Laboratory of Developmental Je Dr. Nancy Jenkins, University of Cincinnati School of Biology and Anomalies, National Institute of Dental Medicine, Department of Microbiology and Molecular Research, Bldg. 30, Room 412, Washington, DC Genetics, 231 Bethesda Ave., Cincinnati, OH 45267 20205 Jem Hebrew University-Hadassah Medical School, Experi- Â«su Kansas State University, Animal Resources Facility, mental Medicine and Cancer Research, Jerusalem, Department of Laboratory Animal Medicine, Manhat Israel (Dr. Michael Schlesinger) tan, KS 66502 Dr. Harold Kalter, Children's Hospital Research Foun- Jena Institut fÃ¼rMikrobiologie und experimentelle Therapie Kt

CANCER RESEARCH VOL. 45 MARCH 1985 972

dation, Eiland Ave. and Bethesda, Cincinnati, OH |_sh London School of Hygiene and Tropical Medicine, 395 45229 Hatfield Road, St. Albans, Hertfordshire, England Kun Katholteke UniversitÃ¤t, Central Animal Laboratory, Lt Dr. Edward H. Leiter, The Jackson Laboratory, Bar Nijmegen, The Netherlands (F. G. J. Janssen) Harbor, ME 04609 Kw Department of Animal Genetics and Organic Evolution, Lub Medizinische Hochschule LÃ¼beck,2400 LÃ¼beck1, Jagiellonian University, Karasia 6,30-060 Krakow, Po BRD land (Dr. Haiina Krzanowska) Lw Dr. L. W. Law, National Cancer Institute, Washington, Kx Dr. W. Eugene Knox, Cancer Research Institute, New DC 20205 England Deaconess Hospital, 194 Pilgrim Road, Bos- Lws Dr. Susan E. Lewis, Life Science and Toxicology Divi ton, MA 02115 sion, Research Triangle Institute, Research Triangle L Lilly Research Laboratories, Eli Lilly and Co., Indian Park, NC 27709 apolis, IN 46206 (Dr. T. T. Yen) Ly Dr. Clara Lynch (retired) Lac Experimental Embryology and Teratology Unit, MRC M Memorial Sloan-Kettering Institute Cancer Center, 410 Laboratories, Woodmansterne Road, Carshalton, Sur E. 68th Street, New York, NY 10021 rey SM5 4EF, England (Dr. D. Whittingham) Ma Dr. E. A. Mirand, Roswell Park Memorial Institute, Lati Laboratory Animals Institute, Tancsics M. Road, Go- Buffalo, NY 14203 dÃ¶llÃ¶,Hungary Mac Massey Universityof Manawatu and Palmerston North Lay W. M. Layton, Department of Anatomy, Dartmouth General Hospital, Palmerston North, New Zealand (Dr. Medical School, Hanover, NH 03755 R. E. Munford) Lb Dr. Miriam Ueberman, Department of Radiology, Stan- Mai M.A. Bioproducts, Biggs Ford Road, Walkersville, MD ford University School of Medicine, Palo Alto, CA 21793 (W. L Athey) 94305 Man Dr. Stanley J. Mann, Temple University Health Sci Ld Dr. J. Russell Undsey, University of Alabama, Depart ences Center, Central Animal Facilities, 3400 North ment of Comparative Medicine, 1919 7th Ave. South, Broad Street, Philadelphia,PA 19140 Birmingham, AL 35233 Mar Royal Marsden Hospital, Radiotherapy Research Unit, Le Mrs. Priscilla W. Lane, The Jackson Laboratory, Bar Downs Road, Sutton, Surrey, England Harbor, ME 04609 Mas University of Massachusetts, Department of Zoology, Lee Leeds University School of Medicine, Laboratory Ani Amherst, MA 01002 (Dr. H. Rauch) mals Department, Thoresby Place, Leeds LS2 9NL, Max Max-Planck-Institut fÃ¼rImmunbiologie, StÃ¼beweg51, England Freiburg i Br., BRD Lei Dr. W. Hijmans, Research Laboratories, Department Mb Max-Planck-lnstitut fÃ¼rBiochemistry,D-8033 Martins of Rheumatology, University Hosital, Leiden, The Neth ried, BRD erlands Mcd Dr. Hugh 0. McDevitt, Stanford University School of Lhm London Hospital Medical College, Department of Can Medicine, Department of Medical Microbiology, Stan cer Research, Ashfield Street, Whitechapel, London E. ford, CA 94305 I.England Mel Dr. Anne McLaren, UniversityCollege London, Wolfson Lhr London Hospital Research Laboratories, Animal House, 4, Stephenson Way, London, England House, Ashfield Street, Whitechapel, London E. 1., Me Sir Peter B. Medawar, Clinical ResearchCentre, North- England wick Park Hospital, Watford Road, Harrow, Middlesex U Dr. C. C. Little (deceased) HA1 3UJ, England Lia Liverpool University, Department of Anatomy, P. O. Mei Experimental Animal Research Laboratory, Meiji Uni Box 147, Liverpool L69 3BX, England versity, Tama-ku, Kawasaki, Kanagawa 214, Japan Lid Liverpool University, School of Dental Surgery, Bound (Dr. Hiroshi Nagasawa) ary Place, Liverpool 7, England Mel Dr. Roger Melvold, Department of Microbiology and LJI Dr. Frank Lilly, Department of Genetics, Albert Einstein Immunology, Northwestern University School of Med College of Medicine, Bronx, NY 10461 icine, 303 E. Chicago Ave., Chicago, IL 60611 U Laboratory Animals Centre, Polish Academy of Sei- Mg Prof. Walter Morgan, South Dakota State College, enees, Lomna Las k. Warsaw, Poland Department of Animal Science, Brookings, SD 57006 Ln Dr. J. B. Lyon, Department of Biochemistry, Emory Mib Genetic Laboratory of the Institute of Experimental University, Atlanta, GA 30322 Biology, Academy of Medical Sciences of the USSR, Lo Los Alamos Scientific Laboratory, P. O. Box 1663, Los Baltiskaya 8, Moscow A-315, USSR (Dr. B. V. Konyu- Alamos, NM 87544 (Dr. J. F. Spalding) khov) Lp Dr. W. S. Lapp. Department of Physiology, McGill Mk seeHok University, Montreal, Quebec, Canada H3A 1B1 Ml Dr. James R. Miller, Central Research Division,Takeda Ls Dr. Edwin P. Les, The Jackson Laboratory, Bar Harbor, Chemical Industries, Ltd., 2-17-85 Jusohonmachi, Yo- ME 04609 dogawa-ku, Osaka 532, Japan Lsb Division of Health Effects, Environmental Health Mo Dr. R. H. Mole, Radiobiology Unit, Harwell, Didcot, Centre, Department of National Health and Welfare, OXON 0X11 ORD, England Tunney's Pasture, Ottawa, Ontario, Canada K1A OL2 Mob Dr. Larry E. Mobraaten, The Jackson Laboratory, Bar (Dr. Souheil Laham) Harbor, ME 04609

CANCER RESEARCH VOL. 45 MARCH 1985 973

Mol Veterinary Surgeon Mollegaard's Breeding LabÃ³ralo- Nip Nippon Rat Co., Ltd., 608-3, Negishi, Urawa, Saitama, ries, Ltd., 4623 LI. Skensved., Ejby, Denmark Japan Mp Dr. E. D. Murphy (deceased). Contact Mr. John Roths, Nmg Department of Zoology, Toemooiveld, Nijmegen, The The Jackson Laboratory, Bar Harbor, ME 04609 Netherlands (Dr. J. H. F. van Abeelen) Mq Dr. Jacqueline Mouriquand, Centre d'Etudes Nu- Nnd National Institute for Nutritional Diseases, S. A. Medical clÃ©airesde Grenoble, B.P. 269, Grenoble, France Research Council, Private Bag 380, Pretoria, South Mr Dr. E. W. Miller, Cancer Research Laboratory, Depart Africa ment of Pathology, Royal Victoria Infirmary, Newcastle No Dr. D. J. Nolte, University of the Witwatersrand, Ge upon Tyne 1, England netics Laboratory, Milner Park, Johannesburg, South Ms National Institute of Genetics, Yata 1111, Misima, Si- Africa zuoka-ken, Japan Not Cancer Research Laboratory, The University, Univer Mts MTS Laboratories, P. O. Box 22091, San Diego, CA sity Park, Nottingham, England 92122 (Marc H. layman) Nrs National Institute of Radiological Sciences, 4-9-1, An- Mu Dr. Irving Mauer, Environmental Protection Agency, agawa, Chiba, Japan 280 (F. Nagasawa) 1400 S. Joyce St., Suite B-1605, Arlington, VA 22202 Ns Dr. Muriel Nesbitt, Department of Biology, University Mv Dr. N. N. Medvedev (retired) of California at San Diego, San Diego, CA 92037 My Dr. W. S. Murray (deceased) Nvs Nevis Biological Station, Irvington, NY 10533 Mza Dr. J. Echave Llanos, Instituto de Patologia General y Nya New York State Department of Health, Tower Bldg., Experimental, Facultad de Ciencias MÃ©dicas,Univer Empire State Plaza, Albany, NY 12201 (Dr. Ronald F. sidad Nacional de Cuyo, Mendoza, Argentina Gruhn) N Veterinary Resources Branch, Bldg. 14A, Room 102, O Universitetets Institutt for Generell og Eksperimental National Institutes of Health, Washington, DC 20205 Patologi, Oslo, Norway (Dr. K. Amesen) (Dr. Cari Hansen) Oci Ontario Cancer Institute, University of Toronto, 500 Na Dr. Joseph H. Nadeau, The Jackson Laboratory, Bar Sherboume St., Toronto, Ontario M4X 1K9, Canada Harbor, ME 04609 Odn Odense Universitet, Laboratory Animal Unit, J. B. Wins- Nac National Cancer Center, Research Institute, Chuo-ku, lows vej 21, 5000 Odense C, Denmark Tokyo, Japan (Dr. Hiroshi Nagasawa) Ok Division of Inbred Strains of Experimental Animals, Nag Nottingham University, School of Agriculture, Joint An Animal Experiment Center, Okayama University Medi imal Breeding Unit, Sutton Bonington, Nr. Loughbor- cal School, Okayama 700, Japan ough, Leicestershire, England Ola Oxfordshire Laboratory Animal Colonies, Shaws Farm, Nar Nara Medical College, Department of Pathology, 840 Bicester, OXON, England Shijo-cho, Nara-ken, Japan (Prof. Dr. Y. Tsubura) Omr University of Otago Medical School, Department of Nav Naval Medical Research Institute, Laboratory Animal Medicine, Wellcome Medical Research Institute, P. O. Science Branch, Bldg. 21, Bethesda, MD 20814 Box 913, Dunedin, New Zealand Nb Dr. R. L. Noble, Cancer Research Centre, University Onl Oncological Institute, Bd I Mac II, P3 5916, Bucharest of British Columbia, Vancouver V6T 1W5, British Co 12, Romania lumbia, Canada Org Organon Laboratories, Ltd., Newhouse, Lanarkshire, Ncr Nottingham University, Cancer Research Campaign, Scotland Centre de L'Ã‰lectionet d'Elevage d'Animaux de La Nottingham, England Ori Nctr National Center for Toxicological Research, Jefferson, boratoire, 45 OriÃ©ans-la-Source, France [formerly Gif] AR 72079 (Mr. Harvey Kalbach) Ort Institute of Orthopaedics, Royal National Orthopaedic Ndri Naval Dental Research Institute, Great Lakes Naval Hospital, Brockley Hill, Stanmore, HA7 4LP England Base, Great Lakes, IL 60088 (Dr. S. Yousuf Ali) Nem Nagoya University, Research Institute of Environmen- Os Osaka University, Institute for Cancer Research, Do- tal Medicine, Furo-cho, Chikusa-ku, Nagoya (Sen-ichi jima-HamadÃ´ri, Fukushima-ku, Osaka, Japan (Dr. Ya- Oda) suyuji Akamatsu) Nga Nagoya University School of Agriculture, Department Osb Osaka University, Department of Experimental Chem of Animal Genetics, Furo-cho, Chikusa-ku, Nagoya- otherapy, Research Institute for Microbial Diseases, shi, Japan Yamadakami, Suita, Osaka-fu, Japan (Dr. Jun-ichi Ka- Ni Dr. Robertha van Nie, Antoni van Leeuwenhoekhuis, wamata) Netherlands Cancer Institute, Plesmanlaan 121, 1066 Osu University of Otago Medical School, Department of CX Amsterdam, The Netherlands Surgery, Dunedin, New Zealand Nia National Institute of Aging, Bldg. 31, Washington, DC Ott Genetics Section, Animal Research Institute, Central 20205 (Dr. Don Gibson) Experimental Farm, Ottawa, Ontario, Canada (Dr. R. Nii National Institute of Immunology, P. 0. Box 4922, New S. Gowe) Delhi 11029, India (Dr. R. K. Anand) Ou Dr. Henry C. Outzen, Department of Medical Pathol Nimr National Institute for Medical Research, Mill Hill, Lon ogy, University of California College of Medicine, Davis, don NW7 1AA, England CA95616 Nin National Institute of Nutrition, Indian Council of Medical Ow Dr. Ray D. Owen, Division of Biological Sciences, Research,Jamei-Osmania,Hyderabad7,India California Institute of Technology, Pasadena, CA

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91109 Rap Breeding Farm Rappolova, Laboratory of Inbred Ani Oxf Oxford University Cellular Immunology Unit, Sir William mals, Academy of Medical Science, Solyanka 14, Mos Dunn School of Pathology, Oxford, England cow, USSR Pa Dr. Virginia Papaioannou, Tufts University School of Rb Dr. R. G. Busnel, Institut National de la Recherche Medicine, Department of Pathology, 136 Harrison Agronomique, Laboratoire de Physiologie Acoustique, Ave., Boston, MA 02111 Jouy-en-Josas (S. & 0.), France Pap Papanikolaou's Research Center of Oncology and Ex- Rbt Dr. Roy RiWet, Institute of Cancer Research, 7701 perimental Surgery, Hellenic Anticancer Institute, 171 Burholme Ave., Philadelphia, PA 19111 Alexandras Av. 603, Athens, Greece (Dr. T. Sirmake- Rd Dr. G. Rudali (deceased) chian-Karra) Re Dr. Elizabeth S. Russell (retired) Pas Pasteur Institute, UnitÃ©de GÃ©nÃ©tiqueCellulaire,DÃ©- Rg University of Reading, Department of Physiology and partment de Biologie MolÃ©culaire,25, rue du Docteur Biochemistry, Reading, Berkshire, England (R. Batt) Roux, 75015 Paris, France (J. L. GuÃ©net) RhÃ´ RhÃ´ne-Poulenc SantÃ©,Department of Biology, Re Pat Paterson Laboratories, Christie Hospital and Holt Rad search Centre, B. P. 14, F94407 Vitry sur Seine Cedex, ium Institute, Manchester, England M20 9BX France (Dr. Lavelle) Pe Dr. P. R. Peacock (retired) Rij Radiobidogical Institute TNO, P. O. Box 5815, NL- Per Division of Cancer Research, University of Perugia, 2280 HV Rijswijk, The Netherlands Perugia, Italy (Prof. Lucio Severi) Rk Dr. Thomas H. Roderick, The Jackson Laboratory, Bar Pfd Proefdierencentrum K.U.L., deCroylaan 34, B-3030 Harbor, ME 04609 Heverlee (Leuven), Belgium Rku Rockefeller University, 1230 York Ave., New York, NY Pfi Pfizer, Ltd., Parasitology Research Department, Sand 10021 (Dennis Stark) wich, Kent, England Rl Drs. W. L. and L. B. Russell, Biology Division, Oak Pgi Population Genetics Institute, Life Science Bldg., G- Ridge National Laboratory, Oak Ridge, TN 37830 117, Purdue University, Lafayette, IN 47907 (Dr. T. G. Rma Istituto di Anatomia Comparata, UniversitÃ di Roma, Martin) Via Alfonso Borelli, 50, Rome, Italy (Dr. M-V. Civitelli) Ph Czechoslovak Academy of Sciences, Institute of Ex- Rn Dr. Eugene M. Rinchik, Division of Immunology, Duke perimental Biology and Genetics, Budejovicka 1083, University Medical Center, Durham, NC 27710 Prague 4, Czechoslovakia (Doc. MUDr. Milan Hasek) Ro Dr. U. Roth, Zoologisches Institut, Jungiusstr. 6, Ham Pha Slovak Academy of Sciences, Institute for Experimen burg 36, BRD tal Pharmacology, DobrÃ¡Voda pri Trnave, Czechoslo- Ros Roswell Park Memorial Institute, West Seneca Labo vakia ratory, 2863 Clinton St., West Seneca, NY 14224 Pi Dr. H. I. Pilgrim, University of Utah College of Medicine, (Barbara Holdridge) Department of Surgery, Salt Lake City, UT 84112 Rot Dr. Med. W. Rotzsch, Physiologisch-Chemisches In Pm Dr. Paul C. Montgomery, Department of Microbiology, stitut der UniversitÃ¤t Leipzig, Ã¼ebigstr. 16, Leipzig, School of Dental Medicine, University of Pennsylvania, DDR Philadelphia, PA 19104 Rp Dr. Rosemary W. Elliott, Department of Molecular Bi Pms Royal Postgraduate Medical School, Hammersmith ology, Roswell Park Memorial Institute, Buffalo, NY Hospital, Ducane Rd., London, W. 12, England 14263 PÃ´ Dr. E. E. Pogosianz, Institute of Experimental and Rr Dr. M. N. Runner, University of Colorado, Department Clinical Oncology, Kashirskoje sh.6, Moscow M-478, of Biology, Boulder, CO 80304 USSR Rt Mr. John B. Roths, The Jackson Laboratory, Bar Har Pol School of Pharmacy, The Polytechnic, Department of bor, ME 04609 Pharmacology, Chester Road, Sunderiand, Durham, S Department of Life Sciences, Bar-Han University, Ra- England mat-Gan, Israel (Dr. Kurt Stern) Pp Drs. Raymond and Diana Popp, Biology Division, Oak Sa Research Institute for Tuberculosis, Leprosy and Can Ridge National Laboratory, Oak Ridge, TN 37830 cer, Cancer Research Laboratory, Tohoku University, Pr Dr. Louis J. Pierre, University of Connecticut, Depart Sendai, Japan (Dr. Haruo Sato) ment of Animal Genetics, Storrs, CT 06268 Sab S.A. Bureau of Standards, Private Bag 191, Pretoria, Ps Dr. Donald D. Porteous, SUNY Downstate Medical South Africa Center, Department of Radiology, 450 Clarkson Ave., Saf Southern Animal Farms, 475 E. Main St., Prattville, AL Brooklyn, NY 11235 36067 Psy Institute of Psychiatry, Animal Psychology Laboratory, Sb Dr. Arthur G. Steinberg, Biological Laboratory, Case- Bethlem Royal Hospital, Monks Orchard Road, Beck- Western Reserve University, Cleveland, OH 44106 enham, Kent, England Sbh Department of Serology and Bacteriology, University Pt Dr. Michael Potter, Laboratory of Genetics, National of Helsinki, Helsinki, Finland (Prof. O. MÃ¤kelÃ¤) Cancer Institute, Bldg. 37, Room 2B03, Washington, Sc Dr. J. P. Scott, Tufts University, Department of Psy DC 20205 chology, Medford, MA 02155 Pu Dr. B. D. Pullinger (retired) Scr Scripps Clinic and Research Foundation, Department Ra Dr. Harold Rauch, Zoology Department, University of of Experimental Pathology, 476 Prospect St., La Jolla, Massachusetts, Amherst, MA 01003 CA 92037 (Mr. Steven Wilson)

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Sd Dr. K. L. Sydnor, Department of Medicine, University bor, ME 04609 of Kentucky College of Medicine, Lexington, KY 40506 Sx Dr. David H. Sachs, Transplantation Biology Section, Sda Tohoku University, Laboratory of Animal Breeding, Immunology Branch, National Cancer Institute, Wash Department of Animal Husbandry, Faculty of Agricul ington, DC 20205 ture, 210 Kita-6-bancho, Sendai, Japan (Dr. Shusaku Sy Dr. A. Symeonidis (deceased). Contact Dr. C. G. Ga- Nishida) brielides, Cancer Institute, Theagenion Memorial, Se Prof. Lucio Severi, Istituto di Anatomia e Istologia Thessaloniki, Greece Patologica dell' UniversitÃ degli Studi di Perugia, Pe- Sz Dr. Leonard D. Schultz, The Jackson Laboratory, Bar rugia, Italy Harbor, ME 04609 Sed Dr. Robert S. Sedlacek, Massachusetts General Hos- T Department of Zoology, University of Toronto, Toronto pital, Department of Radiation Medicine, Boston, MA M5S 1A8, Ontario, Canada 02114 Ta Takatsuki Animal Farm, Takeda Chemical Industries, Seg Dr. Albert SegaloÂ«, Division of Endocrinology, Alton Kyoto, Japan Ochsner Medical Foundation, 1520 Jefferson Hwy., Tac Taconic Farms, Inc., Hover Ave., Germantown, NY New Orleans, LA 70121 12526 (Mr. Joseph W. Phelan) Sel Laboratorio Bioterapico Milanese, Selvi and C., Milan, Tach Dr. Takehiko Tachibana, Virology Division, National Italy (Dr. W. Murmann) Cancer Center Research Institute, Chuo-ku, Tokyo Sf Dr. Donald C. Shreffler, Washington University School 104, Japan of Mediane, Department of Genetics, St. Louis, MO Tar Dr. A. K. Tarkowski, Department of Embryology, Insti 63110 tute of Zoology, University of Warsaw, 00-927 War Sfd Stanford University School of Medicine, Department of saw, Poland Anatomy, Pato Alto, CA 94304 Tb Dr. S. A. Bamett, Australian National University, De Sg Dr. Jack Stimpfling, The Mclaughlin Research Insti partment of Zoology, Canberra ACT 2600, Australia tute, Columbus Hospital, Great Falls, MT 59401 Tbi Tokyo Biochemical Research Institute, 41-8 Takada 3, Shi Shionogi and Co., Ltd., Research Laboratory, Sagisu- Toshima, Tokyo, Japan kamidori, Fukushima-ku, Osaka, Japan (Dr. Yasunao Tbr Dr. Yoshihiko Tsubura, 2nd Department of Pathology, Ogawa) Nara Medical College, Kashihara-shi, Nara-ken, Japan Si Dr. Morten Simonsen, Queen Victoria Hospital, East Ten University of Tennessee, Memorial Research Center, Grinstead, Sussex RH19 3DZ, England Knoxville, TN 37920 (Dr. J. B. Jones) Sid Dr. Richard L. Sidman, Department of Neuroscience Th Dr. Karl Theiler, Anatomisches Institute der UniversitÃ¤t, G-2, Children's Hospital Medical Center, Boston, MA Gloriastr. 19, 8006 Zurich, Switzerland 02115 Tif Tierfarm AG, 4334 Sisseln, Switzerland (Dr. H. Humi) Sim Simonsen Laboratories, Inc., Route 1, Box 129, Day Toni Tohoku University School of Medicine, Central Farm Road, Gilroy, CA 95020 (Dr. James Russell) for Experimental Animals, Sendai, Japan Sk Dr. H. E. Skipper, Southern Research Institute, Bir- Tor Dr. S. Tores, Instituto Nacional do CÃ¡ncer, Sezao de mingham, AL 35205 Pesquisas, Pea, da Druz Vermelha 23, Rio de Janeiro, Skh Skin and Cancer Hospital, Temple University, Health Guanabara, Brazil Services Center, Philadelphia, PA 19140 Tox MRC Toxicology Unit, MRC Laboratories, Woodman- Sm Dr. David Steinmuller, Mayo Clinic, Department of Im steme Road, Carshalton, Surrey SM5 4EF, England munology, Rochester, MN 55901 (Dr. J. B. Greig) Smh St. Mary's Hospital Medical School, Department of Tr Dr. John J. Trentin, Division of Experimental Biology, Pathology, Paddington, London W2 1PG, England Baylor University College of Medicine, Houston, TX Smn Dr. Charles L. Sidman, The Jackson Laboratory, Bar 77025 Harbor, ME 04609 Tru Trudeau Institute, P. O. Box 59, Saranac Lake, NY Sn Dr. George D. Snell (retired) 12983 (David P. Kirstein) Sp Dr. William L. Simpson, Wayne State University School Tu Max-Planck-lnstitut fÃ¼rBiologie, Abt. Immungenetik, of Medicine, Detroit, Ml 48202 7400 TÃ¼bingen1, BRD (Dr. Jan Klein) Sr Dr. Howard A. Schneider (retired) Tw Dr. Noboru Takasugi, Zoological Institute, Faculty of Sri Stanford Research Institute, Department of Experi Science, University of Tokyo, Hongo, Bunkyo-ku, To mental Therapeutics, Mento Park, CA 94025 kyo, Japan Ss Dr. Willys K. Silvers, Department of Human Genetics, Ty Dr. Benjamin A. Taylor, The Jackson Laboratory, Bar University of Pennsylvania School of Medicine, Phila Harbor, ME 04609 delphia, PA 19104 Ucsd University of California at San Diego, Department of Ssc State Seruminstitute, Copenhagen S, Denmark (Dr. Pediatrics, P. 0. Box 3548, San Diego, CA 92103 (Dr. Fennestad) G. F. Chemoff) St Dr. Leonell C. Strong (deceased) Uct Animal Unit, Medical School, University of Cape Town, Sto Breeding Farm Stolbovaya, Laboratory of Inbred Ani Observatory, 7925, Cape Town, South Africa (M. E. mals, Academy of Medical Science, Solyanka 14, Mos Howard-Tripp) cow, USSR Uip UnitÃ©d'lmmunopathologie IRSE, C.N.R.S., B. P. 8,94 Sv Dr. L. C. Stevens, The Jackson Laboratory, Bar Har Villejuif, France

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Urne University of Minnesota, Department of Laboratory Wmr Dr. Willie M. Reams, Jr., Department of Biology, Uni Medicine and Pathology, Minneapolis, MN 55455 (Miss versity of Richmond, Richmond, VA 23137 June Smith) Wms Dr. R. Michael Williams, Sidney Farber Cancer Insti Umm University of Missouri-Columbia, School of Medicine, tute, Division of Tumor Immunology, 44 Binney St., Columbia, MO 65201 (Dr. Ronald M. Mclaughlin) Boston, MA 02115 Un Dr. A. C. Upton, Institute of Environmental Medicine, Wn Weizmann Institute of Science, Laboratory Animals NYU Medical Center, New York, NY 10021 Breeding Center, Rehovot, Israel Uni Unilever Research Laboratories, Biology Division, Col- Wo Dr. James E. Womack, Institute of Comparative Med worth House, Sharnbrook, Bedford, England icine, Texas A and M University, College Station, TX Up Miss Delta E. Uphoff, National Cancer Institute, Wash 77843 ington, DC 20204 Wq Dr. Walter C. Quevedo, Jr., Brown University, Division Upj Upjohn Co., Animal Rearing and Procurement Unit, of Biological and Medical Sciences, Providence, Rl Kalamazoo, Ml 49001 02912 Urd Urology Research, Duke University, Durham, NC Wr University of Wisconsin Medical Center, Department 27710 (Susan Poulton) of Radiology, 1300 University Ave., Madison, WI 53706 Vir Institute of Virology, Church Street, Glasgow, Scotland (Dr. Kelly H. Clifton) Vsp Dr. Michale E. Keeling, University of Texas System Wrm Walter Reed Army Institute of Research, Chief, De Cancer Center, Science Park, Veterinary Resource partment of Animal Resources, Washington, DC 20307 Division, Box 151 B1, Bastrop, TX 78602 Ws Dr. John West, Sir William Dunn School of Pathology, W Instytut Onkologii Â¡mMarii Sklowdowskiej-Curie, Zak- University of Oxford, South Parks Road, Oxford, 0X1 lad Biologii Nowotworow, Warszawa, ul. Wawelska 3RE, England 15, Poland (Dr. Alina Czamomska) Wsl Dr. H. Bazin, UniversitÃ©Catholique de Louvain, Ecole Wa Department of Genetics, Agricultural University, Gen. de SantÃ©Publique, Ave. Chapelle aux Champs 4,1200 Foulkesweg 53, 6703 BM Wageningen, The Nether Brussels, Belgium lands (Dr. P. de Boer) Wt Dr. Wesley K. Whitten, Hobart, Tasmania Wak Wakayama Medical College, Department of Phystol- Wts Dr. Peter J. Wettstein, Department of Microbiology, ogy, Wakayama, Japan (Dr. H. Matsushita) USC School of Medicine, Los Angeles, CA 90033 Wai Wallaceville Animal Research Centre, Department of Ww Mrs. E. F. Woodworth (retired) Agriculture, Private Bag, Wellington, New Zealand Wy Dr. G. W. Woolley, Institute of General Medical Sci We Dr. J. A. Weir, University of Kansas, Department of ences, National Institutes of Health, Washington, DC Zoology, Lawrence, KS 66045 20205 Wehi Walter and Eliza Hall Institute of Medical Research, Y Yuriovo Laboratory of Experimental Animals, Depart Melbourne 3050, Australia (Dr. G. J. V. Nossal) ment of Genetics, Yurtovo Post Office, Khimki Town, Wf Dr. George L. Wolff, National Center for Toxicological Moscow Region, USSR Research, Division of Mutagenic Research, Jefferson, Yok Department of Veterinary Science, National Institute of AR 72079 Health (Yoken), Kamiosaki, Shinagawa-ku, Tokyo 141, Wg Dr. H. E. Walburg, Jr., Oak Ridge National Laboratory, Japan (Drs. Masara Nakagawa and Toshihiko Asano) Comparative Animal Research Laboratory, Oak Ridge, Zal Dr. M. B. Zaleski, Department of Microbiology, SUNY TN 37830 Buffalo, Buffalo, NY 14214 Wh Dr. Abraham White, Department of Biochemistry, Al- Zbz UniversitÃ¤t Zurich, Biologisches Zentrallaboratorium, bert Einstein College of Medicine, 1300 Morris Park Kantonsspital, Ramistr. 100, Zurich, Switzerland Ave., Bronx, NY 10461 Zgm Medical Faculty, Department of Physiology, Salata 3, Wi Dr. J. W. Wilson (deceased) 41000 Zagreb, Yugoslavia (Prof. Dr. Filip Culo) Institut "Ruder Boskovic," 41001 Zagreb, Bijenicka 54, Wim Drs. Richard E. and Cynthia Wimer, City of Hope Zgr Medical Center, Quarte, CA 91010 Yugoslavia (Dr. Lidija Suman) Wis Wistar Institute of Anatomy and Biology, 36th Street ztk Zentrale Tierversuchsanlage des Klinikums der Johann at Spruce, Philadelphia, PA 19104 Wolfgang Goethe-UniversitÃ¤t, D600 Frankfurt, Theo- WI Dr. H. J. Wolfe, University of Kansas, Department of dor-Stein-Kai 7, BRD Zoology, Lawrence, KS 66045 Ztm Zentrales Tierlaboratorium der Medizinischen Hochs Wm Dr. William H. Murphy, University of Michigan, Depart chule, Roderbruchstr. 101, 3 Hannover, BRD ment of Microbiology, East Medical Bldg., Ann Arbor, Zur Institut fÃ¼rZuchthygiene der UniversitÃ¤t ZÃ¼rich,Win- Ml 48104 terthurerstr. 260, CH 8057 ZÃ¼rich,Switzerland

CANCER RESEARCH VOL. 45 MARCH 1985 977

Joan Staats

Cancer Res 1985;45:945-977.

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