Cancerresearch

CancerResearch

VOLUME 32 AUGUST 1972 NUMBER 8

ICANCER RESEARCH 32, 1609â€”1646, August 1972] Standardized Nomenclature for Inbred Strains of Mice: Fifth Listing'

Prepared by Joan Staats The Jackson Laboratory, Bar Harbor, Maine 04609

For The Committee on Standardized Genetic Nomenclature for Mice2

Previous issues of Standardized Nomenclature for Inbred and 232 in the fourth. Appendix 2 is a list of standard Strains of Mice appeared in CANCER RESEARCH in 1952 abbreviations for the names of persons or institutions (1), 1960 (2), 1964 (5), and 1968 (6). The wide demand for maintaining inbred strains. The principal use of these this compendium warrants its continuance. Between issues, abbreviations is in designating substrains. For example, additions and deletions to strain holdings appear in Mouse Deringer's HR strain, upon transfer to the Institute of Cancer News Letter (4) and Inbred Strains ofMice (3). Research, becomes HR/Delcr. Appendix 3 lists recommended Material in this issue is arranged in several sections, with a abbreviations for some of the more widely used inbred strains few changes in coverage or arrangement from previous issues. when coining hybrid designations or when brevity is desired There has been no change in the rules for designating inbred for other reasons. strains of mice since the Fourth Listing; therefore, those rules The Committee stresses the importance of using full strain have been omitted to save space. The data on biochemical or substrain designations in publications. The truncated polymorphisms are arranged in a table, both to avoid repeating symbol C57, for example, could refer to seven or eight long lines of alleles after each strain name and to make the different strains. Often it is sufficient to use the full material more conveniently accessible. designation under â€œMaterialsand Methodsâ€• and the shorter Most fostered and otherwise manipulated lines, named genes symbol alone elsewhere in the text. The many well-established on inbred backgrounds, and congenic histocompatibility cases of differences between substrains emphasize the strains have been omitted, to keep the list to a manageable size necessity of using full designations. For example, CBA/J and to avoid duplication. Dr. Jan Klein of the University of carries the gene for retinal degeneration whereas CBA/Ca does Michigan is preparing a list of congenic strains, to be published not; the two differ in radiosensitivity, and they are not in Transplatztation. histocompatible. We also stress the importance of identifying Appendix 1 is the index list of inbred strains and some the sex of the parents when listing hybrids. It is customary to clearly defined substrains. It contains 244 entries, compared list the female first. Thus, C57BL/6J 9 X DBA/2J d is with 124 in the first issue, 202 in each of the second and third, B6D2F1 , and DBA/2J 9 X CS7BL/6J d is D2B6F1.

1 Address requests for reprints to Dr. Joan Staats, The Jackson Laboratory, Bar Harbor, Maine 04609; to Dr. A. G. Searle, M.R.C. REFERENCES Radiobiology Unit, Harwell, Didcot, Berks., United Kingdom; or to Dr. I. K. Egorov, Institute of General Genetics, USSR Academy of 1. Committee on Standardized Nomenclature for Inbred Strains of Sciences, Moscow B-133, USSR. Mice. Standardized Nomenclature for Inbred Strains of Mice. Cancer 2 The Committee: P. DÃ©mant, Institute of Experimental Biology and Genetics, Czechoslovak Academy of Sciences, Praha 4; I. K. Egorov, Res.,12:602â€”613,1952. Moscow; M. C. Green, The Jackson Laboratory; H. Gruneberg, 2. Committee on Standardized Genetic Nomenclature for Mice. University College London, 4 Stephenson Way, London, NW! 2HE; J. Standardized Nomenclature for Inbred Strains of Mice, Second J. Hutton, University of Kentucky, Lexington, Ky. 40506; K. Kondo, Listing. Cancer Res., 20: 145â€”169, 1960. Department of Animal Genetics, Nagoya University, Nagoya-shi; M. F. 3. Inbred Strains of Mice: An informal biennial document listing Lyon, Radiobiology Unit, Harwell, Didcot, Berks.; 1. H. Roderick, The laboratories maintaining inbred strains of mice; the companion Jackson Laboratory; M. Sabourdy, C.S.E.A.L., C.N.R.S., document to Mouse News Letter. It is prepared by Joan Staats and 45-Orleans-la-Source (ICLA representative); R. Schmidt, Biologisches distributed by The Jackson Laboratory, Bar Harbor, Maine. ISM #7 Institut, Halle-Saale; A. G. Searle, Radiobiology Unit, Harwell, Didcot, Berks.; J. Staats, The Jackson Laboratory. Preparation of this paper was appeared in July 1971 and contained contributions from 96 supported in part by Grant GB27487 from the National Science laboratories. Fo:indation. 4. Mouse News Letter: An informal semiannual document carrying Received and accepted April 1 1, 1972. information on mutant genes, research stocks of mice, and research

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news. There is a bibliographic supplement with each issue. MNL is A Inbr (St): 161. Genet: a, b, c. Origin: currently edited by A. G. Searle, distributed to the Western Strong, 1921 , from cross of Cold Spring Hemisphere and Japan by The Jackson Laboratory and to the rest of Harbor albino and Bagg albino. Majority of the world by the Laboratory Animals Centre, Carshalton, Surrey. sublines trace to a stock which Bittner MNL #46 appeared in February 1972. obtained from Strong in 1927. Charac: lung 5. Staats, J. Standardized Nomenclature for Inbred Strains of Mice, tumors in 9? 5.8%, leukemia in 99 7.2% Third Listing. Cancer Res., 24: 147â€”168, 1964. 6. Staats, J. Standardized Nomenclature for Inbred Strains of Mice, (Bin); relatively susceptible to GraffI Fourth Listing. Cancer Res., 28: 391â€”420,1968. leukemia agent (Bln); mammary cancer 80% in breeders, 30% in virgins (Ki); reticular tissue neoplasms 4% in breeders, 12% in dd APPENDIX 1 (Ki); no mammary tumors in virgins (H); few skeletal variants (Gr); high incidence of List of inbred strains of mice and their clearly defined renal disease in old animals; 40% of 99 have substrains. positive LE cells or antinuclear antibodies by 6 mo., complement not detectable (Umc); Abbreviations 84% neonatally thym'ectomized develop runting syndrome (Umc); high incidence of Inbr = number of generations of brother X sister lung tumors in virgins and breeders (Dm); inbreeding. The substrain on which the cleft lip and palate occur sporadically, easily figure is based is indicated in parentheses. If induced with a variety of agents. Maintained a line has been produced by appropriate by: A, Bcr, Dm, Gr, H, Icrf, Ki, Mann crosses to an inbred strain, the number of (Philadelphia), Miroff (Schenectady), Ph, Ss, generations is preceded by N. St, Sy, Tarkowsky (Warsaw), Tr, Umc, Wis, Woodruff (Edinburgh). Genet = genetic constitution, mainly mutant coat and eye colors. Genes for biochemical A/He Inbr (J): 153. Origin: Strong to Heston polymorphisms and histocompatibility are 1938, He to J 1948. Charac: lung tumors 5% listed in Table 1. in 99, leukemia 7% in 99 (Lac); 58% mammary tumors in breeders at 414 days, Origin = origin. In some cases references are given. A 12.3% primary lung tumors, 10.8% table in Chap. 1 of BLM-2 gives more hepatomas, 12.3% leukemias in breeders at extensive information. 550â€”650 days (Y); mammary tumors about 40%, high lung tumor, amyloid and nephritis BLM-2 = Green, E. L. (ed.). Biology of the (He), median life span 400 days (Advan. Laboratory Mouse, Ed. 2. New York: Genet., 16: 305, 1971), mean life span in McGraw-Hill, 1966. fostered SPF 99 558 days, @d512 days (Lab. Animals, 5: 179, 1971). Maintained Charac = characteristics. In some cases journal references are given. Letters in parentheses by: An!, Cam, Crgl, He, Ibg, Icr, J, Kun, Lac [SPF] , Mk, Ms, Mt, Mv [f] , N, Rank indicate specific contributions to Inbred Strains of Mice. The key to the letters will (MUnchen), Rl, Sn, Sto, We, Y. be found in Appendix 2. In a few cases information has been obtained by A/J Inbr (J): 150. Origin: see strain A. Strong to correspondence. Cloudman 1928, survivors of Bar Harbor fire to Jax 1947 at F73. Charac: spontaneous Maintained by = persons or laboratories maintaining each malformations: in newborn, 6.9% cleft lip strain, insofar as information is available, are with or without cleft palate, 7.6% open indicated by substrain symbols. eyelid(s) (4.2% in 99, 11.2% in dd), 0.5% preaxial polydactyly of hindfoot, 0.5% b X s = brother X sister inbreeding. isolated CP (Kt); fairly high incidence of lung tumors (Umc); mammary tumors in GF, SPF, f = germ-free, specific pathogen-free, fostered. 25% of breeders, primary lung tumors in Information on bacteriological status was 40% of dd, 30% of 99 (J. Nat!. Cancer Inst., supplied by the holder of the strain as of 36: 921 , 1966); lower percentage of April 1971 . For example, the Radiobio granulocytes than other A sublines (Proc. logical Institute TNO has two lines of C3Hf, Soc. Exptl. Biol. Med., 78: 761, 1951); high one maintained under conventional condi incidence of renal disease in older animals. tions and one maintained under germ-free Blood pressure lowest of 8 strains tested conditions. This appears as â€œRij[cony. & (Nature, 212: 5 19, 1966). Uniformly GFI.â€• susceptible to P. berghei infection (Military

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Med., 131: 915, 1966). Very sensitive to by Furth as a high leukemia strain from X-irradiation (BLM-2); some heart lesions in 1928 to 1936, then random-bred at old breeders (BLM-2); moderately Rockefeller Inst. for several generations. b X susceptible to audiogenic seizures over a long S mated 9 gen. by Mrs. Rhoades and 2 1 by period up to 245 days (J. Psycho!., 43: 111, Lynch. Charac: reproduction poor under 1957). Maintained by: Ani, Born, Eg, Fr, Fs, conventional conditions, adequate in axenic Friedmann (Paris), J, Jms, Kt, Ml, Nirnr, Orl, and SPF state (Tif); deficiency of Umc. complement C'S (Tif); lymphatic leukemia 90% (Rd), 76% (Ms), 83% in 29 and 68% in A/WySn Inbr (SI): 138. Origin: see strain A. Strong dd (Ki), 90%bothsexes(Lac),91%in 99 at to Bittner 1927, maintained in Bar Harbor 300 days (Y); 88% in 29 (Life Sd., 9 (II): after Bittner's departure in 1942; recovered 107 1, 1970); sensitive to Graffi leukemia after fire from pedigreed sibs in market (myeloid) agent (Acta Biol. Med. Ger., 7: section, F75, and maintained by Woolley; 306, 1961); Oslo subline source of about 30 pairs to Snell in 1951 at F84-86. adrenocortical lipid depletion gene (Acta Used in transplantation studies. Charac: 25 Pathol. Microbiol. Scand., 58: 212, 1963); presacral vertebrae 7/ 13/5 . Large amount of blood catalase activity high (Z. lipid in adrenal glands (BLM-2). Maintained Versuchstierk., 1: 173, 1962); low by: A, Friedrnann (Paris), Grf, Klj, Sf, Sn. concentration of lipid in adrenal glands (BLM-2); mean life span 279 days in virgin AB Inbr (Jena): 35+. Genet: c. Origin: Agnes 99, 326 daysin dd (J. Gerontol.,21: 404, Bluhm to Hertwig in 1934, to Fortner in 1966); mean life span in fostered SPF 99 1945, to RÃ¶hrer in 1949, to Jena in 1952. 312 days, dcc 350 days (Lab. Animals, 5: Random-bred 1945â€”1949, b X s started 179, 1971). Maintained by: A, Bln, Born, 1959. Charac: 35â€”54% leukemia and @ Drn, Ep, Friedmann (Paris), Grf@Icr, lcrf, J, â€˜ reticulosarcomatosis in virgin 29; 15â€”30% Jamra (Sao Paulo), Ki, Lac [SPF] , Mk, Ms, fibrosarcoma in virgins; moderate incidence N, Orl, Rij, Rudali (Paris), Sm, Sn, Sy, Tif, of primary lung tumors in both sexes; Umc, Wak, We, Y. sensitive to casein-induced amyloidosis (Frankfurter Z. Pathol., 75: 164, 1966); tail AL Inbr (N): 157. Genet: a, b, c. Origin: length as long as or longer than body length believed to have originated from strain A (Z. Versuchstierk., 5: 78, 1964); good outcrossed to unknown strain followed by b vitality and fertility (Hg). Maintained by: x s mating.Shouldnotbe considereda Hg, Jena. strain A subline. Charac: good fertility; very AE Inbr (WI): 27. Genet: ae, b, d, se, p. Origin: low mammary tumor incidence. Maintained Hollander, Iowa, 1962. Maintained by: Wf. by: N.

AG/Cam Inbr (Cam): about 118; since A@a@central AU Inbr (J): 16 sin@cetransfer to J. Genet. : a/a, U, line, Fl8. Genet: AY/ae X AY/a@,with Aâ€•-', rd@. Origin: R. A. Fisher, about 1937. 50% A, As, at, a, and p continually backcrossed GrUneberg's CBA, 28.5% Fisher's to AY/ae line. Origin: R. A. Fisher; â€œAâ€• color stocks, and 21 .5% GrUneberg's wavy from GrUneberg in 1945 at F34 (a CBA stock, the latter two being unrelated to subline, J. R. Morton, personal communica strains of American origin (J. R. Morton lion). Various A-locus alleles introduced by personal communication). To Medawar, backcrosses, stock maintained mainly by 1947, to Silvers at F23 in 1957, to Jax sib-mated sublines until 1959. Backcrossing 1967. Charac: 99 do not reject d isografts. to one Ar/a X AY/a line started 1959; Maintained by: J, Re. central line now replaced by AY/ae X AY/ae. Charac: high penetrance of Nil, 0% pene A2G lnbr (A): 99. Genet: c, carries agouti. trance of chylous ascites in Ra (J. Med. Origin: strain A from GrUr@ebergto Glaxo Genet., 1: 10, 1964). Maintained by: Cam. Labs in March 1942; contaminated with nonstrain mating 1942â€”1950; inbred as AIK Inbr (Kga): 55+. Genet: +. Origin: cross A2G since then. Charac: useful for between Japanese fancy mice and Swiss endocrine work, especially gonadotrophin albino in 1949. Charac: litter size 4.6 Â±1.9 assay (Lac); Barnett has 2 colonies, 1 at 20Â° (Agr. Bull. Saga Univ., 10: 1, 1960). and 1 at â€”3Â°;mean life span in fostered SPF Maintained by: Kga. 99 644 days, dd 640 days (Lab. Animals, 5: 179, 1971). Maintained by: A, Ep, Lac AKR Inbr (N): 117. Genet: a, B, c. Origin: carried [SPF] , Tb.

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AlilInbr Charac:between(Nga): 41 . Genet: +. Origin: crossTruslove, Univ. London, 1957. anmember KSA and KB in 1958 (KB was asegregates for Hertwig's anemia; all b an/b days,Charac:of Kasukabe group, extinct 1959).mice are born alive; mean survival 212 carriersMaintainedgood reproductive performance.median 63 days. Heterozygous wellBAlnbr by: Nga.develop dermatitis. Hematology Re.P. (BLM-2). Maintained by: (Nmg): 22. Genet: b, At/At. Origin: Dr.characterized H. W. van der Kroon. Charac: good (J): 8 1. Genet: a, b, d, p, Se. Origin: W. reproductive performance; no known H. Gates, inbred since 1926; dilute brown 9 tumors.StrongInbr Maintained by: Nmg.BDPInbr from Little X pink-eyed d from 12: 295, 1927). Charac: frequent BALB/c (N): 152. Genet: b, c. Origin: albino mammary tumors; ovaries hemorrhagic and stock acquired by Bagg in 19 13 ; inbreeding necrotic ; kidneys polycystic or granular; started by MacDowel in 1923. Prior nervous behavior; mean life span in 99 468 inbreeding uncertain (J. Gen. Physiol., 11: days, 421 days in dd (J. Gerontol., 21: 404, J.distributed,57, 1927). MacDowell to Snell (who added 1966). Maintained by: Eg, the /c) in 1932 at F26; subsequently widely(Genetics, especially by Andervont. (Ms): 101 . Genet: a, b, c. Origin: Charac: low mammary tumor incidence but Lynch, from Bagg stock via Strong, susceptible to agent; some ovarian, adrenal, maintained at Rockefeller Inst. since 1921. and lung tumors. Susceptible to chronic Ly to De in 195 1 at F54. Charac: low pneumonia ; extremely sensitive to radiation mammary tumor, some lung tumor in old (BLM-2);Ms.1966). long breeding life. Blood pressure mice. Maintained by: Hf, highest of 8 strains tested (Nature, 212: 519,BLInbr Some heart lesions in old breeders; (Nvs): 40+. Genet: a, B, s, T Origin: L. arteriosclerosis common in both sexes fostersubline C. Dunn. Charac: large litters, good (BLM-2). Relatively nonaggressive. Cd (F34)BLPBRInbr mothers. Maintained by: Nvs. bilateraladenocarcinomadevelops spontaneous of the kidney: 60â€”70%in both sexes at 9â€”15months; adenocarcinoma (W): 40. Genet: c. Origin: Anna Dux, cells inhibit body growth when grafted into Gliwice, Sept. 1950 from unknown parents. homologous or other strains; this property F13 taken to Warsaw, June 1956, where it retained through more than 275 passages was split into 2 substrains, inbreeding into hosts of the same strain. 58% neonatally continued (Nowotwory, 7: 67, 1957). thymectomized develop runting syndrome Charac: no tumors; used for carrying (Umc). Very large reticuloendothelial organs transplantable vaginal epithelioma G93 relative to body weight (RES J. (Acta Unio Intern. Contra Cancrum, 16: W.lungReticuloendothelial Soc., 8: 421, 1970);BN/aInbr 172, 1960). Maintained by: 8%,angiomastumors 21%, reticu!ar tumors 4.5%,BN/bmammary6%, lymphosarcomas Inbr (W): 42. Genet: c. Origin: see BN/a. BALB/cPi[GF]tumors 3% of 99 all in Charac: lung tumors 25%, chronic nephntis 138:542,(Proc. Soc. Exptl. Biol. Med., 13%; used for carrying transplantable vaginal spleenamyloidosis1971); almost all dd show epithelioma G94. Maintained by: W. Inst.,47: by 20 mo. (J. Nat!. Cancer aSPF1241, 1971);meanlife spanin fosteredBRSUNTInbr (N): 116. Genet: a, b. Origin: Strong, continuedAnimals,99 56 1 days, dd 509 days (Lab.branch of BRS (from strain NH) 5: 179, 1971); high complementwithout further methylcho!anthrene treat activitygastric1971). (Japan. J. Exptl. Med., 41: 31 1,ment (UNT untreated). Charac: St.[SPF] Maintained by: A, Anl, Ar, Bdlesions, adiposity. Maintained by: N, Ep,Friedmann, Bom, Bre, Bsp, By, Cd, Crgl, Dp, at(Budapest), (Paris), Fs, Gh, Grf, GyorffyBRVRInbr: 72+. Genet: c. Origin: Webster 261,Ki, He, Hf, Ibg, Icr; Icrf, J, Jic, Ka,Rockefeller Inst. (J. Exptl. Med., 65: someN,Kon, Kt, Kun, Lac [SPFJ , Mk, Ms, Mv,1937). Charac: resistant to salmonella, experimental[cony.Nimr (GF] , Or!, Rank (MUnchen), Rijencephalitic viruses, and @ thymusUmc,+ GFJ Rl, 5cr, Sf, Sm, St, Tif [I] ,allergic encephalomyelitis. Has larger Varga (Budapest), W, We.than BSVS, and it increases more under antigenic stimulation (RES J . Reticu!oendo BAN/Re by:noninbredInbr (Re): 38. Genet: a, b, an/+ +. Origin:thelial Soc., 4: 438, 1967). Maintained b an mice received from G.P1, Wis.

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BR6 Inbr: 60+. Origin: C57BL 9 X RIlI d, Sept. Animals, 5: 179, 1971). Maintained by: B!n, 1945, descendants inbred b X s (Brit. J. Cam, Cl, Dept. Surg. Edinb., Eg, Fa, Gyorffy Cancer, 1: 362, 1947; Brit. J. Cancer, 3: (Budapest), H, Ht, J, Lac [SPF] , N, Nimr 230, 1949). Charac: 95% mammary tumor [cony. + GF] , Ph, Ss, Tarkowski (Warsaw), incidence in breeders having 2 or more Tif, TU, Umc, Y. litters, 46% in virgins, 0% in dd (Brit. J. Cancer, 15: 561, 1961). There have been CBA/J Inbr (J): 152. Origin: Strong to Andervont several tumor-free sublines. Maintained by: 1947, to Jax 1948. Charac: 60â€”65% Icrf. mammary tumor incidence in breeders at less than 1 year; susceptible to whole-body BSVS Inbr (Wis): 85. Genet: c. Origin: Webster at irradiation; blood pressure relatively high Rockefeller Inst. (J. Expt!. Med., 57: 793, (Nature, 212: 519, 1966); mid-range of I 933). Charac: susceptible to salmonella, radiation resistance (BLM-2). Mean life span some encephalitic viruses, and experimental in 99 and dd 527 days (J. Gerontol., 21: allergic encephalomye!itis. Maintained by: 404, 1966); d@3have 65% hepatomas (J. P1,Wis. Gerontol., 21: 404, 1966). Maintained by: J, Kch, Kon, Mk, Ml, Ms@Or!, Ph, Sm, Th, BT Inbr (Kt): 35. Genet: a, b, d, bt. Origin: Wak,Yok. unidentified mice thought to be from Jax segregating at b, d, and bt. Dominant alleles CBA/St Inbr (Man): 147. Charac: mammary tumor were eliminated during inbreeding. Charac: incidence high in both breeders and virgins; cortisone causes high fetal death rate but long lived (Man, St); some mammary tumors low incidence of cleft palate in survivors. in breeders (Lac); low or no mammary Short hind limbs. Maintained by: Kt. tumors (Umc). Maintained by: Gr, Ki, Kw, Man, No, St, Umc. BUA Inbr: 59. Genet: a, c. Origin: from albinos of unknown ancestry at Brown University; CBA/H-T6 Inbr (J): N13F40. Origin: animals carrying maintained by random breeding until 1945. the T(3 ;?)6Ca (T6) trans!ocation were Charac: selected for good growth and backcrossed to CBA/H by M. F. Lyon reproductive performance ; no known several times, eventually sib-mated. Charac: tumors. Maintained by: Hn. homozygous for small marker chromosome of T6. Congenic with CBA/H. Maintained BUB Inbr (J): 78. Genet: a, c, rd. Origin and by: Ei, Gyorffy (Budapest), Lac [SPF], charac: as BUA. Bn has a line BUB/Bn-C, Nimr [GF] , Or!, Ph, Rij, Tif, Umc. outcross of BUB/Bn to C57BL/6J with repeated backcrosses to BUB, useful for CC57BR Inbr (Mv): 7 1. Genet: a, b. Origin: transplantation experiments (now at N43). Medvedev, 1943, BALB/cN 9 X C57BL/N d. Maintained by: Bn, Ch, J. Charac: no spontaneous mammary tumors but about 60% when milk agent is C Inbr (Man): 118. Genet: b. Origin: see introduced; primary lung tumors 22.5%. C3H/St. Charac: moderate mammary tumor Incidence of all other tumors less than 1%. incidence. Maintained by: Man, St. Maintained by: Mv, Sto, Y.

CBA/Br Inbr (A): ? + 164. Genet: 1-, not H-2'@. CC57W Inbr (Mv): 68. Genet: a, b, c. Origin: Origin: see C3H/St. Jax to Haldane and Medvedev, same as CC57BR. Charac: almost Grtineberg 1932, to Bonser (Leeds) approx. no mammary tumors, but about 60% when 1933. Maintained by: A, Nmg, Rij [cony. + milk agent is introduced; primary lung GF],Sel. tumors 24.5%; incidence of all other tumors less than 1%. Maintained by: Mv, Sto, Y. CBA/Ca Inbr (J): 70. Origin: see C3H/St. Jax to Haldane and GrUneberg 1932, to Carter CE Inbr (J): ? + 58. Genet: Aw, ce,rd+. Origin: through Royal Cancer Hosp. and Brit. Emp. wild mutant trapped in Illinois by J. E. Cancer Campaign. Charac: absence of lower Knight. Color genetics studied by Detlefsen. third molars in about 18%, few skeletal Inbred by Eaton at least 15 gen., some sent variants (Gr); moderate mammary tumors in to Woolley. Speirs (2 gen. from Wy) to Wy breeders. Foam cell reticulosis mutant found and Jax in 1948. Charac: mammary tumor in CBA/H; dd sensitive to vitamin K 3% in virgins (Ki); 33% ovarian tumors after depletion (Tifl; mean life span of fostered 20 mo. (Di); many tumor types; high adrenal SPF 99 825 days, dd 486 days (Lab. cortical carcinoma incidence in both sexes

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after neonatal gonadectomy. Poor breeders. 100% brachypodism, due to a single Large amount of lipid in adrenals (BLM-2); recessive gene. Maintained by: Cpb. mean life span of fostered SPF 99 703 days, dc@ 498 days; high incidence of hepatomas CPB-N Inbr (Cpb): 40. Genet: a, b, p. Origin: as (Lab. Animals, 5: 179, 1971). Maintained CPB-F. Charac: normal sex difference in by: Ep, J, Ki, Lac [SPFJ. major urinary protein content of serum and in reaction to hexobarbital. Maintained by: CFCW Inbr (RI): 76. Genet: c, Ca. Origin: Cpb [conv.+SPF]. Carworth Farms 1/3/48 to Ri, b X s inbreeding by Ri. Maintained by: Rl. CPB-NIZ Inbr (Cpb): 35. Genet: a, b, p. Origin: cross of strains CPB-N and CPB-I (now extinct), CFW/Jic Inbr (Jic): 26. Genet: c. Origin: from 1956. Selected since 1956 for high body noninbred CFW mice, inbreeding started weight. Maintained by: Cpb. 1964. Maintained by: Jic. [Editor'snote. There are severalother CPB-P Inbr (Cpb): 32. Genet: a, b, c, d, p. Origin: inbred CFW lines (Ms, Jena, Ri); many have as CPB-F. Charac: reacts with head twitching been reported for previous issues of this to LSD. Maintained by: Cpb. compendium.] CPB-Q lnbr (Cpb): ? + SO. Genet: a, B, ce, D, P. CHI Inbr (Man): 126. Genet: +. Origin: see Origin: Hagedoorn, Holland, to Hirschfeld C3H/St. Charac: as C3H. Maintained by: 1937, to Cpb 1949. Charac: more suscepti Man, St. b!e to tuberculosis than most strains; reacts to LSD with head twitching. Maintained by: CL/Fr Inbr: ? + 22 + 7. Genet: at, b, c. Origin: Cpb. Fraser, stock from Morgan carrying â€œmslâ€• (migratory spot lesionâ€”avariable white spot CPB-R Inbr (Cpb): ? + 44. Genet: a, b, c, D, P. on the retina) crossed to A/i and inbred b X Origin: â€œRhodesfarmâ€•South Africa to 5 with selection for high spontaneous cleft Compton, England, to Hagedoorn, Holland, lip frequency. Charac: Msl now has low to Cpb in 1949. Maintained by: Cpb [cony. penetrance ; cleft lip in 26% of viable 17-day +SPF]. fetuses (Teratology, 3: 295, 1970). Main tamed by: Fr, Jic. CPB-S Inbr (Cpb): ? + 51. Genet: A, B, c, D, P. Origin: a Swiss from Rockefeller Inst. to CPB-F Inbr (Cpb): 45. Genet: b, p. Origin: at Cpb, Laidlaw (Hampstead) to Hagedoorn to Cpb about 1950. Charac: 10% show deformed in 1949. Earlier selected for â€œbacillary toes or polydactylous hind feet. Maintained resistant, virus susceptible.â€• Charac: rather by: Cpb. aggressive, especially dd. Maintained by: Cpb, Gro. CPB-FT Inbr (Cpb): 40. Genet: a, B, c, D, p. Origin: CPB-T Inbr (Cpb): 24 + 14. Genet: a, b, s. Origin: as CPB-F. Charac: major urinary protein in Hagedoorn to Cpb in 1949. Charac: serum abnormally low in males; about 8% of macrocytic anemia. Maintained by: Cpb. newborns show transitory jaundice; does not show the norma! sex difference in reaction CBP-TK Inbr (Cpb): 30. Genet: a, b, d, s, W. Origin: to hexobarbital (Evipan); the sex difference cross between CPB-T and CPB-K in 1953. to hydroxyclione (Viadril) is present. Charac: macrocytic anemia. Maintained by: Maintained by: Cpb. Cpb. CPB-V Inbr (Cpb): 46. Genet: c@ . Origin: CPB-H Inbr (Cpb): 42. Genet: b, d. Origin: as Hagedoom to Cpb in 1949. Charac: males CPB-F. Charac: almost all 99 have a pair of have low major urinary protein in serum; no supernumerary nonlactating nipples lateral sex difference in response to hexobarbital. to pair IV. Maintained by: Cpb. Maintained by: Cpb. CPB-K Inbr (Cpb): 44. Genet: a, B, c, d, P. Origin: CPB-WG Inbr (Cpb): 27. Genet: a. Origin: waltzing as CPB-F. Charac: excitable; small litters; mice from Hagedoorn to Cpb in 1949. amylase type B (other CPB-strains are type Crossed with strain G, now extinct, in 1953. A). Maintained by: Cpb. Charac : carries one of the waltzer-shaker mutants; expression varies from fairly CPB-MO Inbr (Cpb): 28. Genet: c. Origin: Inst. Trop. normal walking to circling; very excitable; Hyg. Amsterdam, to Cpb 1957. Charac: not deaf. Maintained by: Cpb.

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CPB-WV Inbr (Cpb): 30. Genet: J@/w. Origin: C3H/Bi Inbr (Ki): ? + 121 . Genet : +. Origin: see GrUneberg to Cpb in 1956. Charac: C3H/St. Strong to Bittner, 1931, Bi to macrocytic anemia. Maintained by: Cpb. Kirschbaum 1952. Charac: mammary cancer 83% in breeders, variable in virgins; leukemia CPB-Y Inbr (Cpb): 40 + 8. Genet: AY/at. Origin: less than 0.5% in breeding 99, 14% in dd; Hagedoorn to Cpb in 1949. Charac: obesity. hepatomas 10% in dd, none in 99 (Ki); Maintained by: Cpb. mammary tumor 70% in virgins, 85â€”90%in breeders, very susceptible to hepatic carcinogens (Rd). Maintained by: Bd [SPF], CPBNB-1/Pr Inbr (Pr): 23. Genet: a, W/w. Origin: Cpb, Dm, Icrf, Ki, Mai, Rd, Umc, Wr. @ CS7BL/lOChPr, NAW-wa-2 and CP. Charac: microphthalmia and/or corneal opacity in C3H/Fg Charac: lymphocyte leukemia 96% in virgin W/w segregants, 20% in dd, 30% in 99. 99, 89% in dd; mammary tumor 24% in 99, Maintained by: Pr. hepatomas 8% in dd (Anat. Record, 142: 233, 1962). Maintained by: Fg. CPN/Pr Inbr (Pr): 22. Genet: a, W@'/w,s. Origin: CP x NAW@wa@[email protected]:40%incidenceof C3H/He Inbr (He): ? + 133. Genet: +. Origin: see hypoiridis. Maintained by: Pr. C3H/St. Strong to Andervont 1930, An to Heston 1941 after 35 b X s matings by An. CR/Sf Inbr (Sf): 20. Origin: Shreffler, C3H/JSf X Charac: mammary tumor incidence 97% in RIII/Wy. Maintained by: Sf. breeders at average age 7.8 mo., 100% in virgins 10.6 mo. (He); 90% in both breeders CS Inbr (Nga): 48. Genet: a, b, c, s. Origin: and virgins (Crgl); 84% in breeders at 272 established from hybrids between NBC and days (Y). Hepatomas 85% in dd at 14 mo. 511 in 1956. Unrelated to IVCS. Charac: (He); high complement activity (Japan J. good reproductive performance ; quick Exptl. Med., 41: 31 1, 1971). Maintained by: moving; Japanese crooked tail 16%. A, Ar, Crgl, Dp, El, Ep, H, He, Icr, Icrf, Jic, Maintained by: Nga. Ka, Km, Kon, Lac, Mk, Ms, N, Rank (MUnchen), RI, Sto, Sn, Sy, Wak, We, Wis, CXBD Inbr (By): 42+. Genet: +. Origin: Bailey, Y. cross of BALB/cAnN 9 X CS7BL/6JN d, then b X s mated. Charac: carries C3H/HeJ Inbr (J): ? + 130. Genet: +. Origin: see histocompatibiity mutation which has C3H/St. Heston to Jax 1947. Charac: very arisen and been fIxed since FlO. Maintained high mammary tumor incidence in breeding by: By. 99, slightly lower in virgins; hepatomas in The recombinant inbred strains CXBD, dd, low red and white cell counts;high CXBE, CXBG, CXBH, CXBI, CXBJ and mortality in ck@exposed to turpentine and CXBK were each derived from the above chloroform fumes (J). Maintained by: A, cross and thereafter independently sib Bts, Eg, Fs, Grf, J, Kraskovsky (Minsk), Ml, mated. For each strain it has been Mv, Nmg, Orl, Ph, Sf, Sel. determined whether the BALB/c or the CS7BL/6 allele has been fixed at each of the C3H/St Inbr (St): I 43. Genet: +. Origin: Strong, following loci: a, b, c, Ea4, Es-i, Gpd-i, 1920, from cross of 9 Bagg albino X DBA d. Gpi-1,Hbb,Mod-i, as wellasatH-i,H-2, Strains C, CBA, CHI, and Cl21 also H-7, H-8, and 17 other as yet unnamed originated from this cross. Charac: high histocompatibility loci. These strains are mammary tumor incidence in both breeders useful in linkage and p!eiotropism studies and virgins (St). Maintained by: Man, St. (Transplantation, ii: 325, 1971). Main tamed by: By. C3Hf Inbr (N): 90. Origin: Heston 1945, from a litter of C3H born by cesarean section and Cl7/Icrc Inbr (Icrc): 25+. Origin: Ranadive, 1956, foster nursed on C57BL/6. There are several XVII 9 X C57BL/6Jlcrc d. Selected for other fostered C3H lines, not all fostered on dilute brown coat color, b X s mated. CS7BL, and not all from the same C3H Charac: sensitive to skin carcinogenesis by subline. All C3Hf lines lack the milk factor, chemicals, sturdy, long-lived (25.8 mo.), hence are low mammary tumor but highly litter size 7â€”8, incidence of all kinds of susceptible to introduction of the factor; tumors less than 1%. Used for testing weak males have some hepatoma. Life span of carcinogens (Indian i. Med. Res., 57: 521, Umc sublime, both sexes, breeders and 1969). Maintained by: Icrc. virgins, 590 days (J. Exptl. Med., 135: 339,

AUGUST 1972 1615

1972); mean life span of SPF 99 676 days, lymphoma incidence after whole-body cSd590days(Lab. Animals,5: 179, 1971). irradiation (Ka); micro- or anophthalmia Maintained by: A, Ani, Bd[SPF] , Born, Crgl, about 20%, hydrocephaly about 2% (Cpb); Dm, Dp, Gh, He, Icr, Ki, Lac[SPF] , N, hereditary hydrocephalus in 4.1% at 20â€”60 Nimr[GFJ , Rd, Rij [cony. + SPF] , RI, Sm, days old (Brain Nerve, 20: 695, 1968); Tif, Umc. micro- and anophthalmia increased from 10% at +F1 to 34% at +F25 (Ml); type B C3HA Inbr (Y): 70. Genet: +. Origin: Pogosianz, reticular cell neoplasms 74.5% in HeDe C3H 9 X A d, subsequent inbreeding. sublime breeders (J. Natl. Cancer Inst., 40: Charac: originally 30% mammary tumors, 771, 1968); mean life span of fostered SPF gradually decreased (Vopr. Onkol., 7: 58, 99 580 days, ck@645 days (Lab. Animals, 5: 1961); susceptible to hepatic carcinogens. 179, 1971). Maintained by: A, Bcr, Bin, Bre, Maintained by : Y. Bsp, Cam, Cpb, Crgl, Dm, Dp, Ep, Fa, Gr, Gro, H, He, Hf, Hg, Icrf, Ka, Ki, Lac[SPF], C3HeB/De Inbr (Hf): 68. Origin: Deringer, fertilized ova Md, Mv, N, Nimr, Nmg, Rd, Rij, Ri, St, Sy, of C3H transferred to C57BL. Charac: lacks Tif,W,Wehi. milk agent; hepatomas 58% in virgin 99 after 24 mo., 30% in breeders, 38% in force-bred, C57BL/Ks Inbr (J): 81. Genet: a. Origin: C57BL/6J to 90% in breeding dc@;mammary tumor 4% in Biesele in 1947, then pen-bred, to Kaliss virgins, 55% in breeders, 74% in force-bred; 1948. Ks resumed inbreeding, returned them many ovarian tumors (J. Natl. Cancer Inst., to Jax 1948. Tumor EO77 1 originally killed 22: 995, 1959). Maintained by: Bre, Dt, Hf, all animals but, as inbreeding progressed, all Ms. animals regressed the tumor. Charac: high incidence of toe malformations; micro C3HeB/Fe Inbr (J): 78. Genet: +, rd. Origin: Fekete, phthalmia, uniform high fertility (Am. 1948, C3H/HeJ ova transferred to C57BL/6; Zoologist, 3: 223, 1963); the mutation original transplant animals to Hummel, F3 diabetes (db) arose in this strain, which is to Jax in 1950. Charac: low mammary used as a control for it; 77% neonatally tumor incidence, high susceptibility to thymectomized develop runting syndrome agent; 64% ovarian tumors in breeders after (Umc). This strain differs from C57BL/6 at 19 mo., 22% in virgins; hepatomas 64% after 4 histocompatibiity loci. Maintained by: J, 19 mo. (Hu); lowest blood pressure of 19 Ph,Umc, Wak. strains tested (Genetics, 55: 497, 1967); mid-range of radiation resistance (BLM-2); CS7BL/1 Inbr (Umc): 80. Origin: W. S. Murray (C. C. calcareous deposits in heart of almost all Little colony) CS7BL sublines to Andervont. retired breeders (BLM-2); mean life span in One subline of Murray's was selected by virgin 99 657 days (J. Gerontol., 21: 404, Halsey Bagg for low mammary tumor; it was 1966). Maintained by: Ar, Dm, Friedmann called Line-A by Andervont. An Line-A to (Paris), Hb, J, Or!. Bittner in 1947 at F29. Bittner called it B-line-i , shortened to B1 . Charac: 99 reject C57BL Inbr (A): ? + I 10. Genet: a. Origin: Little, c@dskingrafts;reciprocalskingraftswith 192 1, from mating of 9 57 X d 52 from Miss C57BL/4 and with CS7BL/6 are rejected Abby Lathrop's stock. d 52 mated to 9 58 100%; 69% neonatally thymectomized gave rise to C58. Charac: sensitive to Graffi develop runting syndrome (Umc). leukemia agent; no spontaneous mammary Maintained by: Umc. cancer, low susceptibility to induction by chemical carcinogens (Bcr); 6 lumbar C57BL/6J Inbr (J): 107. Genet: a, ra@. Origin: see vertebrae (Md); no mammary cancer in C57BL. Sub!ines 6 and 10 separated prior to breeding 99, reticular tissue tumors less than 1937. Charac: spontaneous malformations: 10% in 99, 4% in c@d(Ki); nonterritorial, no in 2709 newborn, 9.6% microphthalmia and sensitive aggression-flight balance, adapted anophthalmiaâ€”l 6.8% in 99 , 3% in d@; 0.6% to hole-living (Gro); many skeletal variants preaxial polydactylyâ€”hindfoot; 0.4% oro (Gr); sublines He and An are high liver pharyngeal mandibular defects (â€œoto catalase ce in contrast to other CS7BL and cephalyâ€•) (Kt); about I 2% eye defects other C57 strains and C58 which are Ce, (Pr & J); skeletal malformations 13â€”15% mammary tumor incidence less than 1%, (skull 5%, vertebral column 11%, extremities adenomas of the hypophysis in older animals 1.5%), resorptions 16% (Ffm); 1% (He); 7% reticulosarcomas at 14 mo., senile hydrocephalus and 3% malocclusion in 3000 nephrosc!erosis frequent (Rd); 90â€”100% mice 6 wk. old; breast tumors about 1% in

1616 CANCER RESEARCH VOL. 32

breeders, none in virgins; resistant to cross of two brown branches, one of which irradiation; various tumor types in low had previously given rise to C57BR/a. To incidence after 18 mo. (J): leukemia 7â€”16% Heston 1938, to mx 1947 at F66. Charac: in 99 (Life Sci., 9(11): 1071, 1970); high low mammary tumor incidence, some incidence of hepatomas after irradiation hepatomas in dd (J); very resistant to (Compt. Rend. Soc. Biol., 157: 680, 1963); X-irradiation but sensitive to insulin (Lac); blood pressure in mid-range (Nature, 2i2: mean life span in fostered SPF 99 660 days, S 19, 1966); high alcohol preference (Quart. dd 577 days(Lab. Animals,5: 179, 1971); J. Studies Alc., 28: 22, 1967); low mean life span in virgin 99 694 days, 703 concentration of lipid in adrenals, mid-range days in dd (J. Gerontol., 21: 404, 1966); of radiation resistance (BLM-2); incidence of 25% hepatomas in c@d(J.Gerontol., 2i: 404, all types of tumors 70% in both sexes under 1966). Maintained by: Hb, J, Lac[SPF] , N, SPF conditions, maximum life span 1200 Orl,Rl. days [Federation Proc., 30: 341 (Abstract), 197 1] ; mean life span in 99 692 days, 676 C57L Inbr (J): 118. Genet: a, b, ln. Origin: J. days in c@d(J. Gerontol., 21: 404, 1966); Murray, 1933, mutation in F22 of a C57BR median life span 600 days (Advan. Genet., subline which is now extinct. Maintained by 16: 305, 1971); median life span in barrier Cloudman, to Heston 193'8, He to Jax 1947 890 days (Bd); high complement activity at F45. Charac: low mammary tumor (Japan. J. Exptl. Med., 4i: 311, 1971). incidence; some pituitary tumors in old Maintained by: Anl, Ar, Bd[SPFJ , Born, By, animals, hematocrit extremely high, Dt, Eg, Ffm, Friedmann (Paris), Fs, Gh, Grf, congenital cystic ovaries frequent (J); type B Hb, Herberg (DÃ¼sseldorf),Hf, Hn, Ibg, Icr, J, reticular cell tumors 54.5% in breeders (J. Jic, Kch, Ko, Kon, Kt, Mai, Ml, Ms, N, Nmg, Nat!. Cancer Inst., 40: 771, 1968); Or!, Ph, Ra, Rank (MUnchen), 5cr, Sm, Ss, uniformly susceptible to P. berghei infection Sto, Th, TU, Ver!ey (Marquette), Wak, We. (Military Med., i3i: 915, 1966); mean life span in fostered SPF 99 604 days, ck@473 C57BL/lOJ Inbr (J): 111. Origin: see CS7BL/6. Charac: days (Lab. Animals, 5: 179, 1971). occasional vaginal septa, some fusion of Maintained by: Eg, Gh, J, Lac[SPF] , Ms, N, bones in feet (Fo); incidence of eye defects R1,Wak,Y. about 12%, 20% in 99 and 3% in dd; malocciusions and hydrocephalus rarer (J); C58 Inbr (J): 153. Genet: a. Origin: MacDowell, Maintained by: Ch, Fo, Gn, J, Man, Ml, Pr, 192 1, from mating of littermates 9 58 and d Rjb, Rl, Sel, Sf, Shire (Stanford), Sm, Wak. 52 of Miss Lathrop's stock, d 52 mated to 9 57 gave rise to C57 strains. Charac: high C57BL/lOScSn Inbr (Sn): 100Ã·. Origin: see C57BL; Little, incidence of leukemia before 1 yr. of age; to W. L. Russell, to J. P. Scott at F26 as a frequent polyovular follicles; aplasia of separate subline, to Snell at F35-36. Charac: kidney about 10% (J); leukemia, primarily behavior traits differ from C57BL/1OJ lymphatic, 75% 99 and 65% dd (Ki); 95% (Science, i30: 45 1, 1959). Has been used to lymphatic leukemia in both sexes (Umc); provide the genetic background for the leukemia 97% in 99 (Life Sci., 9(11): 1071, production of congenic resistant lines 1970); relatively resistant to P. berghei differing from C57BL/lOScSn primarily by infection (Military Med., i3i: 915, 1966); single histocompatibility loci (Immunology, mean life span 35 1 days in virgin 99, 373 4: 366, 1961). Maintained by: Cpb, Eg, Grf, days in dd (J. Gerontol., 2i: 404, 1966). Gyorffy (Budapest), Hull (Glasgow), Klj, Maintained by J, N, Umc, Y. Lac[SPFJ ,N, Ph, Sn, We, Y. DA/Hu Inbr (Sn): 80. Genet: c, rd. Origin: brother and sister born 12/48 to a nomnbred C57BR/a Inbr (Ms): 52+. Genet: a, b. Origin: see â€œSwissâ€•with a mammary gland tumor. CS7BR/cd. Separated from other brown Charac: low mammary tumor; partitioned lines in gen. 9. Jax to Misima in Dec. 1958 at vaginas. Maintained by: Sn. Fl2. Charac: low mammary tumor. Maintained by: Ms. DBA Inbr (A): ? + 92. Genet: a, b, d. Origin: Little, 1909, from color stocks. The oldest C57BR/cdi Inbr (J): 141. Genet: a, b. Origin: Little, inbred strain. In 1929â€”1930 crosses were from cross that gave rise to CS7BL, made between sublines and several new C57BR/a, and C57L. Black and brown lines sublines were established. Two of these were were separated in the first generation. 12 (now called 1) and 212 (now called 2). Subline cd was established in gen. 13 from a Maintained by : A.

AUGUST 1972 1617

DBA/ 1 Inbr (Eg); 75. Genet: a, b, d, rd@. Origin: see chemical carcinogens (Bcr); mammary DBA. Charac: resistant to most DBA/2 tumors less than 3% in breeders, leukemia tumors; P1 534 grows in 50% ofDBA/l; 591 10% in 99 and 2% in dd (Ki). Maintained by: grows in both; mammary tumors in about A, Bcr, Ki, Ms. 3/4 of breeders over 1 yr and in some virgins after I 8 mo.; susceptible to inoculated TB DD Inbr (He); 50. Genet: A, B, c, S. Origin: (J); high red blood cell count, calcareous from noninbred ddN stock of Central Lab. heart deposits in almost all retired breeders Exptl. Anim. to Osaka Univ (1956); to (BLM-2); 61.5% mammary tumors in Heston 1957, to Nara 1959. Charac: breeders at 460 days, 8.4% leukemias, 3.8% mammary tumors 63% in breeding 99 (Thr); primary lung tumors in 99 (Y); 22% varied mammary tumors 84% in breeding 99, some tumors at autopsy (J. Gerontol., 2i: 404, arising in plaques, and 75% in virgin 99 (He). 1966); uniformly resistant to P. berghei Heston has two fostered lines, one on infection (Military Med., i3i: 915, 1966); C57BL (4% mammary tumor in breeders at mean life span of fostered SPF 99 686 days, 19 mo.) and one on C3H/He (91% in dcc 487 days (Lab. Animals, 5: 179, 1971). breeders at 6.7 mo.). Maintained by: He, Maintained by: Eg, Fs, Glw, J, Kt, Lac[f], Thr. N,Y. DDD Inbr (Jic): 44. Genet: A, B, c, D, S. Origin: DBA/2 Inbr (N): 108. Origin: see DBA. Charac: dd-stock mice taken by Dr. S. Hata from 50% mammary tumors in breeders at 14 mo. Germany to Kitasato Inst. before 1920. (dd (Crgl); mammary tumors 66% in breeders, = Deu tschland-DensenbyoKenkyusho). 30% in virgins; leukemia 6% 99, 8% dd (Ki), Moved to Manchuria (K. Ando) and back to 10% (Bd); resistant to most DBA/1 tumors, Japan; inbreeding begun by Suzuki, 1962, at 591 grows in both; a few mammary tumors Univ. Tokyo (Japan. J. Exptl. Med., 40: in old breeders; audiogenic seizures in 100% 159, 1970). Charac: carries mammary tumor at 35 days, 5% after 55 days; high mortality virus; tumor incidence has declined. in dd exposed to chloroform fumes and Maintained by: Jic, Jms. oxidation products of ethylene oxide, and to a deficiency of vitamin K (J); complement DDK Inbr (Nga): 61 . Genet: A, B, c, D, S. Origin: not detectable (Umc); 18% various tumors in K. Kondo, from so-called German mice (dd dd (J. Gerontol.,2i: 404, 1966);meanlife stock) from Inst. Inf. Dis., Tokyo, in 1944. span in virgin 99 714 days, 707 days in dd Charac: fertility reduced when 99 are (J. Gerontol., 2i: 404, 1966); mean life span outcrossed ; skeletal characters: fusion of of fostered SPF 99 719 days, dd 629 days frontal and parietal bones 94%, interfrontal (Lab. Animals, 5: 179, 1971); blood 78%, parted frontal 4%, predominantly 26 pressure relatively low (Nature, 2i2: S19, (7/ 13/6) presacral vertebrae. RBC count 8.5 1966); low alcohol preference (Quart. J. Â±0.22 X 106/cu mm, hematocrit 48.9% Â± Studies Alc., 28: 22, 1967); relatively 0.9%; WBC count 5.81 Â±1.05 X i0@/cu mm. resistant to P. berghei infection (Military Maintained by: Nga. Med., i3i : 91 5, 1966); high red blood cell count, low concentration of lipid in DDY Inbr (Yok); 60. Genet: a, B/B, c. Origin: adrenals, calcareous heart deposits (BLM-2). from noninbred dd-stock of Inst. Inf. Dis. Maintained by: Ar, Bd[SPF] , Bom[f] , Ch, Univ., Tokyo, 1953. Maintained by: Jic, Crgl, Ep, Friedmann (Paris), Fs, Grf, Ibg, Icr, Yok. Icrf,J,Jic,Ki,Kon, Lac [?f] , Mai[f] , Ml, Ms, N, Nmg, Or!, Rank (MUnchen), Rij [f] , Shire DE/J Inbr (J): 60. Genet: ce, A. Origin: Eaton, (Stanford), Sm, St, Sto, Sy, hf, Iii, Umc, 1940, from cross of CE/Wy X E/Gw, W, Wak, We, Y, Yok. Subline not stated: RI. selected for ce phenotype. Charac: high incidence of amyloidosis; adrenais not DBA/2eB Inbr (Hf): 34 since ova transfer. Origin: responsive after neonatal gonadectomy; have Deringer, transfer of fertilized DBA/2 ova to polydipsia (30â€”50 mi/day) and polyuria C57BL. Charac: low mammary tumor, no (25â€”45 mi/day), more noticeable in 99; sp. agent. Maintained by: Bre, Hf. gr. of urine 1.005 . Polydipsia-polyuria is a unit recessive character; no pituitary lesions, DBAf Several lines. Not all are the same DBA but kidney and adrenal are affected. subline or fostered on the same strain. Maintained by: J, Rank (MUnchen). Charac: free of mammary tumor agent, high susceptibility to leukemia induction by DHS Inbr(Mk): 51.Genet:c.Origin:Germany;

1618 CANCER RESEARCH VOL.32

to Tokyo in about 1910. b X s inbreeding Snell's WA linkage stock; 7 rounds of started in 1957. Charac: high incidence of cross-intercross to C3H by Jay and E. polydactyly (Zool. Mag., Tokyo, 74: 115, Russell; outcross to WB/Re by Re; b X s 1965). Maintained by: Mk. matings offf progeny started 1956. Charac: homozygous w/w f/f stock, with diffuse DKI Inbr (Jko): 52. Genet: a, B, c, S. Origin: hemoglobin, both alpha-chain and beta-chain from noninbred ddN stock of Central Lab. hemoglobins characterized. Fetuses and Expt!. Anim., 1953 (B. Kitasato). Charac: newborn show microcytic, siderocytic uniform sensitivity to infection with S. anemia, completely cured by 14 days. enteritidis (Japan. J. Exptl. Med., 32: 505 Variable belly spotting and tail flexure. and 519, 1962). Maintained by: Jko. Good breeding when young; later impaired by obesity. Maintained by: Re. DL Inbr (Ra): 58. Genet: a, se +/+ d'. Origin: balanced se +/+ d' from Searle to E. S. FL/2Re Inbr (Re): 40 since establishment off7r line Russell, to Kelton 1958. Inbred by Kelton. in 1962. Descended from Nl 3 and Ni 1 of Maintained by: Ra. f/+ on FL/lRe (Genetics, 53: 949, 1966). Genet: a, f. Maintained by: Re. @ DLJ/Le Inbr (Le): 28. Genet: +/+ se@, a. Origin: mutation to d' â€œoccurred in FM Inbr (Jms): 28. Genet: p. Origin: from Ueno AKD2F1 in 1958. Dickie to Lane 1963. Zoo to Dept. Zool., Kyushu Univ., to Natl. Crossed to CBA/CaGn@seC@@andinbred as Inst. Genet. to Jms. Inbreeding started in balanced stock. Charac: homozygous 1958. Charac: over 90% mammary tumors in @ die before weaning. Maintained breeders, 100% in force-bred, but very low by: Le. in virgins by 18 mo. Maintained by: Jms.

DLS/Le Inbr (Le): 45. Genet: d'+/+se, a. Origin: FSB/Gn Inbr (Gn): 46. Genet: a, ft. Origin: mutation mutation to d' occurred in CS7BL/Gr in arose in unpedigreed stock at Ohio St. Univ. 1950. Truslove to E. S. Russell 1957 as in 1951; mutant 99 mated with C57BL/10 balanced stock. To Le 1968 at F32. Charac: dd. Charac:lowfecundityandviability;ft/ft homozygous d'/d' die before weaning. have periodic partial hairlessness; all types of Maintained by: La. hairs are shorter than normal (J. Heredity, 45: 115, 1954). Maintained by: Gn. DM Inbr (Ms): 71. Genet: c. Origin: Germany; to Tokyo, to Hokkaido in 1954. Maintained GLF Inbr (Y): 29. Genet: +. Origin: from Jax as by: Mk, Ms. bearers of gray lethal mutation ; selected for the normal genotype by progeny testing. DTB/Jic Inbr (Jic): 44. Genet: c. Origin: from Nara Maintained by: Y. Med. Univ., 1960, at F 13. Subline o@DHT and DD. Maintained by: Jic. GR/A Inbr (Crgl): 5 1. Genet: a, c. Origin: MÃ¼hlbock obtained breeding pairs of DW/J Inbr (J): 49. Genet: ln, dw/+. Origin: La to J â€œGrunderâ€•micefrom A. Grumbach, Zurich, 1966. Charac: dwarf; useful for endocrine in 1955 and inbred [Hyde Found. Conf. on studies. Maintained by: J, Wf. Mamm.Tumor Virus, Inverness, Calif.(1964), pp. 21â€”22]. MÃ¼hlbockhas several sublines. F/St Inbr (St): 109. Genet: a, b, c'@, d, s. Origin: Charac: breeding 99 have high incidence of Strong, 1926, from a group of unpedigreed mammary tumors which are highly hormone Bussey Institute mice. Charac: high leukemia responsive; carries a mammary tumor agent, in older animals regardless of breeding different from Mu, not dependent on milk conditions. Maintained by: Lac, St. transmission. Maintained by: A, Crgl.

FB/Ki Inbr (Ki): 36. Origin: Kirschbaum GR/R1 Inbr (RI): 29. Genet: A, gr. Origin: from G. 1942â€”1952. Multiple crosses between A, F, D. Snell 12/ 17/5 1. Maintained by: RI. and NH. Charac: reticular tissue neoplasms NOTE: The two GR strains were developed about 50%; some myeloid leukemia. and named independently and should not be Maintained by: Ki. considered related despite similarity of names. FL/iRe Inbr (Re): 53 since establishment of f/f line, 1956. Genet: a, f, rd. Origin: flexed gene HR/De Inbr (Icr): 70. Genet: hr. p. Origin: inbred originally obtained by George Jay from by Deringer from hr stock received from

AUGUST 1972 1619

Carnochan, 1948. Charac: develops IDT Inbr (Jic): 36. Genet: A, B, c. Origin: from papillomas and hemangioendotheliomas (J. Germany by Dr. Inada about 1910. NatI. Cancer Inst., i7: 533, 1956). Low Inbreeding started in 1957. Maintained by: mammary tumor. Maintained by: Icr. Jic.

HRS/J Inbr (J): 45. Genet: hr, b, c, d. Origin: hr IF Inbr (Bcr): 41 . Genet: at . Origin: G. Bonser stock originally from Crew to Carnochan, to (Leeds) in 1932â€”1936; selection for early Heston, to Chase, to E. L. Green 1952, to papilloma development after treatment with Las 1956, to M. C. Green 1959, to Jax 1964. carcinogens. Charac: no mammary tumor Mating pattern always + hr 9 X hr/hr d. agent or spontaneous mammary tumors, but Charac: glassy membrane of hair follicles in highly susceptible to induction by chemicals homozygotes is defective, causing permanent or the agent; susceptible to chemical ovarian near-hairlessness after first moult (Chase). tumor induction; high incidence of Tylotrichs may persist up to I .5 yr (Mat. spontaneous pseudopregnancy . Maintained Record, i 70: 485, 197 1). Some + hr 99 lose by: Bcr. most of their fur after 4 mo. Leukemia incidence of hr/hr 45% at 8â€”10mo., 72% at IS/Cam Inbr (Cam): 27. Genet: +. Origin: Mus mus 18 mo.; in +/hr, 1% at 10 mo. and 20% at 18 praetextus caught in Israel port X Mus mus mo. (Proc. Natl. Acad. Sci. U. 5., 63: 759, musculus. Maintained by: Cam. 1969). The Charles River â€œhairlessâ€•isnot J/Glw Inbr (Glw): 44. Genet: A, b. Origin: the same gene (J. Invest. Dermatol., 56: 170, Falconer. Charac: high frequency of cleft l97i). Maintained by: J, Se!. palate. Maintained by: GIw.

HTG Inbr (Eg): 25. Formerly called 11-2G. JBT/Jd Inbr (Jd): 53. Genet: a, b, bt. Origin: from Maintained by: Eg, Grf, Sn. Falconer's outbred JC stock (J. Cellular Comp. Physiol., 56: 153, 1960). Charac: HTH Inbr (Sf): ? + 22. Formerly called 11-211. very low incidence of congenital Maintained by: Sf. malformations, except for frequent tail kinks. Maintained by: Jd. HTI Inbr (Sf): ? + 20. Formerly called 11-2!. JU lnbr (Cam): 55. Genet: a, c. Origin: Maintained by: Sf. Falconer, 1952, from crosses involving Goodale's and MacArthur's large strains. I Inbr (Umc): 98. Genet: a, b, d, ln, p, s. Bateman's high lactation strain, and various Origin: Strong, 1926, from a group of mutant stocks with about 50% of CS7BL/Fa unpedigreed mice. Charac: resistant to ancestry (Mouse News Latter, i8: 5, 1958). chemical induction of tumors (St); Charac: average first litters 9 (Cam); high complement is not detectable (Umc). prenatal mortality in second litters (50%) Sex-linked phosphorylase kinase deficiency when gestation is concurrent with suckling (Biochem. Genet., 4: 169, 1970). first litter (Fa); low penetrance ofNil (Cam). Maintained by: CrgI, Eg, Fn, J, Ki, Man, Re, Maintained by: Cam, Ct, Fa. Sf, St. Umc, Y. K Inbr (Gh): ? + 13. Genet: b, c. Origin: ICRC Inbr (lcrc): 20. Genet: c. Origin: white mice, Strong. Maintained by: Gh. believed imported from England to Central Res. Inst., Kasauli, India, in 1931 ; 3 99 and KE lnbr (Kw): 56. Genet: a, b, c, P. Origin: I d from Haffkine Inst. to Indian Cancer Krzanowska, 1952, from mice of unknown Res. Ctr., Bombay, in March 1957; inbred origin; cross also produced KP (Mouse News there (Indian J. Med. Res., 4: 562, 1961). Latter, 32: 54, i965). Charac: mean litter Charac: large body size, 55â€”60g at 6 mo.; size 6.1 ; low percentage of fertilized ova prolific breeder; mammary cancer incidence (Folia Biol. Warsaw, 8: 269, 1960); 17.6% of in breeders 5 1%, 31% in virgins; leukemia in spermatozoa have abnormal heads (Genet. both sexes 23%; no adrenocortical response Res., i3: i 7, 1969). Maintained by: Kw. to gonadectomy (J. Endocrinol., 48: 449, 1970); type B virus particles and occasional KI Inbr (Glw): 92. Genet: c, Ki. Origin: Dunn type C particles found in mammary tumor and Gluecksohn-Waelsch. Charac: kink and leukemia, respectively (Texas Rept. incomplete dominant ; heterozygotes show Biol. Med., 29: 359, 1971). Maintained by: tail abnormalities; homozygotes die before Icrc. birth. Maintained by Glw.

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KITF Inbr (Nvs): 20 +. Genet: A/a, B/B, Ki@tf/Ã·, wt. 1.8 g, 28 day wt. 20.1 g, 60 day wt. 37.4 t'2 . Polymorphic for black and tan. g. Average litter size 6, sex ratio 56% &@, Origin: Dunn; noninbred kinky stock mean life span 491 days; docile; thyroid outcrossed to tufted from M. F. Lyon in activity low. Maintained by: J. 1957. Charac: maintains Ki and tf (0.7% @ recombination) and tâ€•-'2 (lethal, LIS/A Inbr (A): ? + 55. Genet: c. Origin: recombination suppressor) in Linkage Group MUhlbock, from Hyg. Inst. Zurich in 1955. IX. Maintained by: Nvs. Charac: low mammary tumor incidence in 99, lung tumors in both sexes. Maintained KK Inbr (Nga): 60. Genet: a, B, c, D, S. Origin: by: A. K. Kondo, 1944, from Japanese dealer stock (Kasukabe group). Charac: poor litter size, LP Inbr (J): 86. Genet: A@Â°,s.Origin: Dunn. S.6. Frequent diabetes mellitus, occasional Charac: 55% late-occurring tumors of obesity in old animals (Endocrinol. Japon., various types in 99, 19% in dd (J. Gerontol., i 7: 23, 1970); skeletal characters: cervical 2i: 404, 1966); mean life span in virgin 99 rib 66%, predominantly 25 presacral 800 days, 750 days in dd; large amount of vertebrae (7/12/6); liver and kidney esterase lipid in adrenal glands in both sexes different from CS7BL/6J and DBA/2; (BLM-2). Maintained by: J, Nimr, Sn. erythrocyte count 9.35 X 106 hematocrit 51.6%, hemoglobin 18.62, leukocyte count LS/Le Inbr (La): 33. Genet: at is/-f +. Origin: 5.23 X l0@. Maintained by: Nga, Jic. mutation to is occurred in C57BL@at at Harwell. Phillips to Lane as balanced stock KP Inbr (Kw): 56. Genet: a, b, p. Origin: 1961 . Charac: homozygous is/is develop Krzanowska, 1952, from mice of unknown megacolon but some live and breed. origin. Charac: mean litter size 5.0; high Maintained by: La. embryonal and postembryonal mortality; frequent sterile copulations; low sperm production and low libido of dd; testis LT Inbr (Re): 80. Genet: a, Bit. Origin: abnormalities: degeneration of some tubules MacDowell, 1950, mutation at the brown and cells, large amount of interstitial tissue locus in strain C58. To Chase, to Re in 1957 (Folia Biol. Warsaw, i3: 297, 1965). at F28. Charac: hair almost white except for Maintained by: Kw. blackish tip. Maintained by: Cli, Re, Sv.

KR Inbr (Nga): 57. Genet: A, B, c, D, S. Origin: LTS/A Inbr (A): ? + 54. Genet: c. Origin: as KK, 1952. Charac: good reproductive MUhlbock, from P. Loustalot, Basle, in performance; liver and kidney esterase like 1954. Charac: high mammary tumor DBA/2 ; imperforate vagina 2%. Maintained incidence in both virgin and breeding 99. by: Nga. Also LTSf/A, a fostered low tumor line. Maintained by: A. KSA Inbr (Nga): 67. Genet: s. Origin: as KK, l944@-l948. Charac : moderate reproductive MA Inbr (J): 9 1. Genet: c. Origin: Marsh's strain performance ; docile ; skeletal characters: 3; started from a pair of mice from interfrontal 86%, parted frontals 92%, Lathrop-Loeb colony; 32 gen. of cousin predominantly 2 5 presacral vertebrae matings by Marsh, to W. S. Murray who (7/13/5); liver and kidney esterase like inbred b X S. Charac: 5% gross tumor DBA/2. Maintained by: Nga. incidence in virgin 99, 0% in dd; polydipsia-polyuria 79% in virgin 99, 12% in KSB Inbr (Nga): 47. Genet: a, B, C, D, s. Origin: d@;25%grosskidneydiseaseind@;meanlife as KSA. Charac: resembles KK. Maintained span in virgin 99 585 days, 460 days in dd by: Nga. (J. Gerontol., 2i: 404, 1966). High resistance to chronic whole-body L Inbr (St): 105. Genet: A'Â°, ca'. Origin: X-irradiation; pituitary cysts in over 50% of Strong, about 1926. Charac: Low mammary animals (J). Maintained by: J. tumor, some lymphoblastoma ; retinal opacity. Maintained by: St. MAS/A Inbr (A): ? + 59. Genet: c. Origin: MÃ¼hlbock,from Hyg. Inst. Zurich in 1955. LG Inbr (J): 52. Genet: a, c, rd@. Origin: Charac: low mammary tumor incidence in . developed by Goodale through selection for 99, high lung tumor in both sexes. large size; inbred by Runner. Charac: birth Maintained by: A.

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MK/Re lnbr (Re): 30. Genet: mk/+. Origin: Jax NC Inbr (Nga): 65. Genet: A, b, C, D, S. Origin: mutant #63â€”36, B6D2F1-mk from M. M. K. Kondo, from Japanese fancy mice Dickie to Re, 1963. Charac: segregates for (Nishiki-Nezumi). Charac: good compensating microcytic anemia. All mk/mk reproduction; erythrocyte count 9.06 X are born alive; 1/3â€”1/2 die before 3 weeks, 106/ml; leukocyte count 2.95 X 103/ml. developing skin lesions and tail amputation, Liver and kidney esterase like DBA/2. but surviving mk/mk are fertile and appear Susceptible to X-ray irradiationâ€”LD5 O/3@ normal except for super-normal numbers of 547 R. Maintained by: Nga, Jic. very small erythrocytes. Hematology well characterized (BLM-2). Maintained by: Re. ND2/Rij Inbr (Rij): 29. Origin: from LOBUND Inst. (Notre Dame) in 1962. Maintained by: Rij. MO/Ko Inbr (Ko): 72. Origin: Kobozieff, 1949, from local mice of unknown ancestry which NGP Inbr (N): 23. Genet: c. Origin: a randomly had cornea! opacity, since shown not to be selected litter from the NIH General Purpose hereditary. Charac: used for the study of noninbred mouse colony. Maintained by: N. longitudinal hemimelia, alopecia, periodic hypotrichosis. Maintained by: Ko. NH Inbr (Ki): 70. Genet: a, d, p, s. Origin: Strong, from crosses involving CBA, N, and MSC-2/Pr Inbr (Pr): 25. Genet: a, B, Miw@@,s.Origin: JK. Charac: low tumor incidence; nodular Schaible, 1963. Charac: virtually 100% hyperplasia and adrenal adenomas in at least hypoiridis, bulbus abnormally large. 10% of old miceâ€”gonadectomy at 6 wk. Maintained by: Pr. enhances adenomas; some obesity; breeding ceases at approx. 9 mo. Maintained by: Ki, MT Inbr (Mk): 55. Genet: c. Origin: Makino, N. from hybrids between Mus m. musculus and Mus m. moiossinus. Charac: high incidence NLC Inbr (Rd): 41. Origin: Lab. GÃ©nÃ©t.,Fond. of exencephalia (Zool. Mag., Tokyo, 74: Curie. Charac: mammary tumors I 5% in 115, 1965). Maintained by: Mk. virgins, 60% in breeders. Maintained by: Rd.

N Inbr (St): 99. Genet: a, b, d, s, rd@. Origin: NMRI lnbr (Sel): 22. Genet: c. Origin: noninbred Strong, about 1926, from a group of Swiss mice from Lynch to Poiley in I937. unpedigreed mice; ancestral to PBR strain. Inbred by P1, known as NIH/Pl. To U. S. Charac: low tumor incidence, resistant to Naval Med. Res. Inst. at F5 I , known as chemical carcinogenesis. Maintained by: St. NMRI. Maintained by: Lac, Se!. NOTE: Many colonies of NMRI, particularly NAW lnbr (Pr): Nl6 F30. Genet: a. Origin: European, are random- or pen-bred. Gowen's marker stock, Iowa State; b X s matings since 1954. W and wa-2 have been NZB Inbr (Bl): 89. Genet: a, B. Origin: see NZO. selected out. Charac: good reproduction; From a black pair of segregants in the F3 of designed for pigmentation studies; NZO. Charac: autoimmune hemolytic completely pigmented except that tips of anemia (Proc. Univ. Otago Med. School, rear toes may occasionally be white. 37(2): 9, 1959); antinuclear antibodies and Maintained by: Pr, WI. kidney lesions, complement not detectable (Umc); extramedullary erythropoiesis (Orl); NBL Inbr (N): 80. Genet: a. Origin: probable lupus-like nephritis (5cr); mean life span of contamination of CS7BL/lOSc (J. Natl. fostered SPF 99 441 days, dd 459 days Cancer Inst., 14: 481 , 1953; J. Exptl. Med., (Lab. Animals, 5: 179, 1971). Maintained 102: 188, l955);should notbeconsidereda by: B!, Bsp, Cpb, J, Lac[SPF] , N, Ph, Scr, CS7BL subline. NIH Black. Maintained by: Umc, Wehi. Hf, N. NZC Inbr (B!): 99. Genet: a, b. Origin: see NZO. NBR Inbr (Nga): 53. Genet: a, b. Origin: from Charac: low mammary cancer, congenital mongrels of Japanese fancy mice cystic kidney, increasing incidence of (Nishiki-Nezumi group) between 1944 and adenoacanthoma (Bl). Maintained by: B!. 1949 (Bull. Exptl. Animals, 6: 107, 1957). Charac: poor reproductive performance; NZO Inbr (GI): 90. Genet: +. Origin: liver and kidney esterase like DBA/2. Bielschowsky, 1948, from the mixed mouse Maintained by: Nga. colony at Univ. Otago Med. Sch., this colony

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had been brought from Imp. Cancer Res. believed not to carry the milk agent, but Fund, Mill Hill, in 1930. Several pairs, susceptible to it and can transmit it to selected for similar coat color but having no offspring (J. Nat!. Cancer Inst., 15: 73, systematic relationship, were obtained from 1954). Maintained by: A, Cpb. the Med. Sch. colony and maintained in the Hugh Adam Dept. of Cancer Res. : no other P/A Inbr (A): 86. Genet: a. Origin: P. Korteweg, introductions have been made since the 1934. DBA 9 X C57BL d, N20 to CS7BL, original ancestral pairs in 1948. NZB, NZY, then b X 5 inbred. Maintained by: A. NZC, and NZX strains are also descended from this colony (Cancer Res., 30: 834, P/i Inbr (J): 111. Genet: a, b, d, se, p. rd. 1970). Charac: obese, low mammary tumor, Origin: Snell, extracted following outcross and benign tumors of small intestine (BI); of similar stock (BDP) developed by W. H. 8.2% (37/451) animals with malignant Gates. Charac: high resistance to chronic lymphomas, 50% of them primary in Peyer's whole-body irradiation. Tumor incidence: patches of the intestine (Cancer Res., 3i: 23% in virgin 99, various kinds, 6% in dd; 2047, 1971). Maintained by: BI, Herberg some polycystic or granular kidneys both (DÃ¼sseldorf), L, Wehi. sexes (J. Gerontol., 2i: 404, 1966). Mean life span in virgin 99 5 10 days, 384 days in Inbr (Umc): 70. Genet: b, c. Origin: W. H. NZW dd (J. Gerontol., 21: 404, 1966). Maintained Hall, Animal Breeding Station, Otago Med. by: Eg, J. Sch., from a pair of pink-eyed white mice of their foundation stock. Charac: hybrids PBA between NZB and NZW develop lupus. Inbr (Bsc): 45. Genet: c. Origin: a single pair nephritis with positive LE cell tests (Lac) of random bred albino stock from a pet shop and antinuclear antibodies (Umc); mean life in Birmingham, Ala., in 1957. Charac: span of fostered SPF 99 733 days, dd 802 relatively large litters but fertility limited by days (Lab. Animals, 5: 179, 1971). early tumor development; lymphomas 100% Maintained by: Cpb, Lac[SPF], N, 5cr, in both sexes at 35 wk; mammary tumors Umc. 75% in breeders at 38 wk; pulmonary adenomas 77% by I yr (J. Natl. Cancer Inst., NZX Inbr (Bl): 54. Origin: see NZO. From an 45: 59, 1970). Maintained by: Bsc. NZC 9 (F33) and an NZY d (F27), offspring b X s mated. Charac: From Fl3 some 99 PBB Inbr (Ld). 21. Genet: B. Origin: P. Bailey, have shown congenital imperforate vagina, from a multicolored stock of pet shop and both sexes have a low incidence of origin. Charac: become obese at maturity on megacolon. Maintained by: Bl. standard 4% fat diet. 65â€”75 g body wt. attained after 12 mo.; occasionally both NZY Inbr (Bl): 82. Genet: b, s. Origin: see NZO; a sexes go over 90 g. Not overly diabetic at piebald @cappeared at F2 which was mated any age (blood glucose < 200 mg/l 00 ml at with a tan sister; at F4 a piebald 5â€”80wk of age). No histological changes in brother-sister appeared; b X s mating with pancreatic islets at any age; mild fatty liver. selection for s led to fixation of the coat Breed well and have normal longevity pattern from F7 on. Charac: high mammary (18â€”22 mo.) (Federation Proc., 31: 245 cancer incidence associated with pituitary (Abstr.), 1972). Useful for dental caries enlargement in breeders ; hereditable research: develops rampant carious lesions megacolon (Bl); highly susceptible to ovarian following purified diet and infection with S. tumor induction by chemicals (Bcr). mutans P5-14. Maintained by: U. Maintained by: Bl. PE lnbr (Ri): 55. Genet: pe. Origin: the NZYf/Bl Inbr (BI): F57 since fostering. Origin: NZY mutation pe arose in C3H/HeRl. B X s at F26 were fostered on NZC. Charac: mated since then (Pe/peXpc/pc). marked reduction in mammary cancer; Maintained by: RI. pituitary tumor incidence unchanged. Maintained by: B!. PET Inbr (Wmr): 64. Origin: from mixed stock of C3H and black pet shop mice, Med. Coll. 020 Inbr (A): I 59. Genet: a, c. Origin: R. Va., 1956, to Wmr 1958. Charac: Pigmented Korteweg, 1931 (Am. J. Cancer, 38: 506, Ex trae pide rmal Tissues, occasional 1940). Charac: mammary tumors 0% in mammary tumors in older 99. Maintained virgins, 5% in breeders, 13% in force-bred; by: Wmr.

AUGUST 1972 1623

PH/Re Inbr (Re): 62. Genet: Ph/+. Origin: dropped from 38.5% to 21.4%, leukemias spontaneous mutation in C57BL/6J. from 31 .5% to 14.7%; both B and C particles Truslove to E. S. Russell, 1957, as noninbred are present, but not A (Compt. Rend., 270: stock. Charac: white-spotted agouti; Ph/Ph is 444, 1970). Maintained by: Mq. lethal. Maintained by: Re. QF-5604 Inbr (Wf); 38. Genet: Aâ€•-',b, in. Charac: PHH Inbr (We): 55. Genet: a, in. Origin: Weir, selected for early sexual maturity of dd. from MacArthur outbred stock obtained Mean age of first fertile mating, 5 1.7 days; from Butler 1949 ; b X s inbreeding with mean body wt. at 100 days, 39.6 g. selection for high blood-pH. Charac: Maintained by: Wf. blood-pH 7.48 Â±0.004, blood lactic acid 3.6 Â± 0.2 .tmoles/ml. CO2 output 5.90 Â±0.01 QF-5612 Inbr (WI): 38. Genet: a. Charac: selected for mg/hr/g body wt., sex ratio 52.8 Â±1.00% dd early sexual maturity of dd. Mean age of (Genetics, 47: 881, 1962). Overall fertility first fertile mating, 49.9 days; mean body low. Maintained by: We. wt. at 100 days, 35.9 g. Maintained by: Wf.

PHL Inbr (We): 60. Genet: at, b, In. Origin: Weir, QF5622 Inbr (WI): 29. Genet: A, b. Charac: selected same as PHH, selected for low blood-pH. for early sexual maturity of dd. Mean age of Charac: blood-pH 7.43 Â±0.004, blood lactic first fertile mating, 55.1 days; mean body acid 5.4 Â±0.3 pmoles/ml, CO2 output 5.90 wt. at 100 days, 38.9 g. Maintained by: Wf. Â±0.03 mg/hr/g body wt., sex ratio 41.8 Â± RAP/Ko Inbr (Ko): 64. Origin: Kobozieff, 1951, 0.93% dd (Genetics, 47: 881, 1962). Overall from a pair of Rockland (USA) mice. fertility high. Maintained by: We. Charac: used for the study of longitudinal hemimelia and periodic hypotrichosis; the PL Inbr (J): 86. Genet: c. Origin: from cataract mutation appeared in this line. noninbred â€œPrincetonâ€•stockstarted in 1922 Maintained by: Ko. from 200 mice purchased from a dealer (J. Infect. Diseases, 82: 169, 1948). Inbred by RF Inbr (J): 65. Genet: a, c. Origin: Furth, Lynch, giving rise to a high leukemia line B 1928, from Rockefeller Inst. general purpose (PL) and a second line A (PLA) with lower stock of domestic origin; transferred to Oak incidence. Charac: 71% tumors in virgin 99, Ridge. History somewhat questionable. 50% leukemia; 19% leukemia in dd, mean Charac: up to 50% leukemia; mean life span life span in virgin 99 448 days, 5 17 days in in virgin 99 452 days, 651 days in dd. Blood dd(J. Gerontol.,2i: 404, 1966).Maintained pressure in mid-range (Nature, 212: 519, by: Eg, J, Sf. 1966). Mid-range of radiation resistance (BLM-2, Chap. 22). Glomerulosclerosis POLY/St Genet: a, b, s. Origin: Strong, from Brpb progressive with age (J. Gerontol., i5: 373, (NH subline).Charac:moderatemammary I 960). High susceptibilityto radiation tumor incidence; high incidence of induced leukemia (Ms). Maintained by: J, polydactylism; several other morphological Ms. variants. There are three lines of this strain based on maternal age. One descent is from RFM/Un Inbr (Rij): 82. Genet: a, c. Origin: Furth, to litters born when the mother was less than Oak Ridge, I949. Charac: Myeloid leukemia 100 days old (F72); one when the mother low (5%) in controls but high (20%) after was 100â€”200 days old (F37); and one when X-irradiation ; radiation-induced leukemia the mother was 200â€”300 days old (F92). reduced to less than 2% in germ-free state Maintained by: St. (Wg). Maintained by: Bts, Pat, Rij [cony. + GF] ,Un,Wg[GF]. PRO Inbr (Blk): 26. Genet: a, ca', p. Origin: E. S. Russell, 129/ReJ X C57BL/6J, progeny RMS Inbr (Mk): 32, Genet: hr'@, Origin: Minima, tested for a, câ€• and p; b X s inbred. to Mk in 1959 at F2. Maintained by: Mk. Charac: hyperprolinemia and prolinuria @ (Science, i 76: 809, i972). Maintained by: RUS Inbr (RI): 66. Genet: at, s. Origin: from Blk, Re. Holman 1/5/48 (â€œF4from Dunn's BT ruby x Holman'sblack,piebald,shaker-lâ€• PS Inbr (Mq): 40. Origin: Mouriquand, at the [MacDowell] ). Maintained by: RI. Institut Pasteur, Lyon, inbred since 1957 (Compt. Rend. Soc. Biol., i54: 632, 1960). RIII/2J Inbr (J): Fl3 since reconstitution. Genet: c. Charac: mammary tumor incidence has Origin: in 1967 both RIII/AnJ (at F66) and

1624 CANCER RESEARCH VOL.32

RIII/J (at F58) stopped producing viable multiple lung cysts, especially in se/se. offspring. The two sublines were crossed and Maintained by: Gn. produced viable fertile offspring. Charac: as RIII/An. Maintained by: J. SEC/iRe Inbr (Re): 100. Genet: a, b, c'@', Origin: from SEC/iGn, short-ear eliminated by E. S. RIII/An Inbr (N): 67. Genet: c. Origin: see RIlI. Russell. Charac: excellent breeder (Re). Charac: 45% mammary tumors in virgin 99, Maintained by: Fs, Re. 10% various tumors in dd; mean life span 655 days in 99, 685 days in dd (J. Gerontol., SF/Cam Inbr (Cam): 43. Genet: +. Origin: wild mice 21: 404, 1966). Mammary tumor incidence trapped in a coal mine and sib-mated to FlO declined from 100% in breeders and virgins by M. Barnawell (Berkeley, Calif.) as â€œCorte in 1954 to less than 3% in 1961 (J. Nat!. Moderaâ€•; to Cambridge 1959. Charac: Cancer Inst., 28: 159, 1962). Laukemia less adrenal X zone relatively and absolutely than 3% (Ki). Maintained by: Crgl, Ki, N, large in 99; very poorly developed zona Rd,Sy. glomerulosa; (Environ. Pollution, i: 175, 1970). Maintained by: Cam. RIII Inbr (Dm): 50. Genet: c. Origin: SF-56l3 Inbr (WI): 31. Genet: a. Charac: selected for D obrovolskaia-Zavadskaia, Paris, 1928 late sexual maturity of dd. Mean age of first (Compt. Rend. Soc. Biol., i04: 1191, 1930). fertile mating, 58.8 days; mean body wt. at Charac: have milk agent; 88% early 100 days, 28.9 g. Maintained by: Wf. mammary tumors in breeders, other tumors rare ; urethan causes hepatic angiomatosis; SF-562 1 Inbr (WI): 29. Genet: A, b. Charac: selected susceptible to Graffi virus; resistant to for late sexual maturity in dd. Mean age of goldthioglucose obesity (Rd). Maintained first fertile mating, 58.2 days; mean body by: A, Dm. wt. at 100 days, 32.3 g. Maintained by: Wf.

S Inbr (Gh): 60 ? + 15. Genet: c. Origin: SHM/2Gn Inbr (Gn): 24. Genet: +/shm. Origin: shm Schott (Genetics, 22: 264, 1937) to Gowen mutation arose in randombred stock in in 1927. Inbred by Gowen and selected for March 1960. This strain descended from resistance to S. typhimurium (Ann. Rev. (SHM/Gn X C57BL/6J) X C3HeB/FeJ Microbiol., 2: 21 5, 1948). Charac: (SHM/Gn discontinued at F35 in 1970). radiation-resistant, salmonella-resistant (Ge Charac: homozygotes have abnormal gait, netics, 50: 1115, 1964). Maintained by: Gh. small body size, phospholipidosis, sterility, low viability (J. Heredity, 58: 65, 1967). SB/La Inbr (Le): 40. Genet: sa, bg, Aw . Origin: Maintained by: Gn. mutations to sa and bg, possibly radiation induced, occurred independently in stocks SIlT Inbr (Nga): 26. Genet: a, b, s. Origin: from used for mutation rate studies at Oak Ridge; hybrids between KSB and NBR in 1964. nonsib pair from RI to La 1961 ; sib-mated Charac: brown piebald, to be used as marker since. Charac: high susceptibility to chronic testing strain. Maintained by: Nga. respiratory disease. Maintained by: La.

SD Inbr (Glw): 7 1. Genet : c, Sd/+. Origin: SJL/J lnbr (J): 59. Genet: c, p, rd. Origin: Dunn and Gluecksohn-Wae!sch. Charac: Sd developed from Swiss Webster stock of three incomplete dominant affecting axial and sources that were brought to Jax between urogenital systems; homozygote lethal after 1938 and 1943. Pen-bred until 1955 when birth. Maintained by: Glw. b X s mating was started. Charac: high resistance to chronic whole-body SEA Inbr (J): 100. Genet: b, d +/d se. Origin: X-irradiation ; relatively large litter size; Green, from BALB/c X P. Charac: host for multicellular reticulum cell sarcomas transplantable rhabdomyosarcoma T8l 1. resembling Hodgkin's disease in 91% virgin Maintained by: J, RI. 99 at av. age 13.3 mo., 88% of breeders at 13.5 mo., 91% ofdd at 12.5 mo. (J). Fastest @@ SEC/RI Inbr (Ri); 65. Genet: a, b, +/dse. heart rate of 7 strains tested (J. Comp. Origin: from E. L. Green 5/19/48 at F20 Physiol. Psycho!. 77: 337, 1971); susceptible and F2 I . Maintained by: RI. to experimental autoimmune thyroiditis [Federation Proc., 30: 306 (Abstract), SEC/lGn Inbr (Gn): 99. Genet: a, b, c@@h+/se.Origin: 1971 1; mean life span ofvirgin 99 395 days, Green, from cross of NB X BALB/c. Charac: 472 days in dd (J. Gerontol., 2i: 404,

AUGUST 1972 1625

1966); low incidence of audiogenic seizures STR/l Inbr (N): 94. Genet: a, b, s. Origin: piebald (J. Heredity, 58: 135, 1967); hepatosplenic branch of STR/N, 1961. Charac: amyloidosis after 6 mo. (Rd); paraproteins osteoarthropathy of the knee joints very elevated (Rd); blood pressure in (Gerontol. Clin., 6: 91, 1962); obstructive mid-range (Nature, 212: 519, 1966). uropathy in dd before 16 mo. (Am. J. Maintained by: J, Mk, Sm, Umc, Wn. Pathol., 4i: 233, 1962). Maintained by: N.

SK/Cam lnbr (Cam): 20. Origin: from 3 mice trapped STS/A Inbr (A): ? + 55. Genet: c. Origin: on Skokholm Island off Pembrokeshire in MUhlbock, from Hyg. Inst. Zurich in 1955. 1962 (R. J. Berry). Charac: fairly large Charac: no mammary tumors; lung tumors litters, the size of which dropped little on in both sexes. Maintained by: A. inbreeding. Maintained by: Cam. SLIMs Inbr (Ms): ? + 50. Genet: A, B, c. Origin: STU Inbr: 57 +. Origin: Swiss, GÃ¶nnert, derived from SMA as high leukemia strain by Bayer-Laverkusen , to Max-Planck-Inst . fÃ¼r M. Tutikawa; in Misima, leukemia incidence Virusforsch. (Thbingen) in 1950. Charac: is low. Maintained by: Ms. used for passage of Ehrlich ascites tumor and Rous sarcoma virus-induced fibrosarcomas, SL/Rl Inbr (RI): 65. Genet: Si/+. Origin: the and for transplantation immunity experi mutation Si arose in C3H/HeR!: b X s ments with Rous sarcomas. Maintained by: mating (Si/i- x +/+) since then. Maintained Bauer (TUbingen). by: Rl. NOTE: The two SL strains were developed Swiss Various lines from mainly commercial and named independently and should not be sources, inbred in different laboratories. considered as related sublines despite similarity of names. Inbr (Ms): ? + 46. Genet: c. Origin: City of Hope Med. Ctr., Calif., to Misima in 1953. SM Inbr (J): 66. Genet: AW/a or a/a. Origin: Maintained by: Ms. MacArthur, 1939, by crossing seven stocks (including DBA) and selecting for small size; SWR Inbr (J): 103. Genet: c, rd. Origin: â€œSwissâ€• to Runner in 1948, who began b X s mating. mice from A. de Coulon of Lausanne, inbred Charac: small body size at birth and at by Lynch (Lab. Animal Care, i9: 214, weaning; relatively small size tends to 1969). Charac: low incidence of mammary disappear as the animals mature; very low tumors in breeders and virgins; about half tumor incidence of any kind; both sexes live primary lung tumors; 99 develop polydipsia 570â€”600 days (J); 100% amyloidosis at 1 yr at 6â€”10mo.; leukemia 10% in 99 (Life Sci., or older (Ml). Maintained by: J, Ml, Ms, Sf. 9(11): 1071 , 1970); high mortality in &@ ST/a Genet: H@2b. Subline separated after exposed to ethylene oxide products and to considerably more than 8 gen., differs from vitamin K deficiency. Mean life span in ST/b (q.v.) at the H-2 locus. Maintained by: virgin 99 496 days with polydipsia, 655 days. M. Simonsen. without; 616 days in dd (J. Gerontol., 21: 404, 1966). Mid-range of radiation ST/b Inbr (J): 97. Genet: a, b, c, rd. Origin: a Mrs. resistance, arteriosclerosis common in both Street started breeding Danish white mice in sexes (BLM-2); resting 02 consumption 1932 as a closed colony; Engelbreth-Holm highest of 7 strains tested (Australian J. started b X s mating about 1940. Eh to Exptl. Biol. Med. Sci., 45: 33 1, I967); Heston 1947 at F23, He to J 1948 at F25. highest blood pressure of 19 strains tested Charac: uniformly sensitive to P. berghei (Genetics, 55: 497, 1967). Maintained by: infection (Military Med., i3i: 915, 1966). Dt,J,Sy. 1â€”2%leukemia including some plasma cell type; other tumors including pulmonary SWV Inbr (Ml): 35. Genet: A, c, unknown coat adenomas and mammary carcinomas, about color dilution gene. Origin: from Central 3% (J). Maintained by: J, N. Animal Depot at U.B.C., 1959, where it has STR Inbr (N): 103. Genet: a, b. Origin: Strong; been a closed colony for 10 yr. Charac: all between F4 and F27 mice were given 99 8 mo. or more have gross polydipsia and injections of methylcholanthrene. Charac: polyuria. Maintained by: Ml. susceptible to periodontal disease (J. Dental Res., 40: 23, 1961); polydipsic. Maintained TB Inbr (Orl): 20. Genet: c, p. Origin: Pasteur by: N. Inst., Paris. Maintained by: Orl.

1626 CANCER RESEARCH VOL.32

TER/Sv Inbr (Sv): 24. Origin: derived from MUhlbock, from P. Schafer (TUbingen) in 129/Sv-W C P, which was developed to 1958. Charac: no mammary tumors; high determine what effect the gene W might incidence of leukosis in both sexes; polyuric. have on teratocarcinogenesis (none detect Maintained by: A. able). W/+ animals were repeatedly back crossed to 129. A W/+9of gen. N8 Till Inbr (Glw): 55. Genet: a, b, t3/t3. Origin: produced 38 male offspring of which 8 had Dunn and Gluecksohn-Waelsch. Charac: t3 testicular teratomas. All TER mice are viable allele at T locus. Maintained by: GIw. descended from that mating. Charac: about 30% incidence of spontaneous congenital VY Inbr (WI): 3 1. Genet: Aâ€•@/a. Origin: testicular teratomas, appearing during the C57BL/6J-Aâ€•@from Dickie, 1962. Charac: 12th and 13th day ofgestation. Tumors may prolific and vigorous; frequency of agouti occur on either side or both and may Aâ€•â€•/aoffspring about 10%. Hepatoma contain tissues derived from all germ layers. incidence in (:cd at 12â€”16 mo.; 24% in Maintained by: Mt, Sv. Aâ€•@/a,13%in a/a. Maintained by: L, Wf.

TH Inbr (Wl): 41. Genet: at. Origin: outbred T WB !nbr (Re): 80. Genet: a, W/w, rd. Origin: W stock from MacArthur (Toronto) who heterozygotes from S. L. Holman and S. G. established the line by crossing 7 strains Waelsch; b X 5 inbreeding started in 1948. (Am. Naturalist, 78: 142, 1944); Wolfe Charac: WW homozygotes are anemic, selected for high blood-pH (Genetics, 46: sterile, lack pigmentation in coat; 55, 1961). Charac: good reproductive heterozygotes have normal blood picture performance. Maintained by: Wl. and fertility, but white ventral spotting; anemics die at approximately 11 days. Many TL Inbr (Wl): 42. Genet: Aug, b. Origin: see TH; other anemia-producing mutant alleles are selected for low blood-pH. Charac: good maintained congenic with this strain. reproductive performance . Maintained by: Maintained by: J. Wl. WC lnbr (Re): 74. Genet. and Origin: same as TM Inbr: 53 +. Origin: Casas, b X s inbred from WB. Charac: same as WB except that mean two unpedigreed Swiss albinos since 1948. age of anemics at death is 14 days with some Charac: no mammary tumors, some surviving to adulthood. The anemia-pro adrenocortical tumors, unusually large ducing S1 mutant is also maintained congenic postcastrational accumulation of body fat, with this strain. Maintained by : Re. no liver tumors. Maintained by: Univ. Puerto Rico. WHT Inbr (Ht): 70 +. Genet: c. Origin: Hewitt, London. Charac: hardy, breeds well; origin TP Inbr (RI): 39. Genet: a, tp. Origin: Jax; of a spontaneous transplantable epidermal taupe mutation arose in CS7BL/1OJ in Dec. keratinizing squamous carcinoma which 1948; after 6 gen. of backcross-intercross to metastasizes to the lymph nodes (Intern. J. CS7BL/lO, b X s inbreeding. Charac: tp/tp Radiation Biol., 12: 535, 1967). Maintained are poor mothers. Maintained by: Rl. by:Ht.

TR Inbr (Ei): 41. Genet: To/+. Origin: Dickie; WLHR/La Inbr (Le): 47. Genet: a, b, wi +/+ hr. Origin: tortoise mutation arose in obese stock (not mutation to wi occurred in pirouette stock inbred) in 1952. Charac: line has been in 1948. Crossed to hr from Hummel 1949. maintained by trio matings for 17 years as Dickie to La 1958 and inbred as balanced offspring do not survive as well from pair stock. Charac: homozygous wi/wi die before matings. To/+ 99 with much white in coat weaning. Maintained by: Le, Ra. usually do not mature; darker ones survive well. In this line no To &$ have been WLL Inbr (A): ? + 84. Genet: c. Origin: Kreyberg, observed. Maintained by: Ei. 1929, from a commercial dealer in Oslo (Brit. J. Cancer, 6: 140, 1952). In 1934 TRE/Ko Inbr (Ko): 64. Origin: Kobozieff, 1937, â€œWhiteLabelâ€•mice were sent to Leeds, from waltzing mice of unknown origin. becoming WLL, and some stayed in Oslo Charac: malformation of one or both ears in becoming WLO (not reported). Maintained by:A. low incidence. Maintained by: Ko.

TSI Inbr (A): ? + 42. Genet: a, c. Origin: WV Inbr (Rl): 49. Genet: a, W'-'/w. Origin: E. S.

AUGUST 1972 1627

Russell, N15 of Wâ€•/won C57BL/6 to Oak Dobrovolskaia-Zavadskaia, C57L X CS7BL Ridge in 1951; b X s (Wâ€•/wX w/w) (Bull. Cancer, 46: 737, 1959). Charac: very inbreeding since. Maintained by: Re. low tumor incidence (Rev. Franc. Etudes Clin. Biol., 9: 632, 1964); hepatomas X/Gf Inbr (GO: 53. Genet: a, B/b, c. Origin: induced by irradiation (Bull. Cancer, 54: 7, unknown. Inbredb X s by Gf since,1954 1967); biochemical polymorphisms (Brit. J. Cancer, 20: 361 , 1966). Charac: no characterized by Moutier (Exptl. Animals tumors of any kind; does not carry milk Paris, 1: 261 , 1968). Maintained by: Orl. agent but produces antibodies against it; give immune responses to SRBC and possess high 10! Inbr (RI): 63. Genet: [email protected]: Dunn (J. phagocytic activity; newborn are moderately Genet., 33: 443, 1936). Charac: low susceptible to Friend leukemia virus, adults mammary tumor incidence; slow to breed, are resistant ; irradiation not carcinogenic fertility moderate (H); high susceptibility to (Texas Rept. Biol. Med., 25: 396, 1967). skin and lung tumor induction. Maintained Maintained by: Gf. by:El,Ep,H, RI.

YBR Inbr (Ki): 94. Genet: AY/a, b. Origin: Little 129/Re Inbr (Wak): 59. Genet: AW @.Chp/c'@' p. to Andervont 1936, to Heston 1946 at An's Origin: see l29/RrJ; a b X s Dy/Dy subline, F30. Charac: amyloid at least 50% in both descended from the 129/Re-dy subline, from sexes with Ar/a or a/a; obesity in hybrids tested Dy/Dy offspring. Maintained by: Jic, between Ar/a and other strains; low tumor. Wak,Wl. Maintained by: Ki. 129/Re-+ dy !nbr (J): 52. Genet: Aâ€•-'c'@'p/cch p. Origin: YS Inbr (WI): 79. Genet: Ar/a, s. Origin: Chase, see 129/Rn ; this subline has been separated 1959. Charac: hepatoma incidence in dd at since 1948. The dystrophic phenotype was 12-16 mo.; 11% in Ar/a, 3% in a/a. first observed in this subline in 1951. Maintained by: L, Wf. Charac: this is the only subline carrying the dy mutant. Maintained at Jax by ovary YZ57S Inbr (Pr): 21. Genet: Ax/a, B, bg, s. Origin: transplants. Maintained by: J, Jic, Wak. bg/bg X YZS7. Charac: extreme basal dilution of hair shaft in yellow segregants. 129/RrJ Inbr (Dt): 76. Genet: AW câ€•@'p/cCh p. Maintained by: Pr. Origin: Dunn, a derivative of strain 101 (Proc. Nat!. Acad. Sci. U. S., 31: 267, 1945, IVCS Inbr (Csk): 36. Genet: a, B, c, S. Origin: and correspondence). Charac : 5% sponta from ddN stock of Central Lab. Exp. Anim., neous congenital testicular teratomas (Sv); selected for regular estrus cycling, 1960. not susceptible to mammary tumor agent; Named 4CS meaning â€œ4-daycycleof vaginal useful for ovary transplant and ova transfer smearâ€•;designation changed to conform to studies; highly sensitive to estrogen at all nomenclature rules. Charac : regular 4-day ages (J). Blood pressure relatively low estrus cycle established by vaginal smear; (Nature, 212: 519, 1966); very resistant to appearance of estrus in the suckling 99 after X-irradiation, high incidence of urinary postpartum estrus; appearance of 3-day calculi (BLM-2); slowest heart rate of 7 estrus cycle by the proximity of males. strains tested (J. Comp. Physiol. Psycho!., Maintained by: Csk, Jic. 77: 337, 1971); mean life span of fostered XVII Inbr (Rd): 75. Genet: c. Origin: SPF 99 666 days, dd 699 days (Lab. Dobrovolskaia-Zavadskaia, 1928; b X s Animals, 5: 179, 1971). Maintained by: Dt, inbreeding since 1943. Charac: no mammary Hb, J, Kt, Lac[SPFJ , N, Ri, Sv, Wak, Y. tumors or leukemia; pulmonary adenomas 19.5% after 13 mo. (Rd); mammary tumors 201/RI Inbr (RI): 42. Genet: Ar/a, pe. Origin: 1.3%, leukemia 99 0.4%, dd I .6%; lung Russell, from PE/Rl and noninbred Ar/a tumors 99 5.1%, dd 8.8% (Bln); sensitive to stock. Mating is always A Y/a pc/pc 9 X a/a Graffi leukemia agent (Arch. Geschwulst pc/pc d. Charac: occasional somatic reverse forsch., 20: 22, 1962); strong reactivity mutations pe to +. Maintained by: Rl. against specific antigens of carcinogen-in duced sarcomas (Acta Biol. Med. Ger., ii: The following strains, included in previous issues of this 572, 1963); very susceptibleto lung compendium, have not been reported. They may or may not oncogenesis by chemical agents (Rd). Main still exist. BALB/Gw, BC, BSL, BUC, BUE, DB, DDM, DLK, tamed by : Bln, Rd. DP, D103, FU, FZ, GFF, GP, HG, HM, IPBR, JB, LAA, LCS, MY, MYA, NCN/a, NCN/b, NS, PBR, PT, Q, QV, SEAC, XLII Inbr (Or!): 42. Genet: b. Origin: STOLI, T, TXXIX, WD, WH, WLO, Y/Wi, Z, ZRDCT.

1628 CANCER RESEARCH VOL.32

Table 1 Strain distribution ofseveral biochemical polymorphisms in the mouse A few data are taken from Inbred Strains of Mice No. 7. All other data are from the open literature. Synonyms or earlier names are given in parentheses (Transplant. Proc., 3: 1133, 1971). distributionReferencesAhhiA/HeJ,LocusAllele Strain

A/i, AU/SsJ, BALB/cJ, BDP/J, BUB/BnJ, CBA/J, CE/J, C3H/HeJ, B. A. Taylor, C3HeB/FeJ, C57BL/KsJ, C57BL/6J, C57BL/1OJ, C57BR/cdJ, C57L/J, C58/J, personal communicationnAKR/J,HRS/J, MA/i, P/i, PL/i, RIII/2i, SM/i, ST/bi39;

29/iAmy-iaAKA, DBA/li, DBA/2i, LG/i, LP/i, RF/J, SJL/i, SWR/i, 1

40bSingle DBA, C3H, IS/Cam, SF/Cam, SK/Cam, ST/Eh, T6, and wild Danish mice35, fancierAmy-2aSF/Cam40bIS/Cam, male from a

SK/CamAmy-3aIS/Cam,

SK/Cam40CeC57BL/6i, SF/Cam,

C58/J25Dip-i C57BL/10, C57BR/cdi, CS7L,

(Pep-i)aBALB/ci, 27bA/HeJ, C57BL/6i, C57BL/10, C58/J, HRS/i, LP/i, SEA/Gn, SEC/lRei16,

AKR/J, AU/Ssi, BDP/J, BUB/Bni, CBA/J, CE/i, C3HeB/FeJ, DBA/2i, DE/i, DW/i, LG/i, MA/i, P/i, PH/Re, PL/i, RF/i, RIII/2i, SiL/i, SM/i, ST/bJ, 129/iEa-iaWild SWR/i,

mice36bWild

mice0C3H/He,

ReiEa-2 C57BR/cdi, DBA/2i, SEC/i

(rho, RZ, RFM, RIII/i H-i4)a C57L36Ea-3 bRF/i, A.CA, AKR, A/Sn, CBA, CFCW, C3H, C57/Ha, C57BL/6, CS7BL/i0, C57BR,

(X)aC57L/i36bA/Mv,

C57BL/10@H@2dEa-4 BALB/cDe, C3H/HeDiSn, CS7BL/He, C57BL/iOScSn,

(D)aA, AKR, BALB/c, BDP, BUB/Bn, CBA/i, CE/i, C3H/He, C57BR/cd, C57L, C58, DA/HuSn, DBA/1, DBA/2, F/St. FL/2Re, HRS, HTG, I, LP, MA/i, NZB, PL, RF/i, 12936bC57BL,C57BL/KsEa-5 RI!!, SEC/iRe, SJL, SM/i, ST/bJ, SWR, WB/Re,

(H-5)aA, 12936bC3H/He, C3H/St, F/St. I, YBR, iKEa-6 C57BL, C58, DBA/1, DBA/2,

(H-6)aA, 12936bBALB/c, AKR, CBA/i, C3H/He, C57BL/6, C58, F/St, I, YBR, iKEa-7 C3H/St, DBA/i, DBA/2,

(T)aBUB/Bn, 12936bA, CBA/J, C3H/He, C58, LP,

AKR, BALB/c, BDP, C57BL/6, C57BR/cd, C57L, CE/i, DA/HuSn, DBA/1, DBA/2, FL/2Re, HRS, HTG, I, MA/i, PL, RF/i, SEC/iRe, SJL, SM/i, ST/bi, WB/ReEs-iaBP/Ww, SWR,

27bA/He, CS7BL/6i, C57BL/iO, CS7BR/cdi, C57L, MWT/Ww, ROP/Gn23,

AKR/i, AU/Ssi, BALB/cJ, BDP/i, BUB/Bni, CBA/J, CE/i, C3H/He, C3HeB/Fei, C58/i, DBA/1, DBA/2i, DE/i, DW/J, HRS/i, IS/Cam, LG/i, LP/J, MA/i, NZB/Hz, P/i, PH/Re, PL/i, RF/i, RIII/2i, SEA/Gn, SEC/lRei, SF/Cam, SiL/i, SK/Cam, SM/i, ST/bi, SWR/i, 129/i, XLII/Orl

AUGUST 1972 1629

a27b IS/Cam, RFM/Un, SK/Cam23,

A/Hei, AKR/.J, AU/SSJ, BALB/ci, BDP/J, BP/Ww, BUB/Bni, CBA/.J, CE/i, C3H/Hei, C3HeB/FeJ, C57BL/6i, C57BR/cdi, C58/i, DBA/2i, DE/i, DW/i, HRS/J, LG/i, LP/i, MA/i, MTW/Ww, NZB/Hz, P/i, PH/Re, RF/i, ROP/Gn, RIII/2i, 129/iC SEA/Gn, SEC/1ReJ, SF/Cam, SiL/i, SM/i, ST/bJ, SWR/i,

PL/JEs-3

a BALB/ci, BDP/.J, BP/Ww, C57BL/6i, C57BL/10, C57BR/cdi, DW/i, HRS/i, SEC/lReJ27b MWT/Ww, NZB/Hz, P/i, ROP/Gn, SEA/Gn,

ST/biC RF/i,

A/Hei, AKR/i, AU/SSJ, BUB/Bni, CBA/i, CE/i, C3H/He, C3HeB/Fei, C58/i, DBA/1, DBA/2i, LIE/i, IS/Cam, LG/i, LP/i, MA/i, PH/Re, PL/i, RIII/2i, SF/Cam, 129/iEs-5 SiL/J, SK/Cam, SM/i, SWR/i,

C57BL/1023g + CBA/i, C3H/He,

gFL8+ AKR, CBA/J, C3H/Bi, C3H/HeHa, C3H/Hei, C3Hp/Ha, C3H/StHa,

A/Ha, A/Hei, A/i, A/St, AL, BALB/cJ, BDP/J, BRS, BRSUNT, C, CBA/St, CE/i, CHI, C3H/Bi, C3H/St, C3HB, C57BL, C58, DA, DBA/2, DE/i, FZ, H, I, IPBR, JK, L, LAA, LOW, LP/i, MA/i, PBR, PIN, P/i, PL/i, POLY, PRUNT, 5-PRUNT, RF/J, 129/RnGot-2 SiL/J, SM/i, ST/i, SWR/i, Y/Wi, YBR, 129/i,

a27b SWR/J6,

A/Hei, AKR/i, AU/SSJ, BALB/ci, BUB/BnJ, CBA/i, CE/i, C3HeB/Fei, C57BL/6i, C57BR/cdi, C58/i, DBA/2i, DE/i, DW/i, LP/J, MA/i, P/i, PL/i, RF/i, RIII/2i, 129/JGpd-i SEA/Gn, SJL/J, SM/i, ST/bJ,

a28b BDP/i, BP/Ww,CE/i, C57BL/6J, C57BR/cdi, C57L, C58/i, DW/i, HRS/i, MWT/Ww, P/i, PL/i, RF/i, ROP/Gn, SEA/Gn, SF/Cam, SK/Cam, 129/i27,

A/Hei, AKR/i, AU/SSJ, BALB/ci, BUB/Bni, CBA/i, C3H/HeOnl, C3HeB/Fei, DBA/2i, DE/i, IS/Cam, LG/i, LP/i, MA/i, NZB/Hz, PH/Re, RIII/2i, SEC/I Rei, XLII/OrlGpi-i SiL/i, SM/i, ST/bi, SWR/i,

a27b A/Hei, AKR/i, BALB/ci, BDP/J, CE/i, C57BR/cdi, C58/J, DBA/2i, DE/i, DW/i, HRS/J, LG/i, LP/J, MA/i, MWF/Ww, NZB/Hz, P/i, PH/Re, PL/J, RF/i, ROP/Gn, RIII/2i, SEA/Gn, SEC/lRei, SJL/i, SM/i, ST/bi, 129/i5,

SWR/iGjx AU/SsJ, BP/Ww, BUB/Bni, CBA/i, C3HeB/Fei, C57BL/6i,

G1x3129/Sv-Sl@@CP37G1x2 CE/i, TER/Sv, 129, 129/Rei-dy, 129/Rn, 129/Sv, IGix' A, AKR, AKR.K, AKRIb2b, A/TL, C3H/He, C58, 101Gjx C3H/An, DBA/2, SiL/i, BALB/c,B10.129(5M),B10.129(9M), B10.129(1OM),B10.129(12M), B10.129(13M), CBA/.J, CBA-T6 (Lyon), C3Hf/Bi (when young), [email protected], C57BL/Ly-A.1, C57BL/Ly-B. 1, C57BL/TL@, CS7BL/6, C57BL/10, C57BR/cdi, SWRThese DBA/IJ, HTG, HTH, HTI, MA/i, RF/J, genes.Hba four classes are quantitatively different phenotypes of an antigen determined by a system of at least two

a A/Hei, AKR/J, BAN/Re, BP/Ww, CE/i, CXBE, CXBG, CXBI, CXBJ, C57BL/6J, 27; E. S. C57BL/10, C57BR/cdi,CS7L, DBA/2i, MA/i, RF/i, WK/Re14, Russell, personal communicationb

SEC/lReJc BALB/cJ, CXBD, CXBH, CXBK, C58/J, DW/i, HRS/i, LT/Re,

BDP/J, C3H/He, C3HeB/Fei, DEli, LS/Le, P/i, SEA/Gn, MK/Re, SiL/J, ST/bi, WH/Red SWR/J, WB/Re, WC/Re,

129/iNot PH/Re, ROP/Gn, SM/i,

c AU/SSJ, BUB/Bni,CBA/J, DBA/1, I/LnJ, LG/i, LP/J, NZB/B1N, PL/i, 129/i

1630 CANCER RESEARCH VOL. 32

Table 1â€”Continued

Locus Allele Strain distribution References

HbbdA/HeJ, 27pAU/SSJ5AIII, AB, AKR/i, AY, BALB/ci, BDP/.J, BP/Ww, BUB/Bni, CBA/J, CXBG, CXBI, C3H/He, C3HeB/Fei, DBA/1, DBA/2i, I/Lni, IS/Cam, iU/Fa, LG/J, LP/i, MK/Re, NZB/Hz, P/i, PL/i, RF/i, SEA/Gn, SF/Cam, SK/Cam, ST/bi, WB/Re, WC/Re, WH/Re, XLII/Onl, 129/i14,

BAN/Re, CE/i, CS, CXBD, CXBE, CXBH, CXBi, CXBK, C57BL/6i, CS7BL/10, C57BR/cdi, C57L, C58/i, DDK, DE/i, DW/i, HRS/J, IDT, ITES, KK, KR, KSA, KSB, LS/Le, LT/Re, MA/i, MWT/Ww, NC, PH/Re, ROP/Gn, RIII/2i, WK/ReHc0A/Hei, SEC/lRei, SIlT, SJL/J, SM/i, SWR/J,

7IBALB/CJ, A/i, AKR/i, AU/Ss, BUA/Wi, BUC/Wi, BUE/Wi, Bl0.D2/o, BRSUNT, CE/i, DBA/2i, DDK, DE/i, DM/Ms, GFF, IF, I/FnLn, iU/Fa, KK, MAS/A, NBL/N, NC, NS/Fr, NZB/B1, PHH, RF/J, SMA/Ms, ST/bJ, SWR/J, YBR/He3,

BDP/i, BRVR/Sr, BSVS/Sr, BUB/Bn, B10.BY, B10.D2/n, B10.LP, CBA/J, C3Hf/BiOci, C3H/Hei, CHI/St, C57BL/6i, CS7BL/lOi, C57BR/cdi, C57L/i, C58/i, DBA/li, F/St, FU/Ri, HR/De, LP, MA/i, MO/Ko, NZO/Bl, PE/RI, PHL, P/i, PL/i, PS/Mq, RIlI/Ani, RIIl/i, RIII/Wyi, SEA/Ga-se, SEC/lGn, SJL/J, SL/Rl, SM/i, 129/iId-iaA/Hei, STOLI/Lw, STR, T6, WHT/Ht 101,

BALB/ci, BP/Ww, CE/i, C3H/He, C3HeB/Fei, C57BL/6i, C57BL/10, C58/i, DE/i, DW/i, HRS/i, LG/i, LP/i, MA/i, MWT/Ww, NZB/Hz, RF/i, RIII/2i, 129/i27bAKR/i, SEA/Gn, SEC/lRei, SF/Cam, SK/Cam, ST/bi, SWR/i,

AU/SSJ, BDP/i, BUB/Bni, CBA/i, C57BR/cdi, DBA/1, DBA/2i, IS/Cam, XLII/OrlIg-iaBALB/ci, P/i, PH/Re, PL/i, ROP/Gn, S1L/i, SM/i,

12bB10.D2/o, BUB/Bn, CBA/i, C3H/He, CHI/Ao, C3H.SW/Hz, C57BR/cdi, C57L/i, 1, C58/i, F/Ao, HTG, JK/Bi, MA/MyJ, MA/i, NZY/B1, PBR/Ao, PL/i, ST/bi, STR/N, 129/i1

B10.D2/n, C57BL/6J, C57BL/1OJ, HTh, HTI, LP/J, SJL/J, SM/J, 101/RicDBA/1, WB/Re, WC/Re, WH/Re, WK/Re,

SWR/idAKR/i, DBA/2i, I/Ao, iB/Di, RF/i,

AL/NeA/i,

NZWfCE/i, NZB/Bl, NZO/Bl,

NH/NgDA/Hu, DE/i, N/Ao,

STBhBDP/i, FZ/Di, RIII/i,

SEC/GnIg-2aBDP/J, BSL/Di, P/i, SEA/Gn,

CBA/J, C3H/He, C57BR/cdi, C57L, C58/i, MA/i, P/i, SEA/Gn, 29/i11CDBA/1, ST/bi, 1

SWR/iJg-3H-A/HeN, DBA/2i,

AL/N17H9BALB/cAnN, AKR/N,

BDP/.J, BL/LyDe, BRSUNT/N, CBA/J, CE/i, C3H/HeN, CS7BL/HeN, C57BL/6N, C57BL/1 OScN, C57BR/cdi, C57L/N, C58/i, DBA/li, DBA/2N, DD/He, DE/i, HR/Dc, I/An, LP/J, MA/i, NBL/N, NH/Lw, PL/i, RF/i, RIII/An, S1L/i, SM/i, 129/iIg-4aBALB/ci, ST/bi, STOLI/Lw, STR/N, STR/1N, SWR/i, YBR/He,

BDP/i, CBA/.J, CE/i, C3H/He, C57L, DBA/2i, DE/i, P/i, 129/i19bC57BL/6i SEA/Gn, SWR/J,

SM/ik+C57BL/FnLn18â€”I/FnLn , C57BL/1 0, LP/J, SiL/i,

AUGUST 1972 1631

Table 1â€”Continued distributionReferencesLdr-1aA/Hei,LocusAlleleStrain

29bDE/i, AU/Ssi, AKR/i, BALB/ci, BDP/J, BP/Ww, BUB/Bni, CBA/i, CE/i, C3HeB/Fei, C57BL/6i, C57BR/cdi, C57L, C58/i, DBA/1, DBA/2, HRS/i, LG/i, MA/i, MWT/Ww, NZB/Hz, P/i, PL/i, RF/i, ROP/Gn, RIII/2i, SEA/Gn, SEC/lRei, SJL/i, SM/i, ST/bJ, 129/i27,

SWR/JLvaA/Hei, DW/J, LP/i, PH/Re,

AKR/i, BALB/ci, CBA/i, CE/i, C3H/He, C3HeB/Fei, C57BR/cdi, CS7L, 27bC57BL/6J, DBA/1, DBA/2i, HRS/J, MA/i, SJL/J, ST/bJ, SWR/i15,

SM/icBUB/Bni, RF/i,

129/iLy-i C57BL/10, C58/i, LP/i, PL/i, SEC/lRei,

(mu, Ly-A)aCBA/i,36bA, C3H/He, DBA/1, DBA/2, FL/2Re, 1K, MA/i2,

AKR, BALB/c, BDP/J, BUB/Bni, CE/i, C57BL/6, C57BL/Ks, C57BR/cdi, C57L, C58/i, DA/HuSn, HTG, HTI, I, LP/i, NZB, PL/i, RF/i, RIII/2i, SEC/lRei, 129/iLy-2 SiL/i, SM/i, ST/bJ, SWR/J, WB/Rei,

(Ly-B)aAKR/i, 36bA, BDP/.J, CBA/J, CE/i, C3H/He, C58/i, DBA/1, DAB/2, I, JK, MA/i, PL/i, RF/i, SM/i2,

AKR.M, BALB/cJ, BUB/Bn, C57BL/Ks, C57BL/6, C57BR/cdi, C57L, DA/HuSn, 129/iLy-3 FL/2Re, HTG, HTI, LP/i, NZB, SEC/lRei, SiL/i, ST/bi, SWR/i, WB/Rei,

(Ly-C)aAKR/i, 36bA, C58, PL/i, RF/i1,

BALB/c,CE/J,C3H/He,C57BL/6,C57BR/cdi, DA/HuSn, DBA/1, DBA/2, 129/iMod-i FL/2Re, HTI, I, LP/i, NZB, SJL/J, SM/i, ST/bi, SWR/i,

(Mdh-i)aA/HeJ,30bAKR/J, BALB/cJ, BDP/J, BP/Ww, BUB/Bni, CE/i, C3H/HeOrl, C3HeB/FeJ, DBA/2J, DE/i, DW/i, IS/Cam, LG/i, LP/i, MA/i, MWT/Ww, PL/i, RF/i, ROP/Gn, SEC/lRei, SF/Cam, SM/i, SWR/i, 129/i27,

AU/Ssi, CBA/i, C57BL/6i, C57BR/cdi, C58/i, HRS/i, NZB/Hz, P/i, XLII/OrlMod-2aSM/i27bA/Hei, PH/Re, RIII/2J, SEA/Gn, 5K/Cam, ST/bi,

AU/Ssi, BALB/ci, CBA/J, CS7BL/6i, C57BR/cdi, DBA/2i, DE/i, LG/J, 129/iMud1AKR/i, MA/i, NZB/Hz, PL/J, RIlI/2J, SiL/i, SWR/i,

BALB/ci, BDP/J, B10.D2/n, B10.D2/o, C57BL/6i, C57BL/1OJ, C57BR/cdi, C57L/i, C58/i, HRS/i, LP/i, MA/i, P/i, PHH, NBL/N, NZO, 129/i212A/Hei, SEA/GnJ, SEC/1ReJ, ST/bi, SWR/J,

A/i, CBA/J, CE/i, DBA/li, DBA/2J, DE/i, FZ/Di, PL/i, RF/i, RIII/Ani, SM/iMup-iaA/He, RIII/AnKi, RIII/Dm, RIIIeB/DeHf, RIII/Ko, RIII/2i, SJL/i,

AKR/Lw, AL/N, BALB/cHf, BL/De, BRSUNT/N, CBAf/Lw, CE/i, CFCW/Rl, C3Hf/De, CS7BR/cdi, DBA/1J, DBA/2eDe, DD/He, I/An, LP/J, NBL/N, 129/i13bC57BL/An,MA/i, NH/Lw, RF/Lw, ST/i, STR/N, STR/1N, SWR/De,

C57BL/He, C57BL/6Hf, C57BL/1ON, C57L/He, C58/Lw, HR/Dc, P/i, YBR/HePca-iaA, RIII/An,

38bC57BL/6, AKR/J, BALB/c, CE/i, C3H/He, MA/i, NZB, PL/i, RF/i, SiL/i36,

129PdaBALB/ci, C58, DBA/2, HTG, HTI, I,

BDP/i, C3HeB/Fei, C57BL/6i, C57BL/10, C57BR/cdi, C58/i, LP/i, 129/i4bSiL/i PL/i, SWR/i,

1632 CANCER RESEARCH VOL. 32

31bAU/Ssi, AKR/J, BALB/ci, BP/Ww, BUB/BnJ, CBA/J, CE/i, C57BL/6i, C57BR/cdi, C57L, C58/i, DE/J, DW/i, HRS/i, LG/i, LP/J, MWT/Ww, RF/i, ROP/Gn, RIII/2i, SEA/Gn, SEC/1ReJ, ST/bi, SWR/J, 129/i27,

BDP/.J, C3H/He, C3HeB/Fei, DBA/1, DBA/2, MA/i, P/J, PH/Re, SWR/JPgm-2aA/Hei, PL/i, SJL/J,

AKR/i, AU/Ssi, BALB/ci, BDP/i, BP/Ww, BUB/Bni, CBA/J, CE/i, C3HeB/Fei, CS7BL/6i, C57BR/cdi, C58/J, DBA/2i, DEli, DW/i, HRS/.J, LG/i, LP/i, MA/i, MWT/Ww, NZB/Hz, P/i, PH/Re, PL/J, RF/i, ROP/Gn, RIII/2i, 129/i27bSM/iPre0AKR/J, SEA/Gn, SEC/lRei, SiL/i, ST/bi, SWR/i,

C57BL/1033aBALB/cJ, C3H/He, C57BL/6i,

DAB/2Sas-i0CBA/J, CBA/i, DBA/1,

ST/bJ41aAKR/J, CE/i, C3H/He, DBA/1, DBA/2i, DE/i, PL/J, SJL/i, SM/i,

BALB/ci, BDP/.J, C57BL/6J, C57BL/ 10, CS7BR/cdi, CS7L, C58/i, LP/i, 129/iSlp0AKR/i, SWR/i,

CBA/J, C3H/He, C57BL/6i, C57BL/lOi, C57BR/cdi, CS7L, C58/i, RF/i22aBALB/ci,DBA/I , MA/i, PL/J,

YBRSs1AKR/J, BDP/J, DBA/2i, P/i,

ST/bJ34hBALB/cJ, CBA/J, C3H/He, CS7BR/cdi,

DBA/2JSvp-iaAKR/i, C57BL/6J, C57BL/10, C57L, DBA/1,

129/i24bA/Orl, C3H/He, DBA/2OrL, XLII/Orl,

C57BR/cdOrlSvp-2aC57BL/6Orl20bAKR/Orl, AL, BALB/ci, CBA/J, C57BL/6i, C57BL/10,

XLII/OrlcA/Orl, CBA/Orl, C57BR/cdOri,

DW/OrlThy-i BALB/cOrl, CBA/H-T6, C3H/HeOrl,

(0)aAKR/i, 36bA, BDP/J, BUB/BnJ, MA/i, PL/J, RF/i, RFM26,

BALB/c, CBA/J, CE/i, C3H/He, C3H/St, C57BL, C57L, C58, DA/HuSn, FL/2Re, 129/iTiaaA, HTG, I, LP/i, SEC/lRei, SM/i, ST/bJ, SWR, WB/Re,

SWR36bAKR, BDP/i, BUB/BnJ, CS7BR/cdi, C58, F/St. HTI, NZB, PL/i, SJL/i,

ST/bicBALB/c, CBA/J, C3H/He, C57BL/6, CS7L, DBA/1, HTG, I, 1K, MA/i, RF/J,

129TrfaCBA,XLII/Orl32bA/Orl, C57BL/Ks, DBA/2, LP,

AKR/Orl, All!, A2G, BALB/cOrl, CS, C3HeB/FeiOrl, C3H/HeOrl, C57BL/6Orl, C57BR/cdOrl, DBA/2Orl, DDK, ITES, JU, KK, KR, KSA, KSB, TB/OrlH-iaB10.C3H(4ONX), LG, NC, 5,SIlT,SWR,

10bBALB/ci, B10.D2(58N), CBA/J, CBA/CaGn, C3H/Bi, C3H/Sn, C3Hf/An, DBA/lSn, DBA/2i, BDP/.J, WB/Re,WC/Re9,

129/SncC57BL/6i, B10.BY, B10.C(41N), B10.129(5M), C3H.K,

C58/iNot C57BL/1 OSn, C57BR/cdi, C57L/i,

a or cA/Hei, A/Sn, AKR/Sn, CE/i, C57BL/Ks, DA/HuSn, FL/2Re, LP/J, PL/J, RF/i, SiL/J, SWR/i, WK/Re

AUGUST 1972 1633

Locus Allele Strain distribution References

H-2 a A, A/He, A/SnSf, A/WySn, AKR.K, AL/N, A2G, B10.A G. D. Snell, personal b ABP/Le, A.BY, BAN/Re, BLPBR, C3H.SW, C3H.B10/Sf, C57BL/6, C57BL/lOSn, communication CS7L, CC57BR, CCS7W, Dl.LP, HG/Hu, SB/Le. ST/a, V/Le

bc Bl0.129(6M), LP/J, 129

d BALB/c,C57BL/Ks, B10.D2, DBA/2i, LG/i, NBL/N, NZB, SEA/Gni, SEC/iGn, ST.T6, WH, YBL/Rr, YBR/Wi, Dl .C f A.CA, B10.M, RFM/Un

g HTG/AoSf

h B10.A(2R), HTH/AoSf

i HTI/Sf, B10.A(5R) I C3H.iK,I/St,iK,N/St(?)

ja B10.WB, WB/Re, WC/Re, WK/Re

k AKR, B10.BR, B10.K/Sf, CBA, CE, CHI, C3H, C57BR/a, C57BR/cd, C58, Dl .ST, DE/J(?), FL/2Re, FL/6Re, FSF/Gn, HRS/i, L/St, MA/i, PH/Re, RF/i, ST/bi, 101

m AKR.M,B10.AKM

0 C3H-H-2Â°,HTO/Sf

p BDP/i, B10.Y, P/Sn, C3H.NB, F/St(?)

q AU/Ssi, BUB/Bn, DBA/1, C/St, C3H/HeNRe, SWR/i, STOLI

qs DA/HuSn

r Bi 0.RIIl(7 1 NS), CR/Sf, C3H.RIII, LP.RIII, RIII/J, RIII/Wy

S A.SW,SiL

I A.TL

u BlO.PL,PL/i

V B10.SM, SM/i

y AQR, B10.T(6R)

H-3 a C57BL/Ks, C57BL/6i, C57BL/1 OSn, C57BR/cdi, C57L/i, WB/Re, WC/Re 9, 10

b C3H/Bi, C3H/Sn, C3Hf/An, C58/i, DBA/lSn, DBA/2i, LP/i, SWR/i, 129/Sn

Not a or b A/Hei, A/Sn, AKR/Sn, BALB/ci, BDP/J, CBA/CaGn, CBA/.J, DA/HuSn, FL/2Re, PL/i, RF/i, SiL/i, WK/Re

H.4 a AKR/Sn, CBA/.J, CBA/CaGn, C3H/Bi, C3H/Sn, C3Hf/An, C57BL/Ks, C57BL/6i, 9, 10 C57BL/lOSn, C57BR/cdi, C57L/i, C58/J, SJL/J, WK/Re

b 129/Sn, BDP/J

Not a or b A/Hei, A/Sn, BALB/cJ, CE/i, DA/HuSn, DBA/lSn, DBA/2i, FL/2Re, LP/i, PL/i,RF/i, SWR/J, WB/Re, WC/Re

H- 7 a BDP/.J,C57BL/Ks, C57BL/6i, C57BL/lOSn, C57BR/cdi, C57L/i, C58/i, 9, 10 DBA/lSn, DBA/2J, GR/A, WK/Re, 129/Sn

b A/Hei, A/Sn, BALB/cJ, C3H/Sn, C3Hf/An, DA/HuSn, FL/2Re

Not a or b AKR/Sn, CBA/CaGn, CBA/i, CE/i, C3H/Bi, LP/J, PL/i, RF/i, SiL/i, SWR/i, WB/Re, WC/Re

1634 CANCER RESEARCH VOL. 32

Table 1â€”Continued distributionReferencesH-8aLocusAllele Strain

10b C57BL/6i, CS7BL/1 OSn, C57BR/cdi, CS7L/i, C58/i9,

DBA/lSn,129/SnA/HeJ, DBA/2i, LP/i,

A/Sn, AKR/Sn, BALB/c, BDP/i, CBA/CaGn, CBA/J, C3H/Bi, C3H/Sn, C3Hf/An, CE/i, CS7BL/Ks, DA/HuSn, FL/2Re, PL/i, RF/i, SJL/i, SWR/i, WB/Re, WK/ReH-9a WC/Re,

10b A/Hei, CE/i, C3H/Sn, C57BL/lOSn, C57BR/cdi, CS7L/i, C3H/Bi, FL/2Re, PL/i, WB/Re9,

C3Hf/AnNot BALB/cJ, CBA/CaGn, CBA/J,

WK/ReH-i2a a or b C57BL/Ks, C57BL/6i, BDP/i, RF/i, SiL/i, WC/Re,

10b A/Sn, BALB/ci, BDP/J, CE/i, C3H/Bi, C3H/Sn, C57BL/6i, C57BL/lOSn, C57BR/cdi, C57L/i, C58/i, DBA/lSn, DBA/2J, FL/2Re, PL/J9,

SWR/iNot 129/Sn,

a or b A/Hei, AKR/Sn, CBA/CaGn, CBA/J, C3Hf/An, C57BL/Ks, DA/HuSn, LP/i, WK/ReH-i3a RF/J, SiL/i, WB/Re, WC/Re,

10b A/Hei, A/Sn, AKR/.J, CBA/CaGn, CBA/J, C3H/Bi, C3Hf/An, C57BL/Ks, C57BL/6i, C57BL/lOSn, C57BR/cdi, C57L/i, DA/HuSn, FL/2Re, RF/i, SWR/i, WC/Re, WK/Re9,

129/SnNot CE/i, C58/i, DBA/lSn, DBA/2i, LP/i,

a or b BALB/cJ, BDP/i, C3H/Sn, PL/i, SiL/i, WB/Re

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of a Gene Locus for @G, Immunoglobulin H Chains and Its 41. Wortis, H. H. A Gene Locus Concerned with an Antigenic Serum Linkage to the H Chain Chromosome Region in the Mouse. Proc. Substance in Mus musculus. Genetics, 52: 267â€”273, 1965. Natl. Acad. Sd., U. S. 58: 188â€”194,1967. 20. Moutier, R., Toyama, K., and Charrier, M. F. ContrÃ¶leGÃ©nÃ©tique des ProtÃ©inesdela SÃ©crÃ©tiondesGlandes SÃ©minaleschezla Souris APPENDIX 2 et le Rat. Exptl. Animals Pans, 4: 7â€”18, 1971. 21. Naylor, D. H., and Cinader, B. Inheritance, Hormonal Regulation and Properties of Polymorphic Murine Antigens Mud 1 and Mud 2. List of Abbreviations for Use in Symbolizing Substrains Intern. Arch. Allergy Appl. ImmunoL, 39: 51 1â€”539, 1970. 22. Passmore, H. C., and Shreffler, D. C. A Sex-limited Serum Protein A Antoni van Laeuwenhoekhuis, Amsterdam Variant in the Mouse: Inheritance and Association with the H-2 C, Sarphatistraat, 108, The Netherlands (Dr. Region. Biochem. 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Biochemical Polymorphisms in Feral and Inbred Mice (Mus Aid A. Leonard, Laboratoire de GÃ©nÃ©tique, musculus). Biochem. Genet., 5: 457â€”466,1971. Ddpartement de Radiobiologie, Centre 28. Ruddle, F. H., Shows, T. B., and Roderick, T. H. Autosomal d'Etude de l'Energie NuclÃ©aire, Mol, Control of an Electrophoretic Variant of Glucose-6-phosphate Dehydrogenase in the Mouse (Mus musculus). Genetics, 58: Belgium. 599â€”606, 1968. 29. Shows, T. B., and Ruddle, F. H. Function of the Lactate A1T@ Dr. J. L. Ambrus, Roswe!I Park Memorial Dehydrogenase B Gene in Mouse Erythrocytes: Evidence for Institute, Buffalo, New York 14203. Control By a Regulatory Gene. Proc. Natl. Acad. Sci. U.S., 61: 574â€”581, 1968. An Dr. H. B. Andervont (retired), National 30. Shows, T. B., and Ruddle, F. H. Malate Dehydrogenase:Evidence Cancer Institute, Bethesda, Maryland 20014. for Tetrameric Structure in Mus musculus. Science, 160: 1356â€”1357,1968. Argonne National Laboratory, Division of 31. Shows, T. B., Ruddle, F. H., and Roderick, T. H. Phosphoglucomutase Electrophoretic Variants in the Mouse. Biological and Medical Research, Argonne, Biochem. Genet., 3: 25â€”35, 1969. Illinois 60439 (Dr. Robert J. Flynn). 32. Shreffler, D. C. Genetic Control of Serum Transferrin Type in Mice. Proc. Nati. Acad. Sci. U.S., 46: 1378â€”1384, 1960. Ao Dr. D. B. Amos, Duke University School of 33. Shreffler, D. C. Inheritance of a Serum Pre-albuminVariant in the Medicine, Durham, North Carolina 27706. Mouse. Genetics, 49: 629â€”634, 1964. @ 34. Shreffler, D. C., and Owen, R. D. A Serologically Detected Variant A.R.S.A.L., Via di Valle Caia, 00040 in Mouse Serum: Inheritance and Association with the Pomezia (Roma), Casella Postale 39 Histocompatibiity-2 Locus. Genetics, 48: 9â€”25, 1963. Pomezia, Italy (dott. Renata Nobili Castelli). 35. Sick, K., and Nielsen, i. T. Genetics of Amylase Isozymes in the Mouse. Hereditas, Si: 291â€”296, 1964. A Dr. Robert Auerbach, University of 36. Snell, G. D. and Cherry, M. Loci Determining Cell Surface u Alloantigens. In: P. Emmelot and P. Bentvelzen (eds.), Proceedings Wisconsin, Department of Zoology, of the Symposium on RNA Viruses and Host Genome in Madison, Wisconsin 53706. Oncogenesis, Amsterdam, May 12â€”15, 1971, pp. 221â€”228. Amsterdam, North-Holland Publishing Co., 1972. Ba Instituto de Medicina Experimental, 37. Stockert, E., Old, L. J., and Boyse, E. A. The Gix System; A Cell Laboratorio de Genetica, Avda. San Martin Surface Allo-antigen Associated with Murine Leukemia Virus; 548 1, Buenos Aires, Argentina. Implications Regarding Chromosomal Integration of the Viral Genome. i. Exptl. Med., 133: 1334â€”1355,1971. B@ Centro per lo Studio e la Cura dei Tumori, 38. Takahashi, T., Old, L. i., and Boyse, E. A. Surface Alloantigensof Busto Arsizio, Italy (Dr. G. Ceriotti). Plasma Cells. J. Exptl. Med., 131: 1325â€”1341, 1970. 39. Taylor, B. A. Strain Distribution and Linkage Tests of 7,1 2-Dimethylbenzanthracene (DMBA) Inflammatory Response in Bcr University of Birmingham, Cancer Research Mice. Life Sci., 10(I): 1127â€”1134, 1971. Laboratories, The Medical School, 40. Wallace, Margaret E. An Unprecedented Number of Mutants in a Birmingham 15 , England (Dr. June Colony ofWild Mice. Environ. Pollution, 1: 175â€”184, 1970. Marchant).

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Bd Biology Division, Oak Ridge National Bsc Birmingham-Southern College, Department Laboratory, P.O. Box Y, Oak Ridge, of Biology, Birmingham, Alabama 35204 Tennessee 37830 (Dr. Conrad B. Richter). (Dr. Paul C. Bailey).

Be Dr. R. A. Beatty, Institute of Animal Bsp FundAÃ§aoMaria Cecilia Souto Vidigal, Rua Genetics, West Mains Road, Edinburgh 9, Henrique Schaumann, 749, Sao Paulo, Brazil Scotland. (Prof. Michel Jamra).

Bi Dr.J.J.Bittner(deceased). Bt Dr. N. Bateman, Field Laboratory, Animal Breeding Research Organization, Dryden Bim Martin-Luther UniversitÃ¤t,Halle-Wittenberg, Mains, Roslin, Midlothian, Scotland. Bio!ogisches Institut der Medizinische, Germany (Dr. R. Schmidt). Bts Radiobiology Department, Medical College of St. Bartholomew's Hospital, London, Bk Dr. Sidney L. Beck, Department of Biology, ECIM 6BQ, United Kingdom (Prof. P. J. Wheaton College, Norton, Massachusetts Lindop). 02766. Bu Dr. Walter J. Burdette, M. D. Anderson Bkr Mrs. Helen Bunker, The Jackson Laboratory, Hospital and Tumor Institute, University of Bar Harbor, Maine 04609. Texas, Houston, Texas 77025.

Bl Dr. M. Bielschowsky, Department of Tumour Biology, University of Otago Bw Dr. Russell V. Brown, North Texas State Medical School, Great King Street, Dunedin University, Department of Biology, Denton, C.l,New Zealand. Texas76201.

Blk Dr. Robert L. Blake, The Jackson By Dr. Donald W. Bailey, The Jackson Laboratory, Bar Harbor, Maine 04609. Laboratory, Bar Harbor, Maine 04609.

Bln Institut fÃ¼rexperimentelle Krebsforschung, C or Cam University of Cambridge, Genetics Deutsche Akademie der Wissenschaften zu Department, Milton Road, Cambridge, Berlin, Berlin-Buch, Germany (Dr. G. England (Dr. M. E. Wallace). Pasternak). Ca Dr. T. C. Carter, University of Edinburgh, Bn Dr. S. E. Bernstein, The Jackson Laboratory, Edinburgh, Scotland. Bar Harbor, Maine 04609. Cag University of Cambridge, School of Bnd Barnard College, Department of Zoology, Agriculture, Downing Street, Cambridge, Columbia University, New York, New York England (Dr. J. R. Morton). 10027. Cbi Chester Beatty Research Institute, Institute Bnr Department of Pathology, University of of Cancer Research, Fulham Road, London, Bonn/Rhein, Germany (Dr. A. Gropp). S. W. 3, England (Dr. P. C. Koller).

Bo Biochemical Department of Cancer Institute, Cd Dr. Albert Claude, UniversitÃ© Libre de 2Iut@ kopec 7, Brno, Czechoslovakia. Bruxelles, Laboratoire de Cytologie et de CancÃ©rologie Experimentale, Brussels, Bom Laboratory Animals Breeding and Research Belgium. Centre, 8680 Ry, Gl. BomholtgArd, Denmark (C. W. Friis). Cg Mrs. A. Cohen, Experimental Oncology Laboratory, Radiation Therapy Department, Br Dr. G. M. Bonser (retired), Department of Johannesburg General Hospital, Johannes Experimental Pathology and Cancer burg, South Africa. Research, School of Medicine, Leeds 2, England. Ch Dr. Herman B. Chase, Department of Biology, Brown University, Providence, Bre Dr. E. J. Breyere, Department of Biology, Rhode Island 02912. American University, 5355 Loughboro Road, N. W., Washington, D. C. 20016. Ci Dr. Ernst Caspari, University of Rochester,

AUGUST 1972 1637

Department of Biology, River Campus Dg Dr. C. P. Dagg, University of Alabama, Station, Rochester, New York 14627. College of General Studies, Department of Biology, Birmingham, Alabama 35233. Ciu Unidad de Investigaciones Cancerologicas, Avenida Cuauhtemoc 240, Ciudad de Di Dr. Margaret M. Dickie (deceased). Mexico, Mexico. Dk Dr. A. G. Dickinson, A.R.C. Animal Ckc Dr. C. K. Chai, The Jackson Laboratory, Bar Breeding Research Organization, West Mains Harbor, Maine 04609. Road, Edinburgh 9, Scotland.

Cl Mrs. Ruth Clayton, Institute of Animal Dm Dr. L. Dmochowski, M. D. Anderson Genetics, West Mains Road, Edinburgh 9, Hospital and Tumor Institute, Virology and Scotland. Electron Microscopy , Houston , Texas 77025. Cn A. L. Chapman, Ph.D., University of Kansas Medical Center, Kansas City, Kansas 66103. Dp Dr. Giuseppe Della Porta, Head, Section of E x p e r imental Carcinogenesis, Istituto Co Columbia University, Department of Nazionale per lo Studio e la Cura dei Zoology, New York, New York 10027. Tumori, Milano, Italy.

Cpb Centraal Proefdierenbedrijf T.N.O., Bilt Dt Dr. Donald P. Doolittle, Purdue University, straat 172, Utrecht, Holland (Miss Drs. A. K. Population Genetics Institute, Agriculture Kremer). Experiment Station, Lafayette, Indiana 47907. Cr Collaborative Research, National Cancer Institute, Bethesda, Maryland 20014 (Mr. Eg Dr. I. Egorov, Institute of General Genetics, Samuel M. Poiley). USSR Academy of Sciences, Moscow B-i 33, USSR. Crgl Cancer Research Genetics Laboratory, University of California, Berkeley, California Eh Dr. J. Engelbreth-Holm (deceased). 94720. Ei Dr. Eva M. Eicher, The Jackson Laboratory, Cr1 Charles River Breeding Laboratories, Inc., Bar Harbor, Maine 04609. Wilmington, Massachusetts 01887 (Dr. Henry Foster). El Dr. U. H. Ehling, Gesellschaft fÃ¼rStrahien und Umweltforschung, 8042 Neuherberg bei Cs R. T. Charles, â€˜Shell'Research Ltd., Tunstall MÃ¼nchen,Germany. Laboratory, Broad Oak Road, Sittingbourne, Kent, England. Ep Dr. Carlos Epper, Radiobiology Laboratory, Csk Research Laboratories, Chugai Pharmaceu Atomic Energy National Commission, Avda. tical Co., Ltd., 8-41-3, Takada, Toshima-ku, del Libertador Gen. San Martin 8250, Tokyo, Japan (Dr. Toshima Nobunaga). Buenos Aires, Argentina.

Ct Dr. Bruce M. Cattanach, M.R.C. Fa Dr. D. S. Falconer, Institute of Animal Radiobiology Unit, Harwell, Didcot, Berks., Genetics, West Mains Road, Edinburgh 9, England. Scotland.

Cu Dr. R. L. Curtis, Department of Anatomy, Fe Dr. Elizabeth Fekete (retired), The Jackson School of Medicine, Marquette University, Laboratory, Bar Harbor, Maine 04609. 561 N. 15th Street, Milwaukee, Wisconsin 53233. Ffm UniversitÃ¤t Frankfurt, Institut fuf Humangenetik und vergleichende Erbpatho Cz Dr. Gustavo Cudkowicz, Roswell Park logie, 6 Frankfurt/Main, Germany (Dr. K.-H. Memorial Institute, Buffalo, New York Degenhardt). 14203. Fg Prof. Frank H. J. Figge, University of Dc Dr. Margaret K. Deringer, 5528 Johnson Maryland School of Medicine, Department Avenue, Bethesda, Maryland 20034. of Anatomy, Baltimore, Maryland 21201.

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Fn Dr. Paul F. Fenton, Brown University, Gr Dr. H. GrÃ¼neberg, University College Biology Department, Providence, Rhode London, Department of Zoology, Gower Island 02912. Street, London, W. C. 1, England.

Fo Dr. P. Forsthoefel, University of Detroit, Grf Dr. Ralph J. Graff, Jewish Hospital of St. Biology Department, McNichols Road at Louis, Department of Surgery, 216 South Livernois, Detroit, Michigan 48221 . Kingshighway, St. Louis, Missouri 63110.

Fr Dr. F. Clarke Fraser, Department of Gro Genetical Institute, University of Groningen, Genetics, McGill University, Montreal, Kerk!aan 30, Haren (Gr.), Netherlands (Dr. Quebec, Canada. G. A. van Oortmerssen).

Fs Dr. Morris Foster, University of Michigan, Gs Dr. Ludwik Gross, Cancer Research Department of Zoology, Ann Arbor, Laboratory, V. A. Hospital, 130 W. Michigan 48 104. Kingsbridge Road, Bronx, New York 10468.

Fu Dr. J. Furth, Department of Pathology, Gw Dr. John W. Gowen (deceased). Francis Delafield Hospital, 99 Fort Washington Avenue, New York, New York H M.R.C. Radiobiology Unit, Harwell, Didcot, 10032. Berks., England (Dr. M. F. Lyon).

G Glaxo Laboratories, Ltd., Greenford, Ha Dr. T. S. Hauschka, Roswell Park Memorial Middlesex, England. Institute, Buffalo, New York 14203.

Ga Dr. Allen H. Gates, Department of Anat- Han Zentralinstitut fÃ¼r Versuchstierzucht, omy, University of Rochester Medical Lettrow-Vorbeck-Allee 57, Hannover Center, 260 Crittenden Blvd., Rochester, Linden, Germany (Dr. W. Heine). New York 14642. Hb H. Everett Hrubant, Ph.D., California State Ge Dr. H. N. Green (deceased). College at Long Beach, Department of Biology, Long Beach, California 90804. Gen Istituto di Farmacologia, UniversitÃ di Genova, Viale Benedetto XV, N.2, Genova, He Dr. W. E. Heston, National Cancer Institute, Italy (Dr. Silvio Parodi). Bethesda, Maryland 20014.

Gf Anna Go!dfeder, D.Sc., M.U.C., Cancer and Hea Dr. M. A. Head, Royal Beatson Memorial Radiobiological Research Laboratory, City Hospital, Cancer Research Department, of New York Department of Hospitals, 99 Glasgow, C.3, Scotland. Fort Washington Ave., New York, New York 10032. Hf Dr. Harold A. Hoffman, National Cancer Institute, Bethesda, Maryland 20014. Gh Dr. Douglas Grahn, Argonne National Laboratory, Division of Biological and Hg Prof. Dr. P. Hertwig (retired), Biologisches Medical Research, 9700 Cass Ave., Argonne, Institut, UniversitÃ¤tsplatz 7, Halle (Saale), Illinois 60439. Germany.

Gl Dr. A. GlUcksmann, Strangeways Research Hn Dr. F. K. Hoornbeek, University of New Laboratory, Wort's Causeway, Cambridge, Hampshire, Zoology Department, Spaulding England. Building, Durham, New Hampshire 03824.

. Ho Prof. W. F. Hollander Department of Glw Dr. S. G. Waelsch, Albert Einstein College of Genetics, Iowa State University, Ames Iowa Medicine, Department of Anatomy, 50010 Eastchester Road and Morris Park Ave., New York, New York 10461 . How Dr. Alma Howard, Paterson Laboratories, Christie Hospital and Holt Radium Institute, Gn Drs. E. L. and M. C. Green, The Jackson Manchester 20, United Kingdom. Laboratory, Bar Harbor, Maine 04609. Hr Dr. G. Hoecker, Catedra de Biologia, Av. Go Dr. Peter Gorer (deceased). Zanartu 1042, Santiago de Chile, Chile.

AUGUST 1972 1639

Ht Dr. H. B. Hewitt, Research Unit in der Wissenschaften zu Berlin, DDR 69 Jena, Radiobio!ogy, Mount Vernon Hospital, Beuthenbergstrasse I 1, German Democratic Northwood, Middlesex, England. Republic (East Germany) (Dr. H. Heinecke).

Hu Dr. Katharine P. Hummel, The Jackson Jic Department of Genetics and Breeding, Laboratory, Bar Harbor, Maine 04609. Central Institute for Experimental Animals, 17-2, Aobadi-2, Meguro, Tokyo, Japan. Hz Dr. L. A. Herzenberg, Department of Genetics, Stanford University School of Jko Keio University School of Medicine, Medicine, Palo Alto, California 94304. Department of Microbiology, Shinano machi, Shinjuku-ku, Tokyo, Japan (Dr. Ibg Institute for Behavioral Genetics, University Daizo Ushiba). of Colorado, Boulder, Colorado 80302 (Dr. G. E. McClearn). Jms Animal Breeding Unit, Institute of Medical Science, University of Tokyo, Shiba Icr Institute for Cancer Research, 7701 Shirokane-Daimachi, Minato-ku, Tokyo, Burholme Ave., Fox Chase, Philadelphia, Japan (Dr. Yoshio Tajima). Pennsylvania19111. Jt Dr. Judith Tennant, Sloan-Kettering Icrc Indian Cancer Research Centre, Parel, Institute for Cancer Research, New York, Bombay 12, India (Dr. B. K. Batra). New York 10021.

Icrf Imperial Cancer Research Fund, Burtonhole Ka Dr. H. S. Kaplan, Department of Radiology, Lane, London, N. W. 7, England (Prof. J. Stanford University School of Medicine, Craigie). Palo Alto, California 94304.

Ig Dr. Rigoberto Iglesias, Director, Instituto de Kb Dr. Berenice Kindred, UniversitÃ¤tKonstanz, Medicina Experimental, Avda. IrarrÃ¡zaval Fachbereich Biologie, 775 Konstanz, 849, Casilla 3401 , Santiago de Chile, Chile. Postfach 733, Germany.

Imr Institute for Medical Research, Copewood Kch Dr. Walter Kocher, Heiigenberg-Institut, Street, Camden, New Jersey 08103. Institut fÃ¼rExperimentelle Biologie, 7799 Heiigenberg/Baden, West Germany. lo Institute of Orthopaedics, Royal National Orthopaedic Hospital, Brocklay Hill, Kd Dr. J. F. Kidwell, Division of Biology and Stanmore, Middlesex, England (Mark Medical Sciences, Brown University, Walton). Providence, Rhode Island 02912.

J or Jax The Jackson Laboratory, Bar Harbor, Maine Kga Kagoshima University, Laboratory of 04609. Animal Breeding, Faculty of Agriculture, Kagoshima, Japan (Dr. Manjiro Taketomi). Jali National Institute of Animal Health, Kodaira, Tokyo-to, Japan (Dr. Takayoshi @j Kirschbaum Memorial Laboratory, Medical mo). College of Georgia, Department of Cell and Molecular Biology, Augusta, Georgia 30902. Jb Dr. Jan Bruell, Psychology Department, Western Reserve University, Cleveland, Ohio Ki Drs. G. and E. Klein, Department of Cell 44106. Research, Karolinska Institutet, Stockholm 60,Sweden. Jd A. Jurand, Institute of Animal Genetics, West Mains Road, Edinburgh 9, Scotland. Klj Dr. Jan Klein, University of Michigan, School of Dentistry, Ann Arbor, Michigan Jem Hebrew University-Hadassah Medical School, 48104. Experimental Medicine and Cancer Research, Jerusalem, Israel (Dr. Michael Km Dr. Robert F. Kallman, Department of Schlesinger). Radiology, Stanford University School of Medicine, Palo Alto, California 94304. Jena Institut fÃ¼r Mikrobiologie und experi mentalle Therapie der Deutschen Akademie Kn Prof. Dr. Fr. Kr5ning, Medizinische

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Forschungsanstalt , Pharmakologische Department of Cancer Research, Ashfield Abteilung, Bunsenstrasse 10, Gottingen, Street, Whitechapel EA , England. Germany. U Laboratory AnimalsCentre,PolishAcademy Ko Dr. N. Kobozieff, Laboratoire de GÃ©ndtique, of Sciences, Lomna Las k. Warsaw, Poland Ecole National VÃ©tÃ©rinaire d'Alfort, (Doc. dr. Czeslaw Maranski). Maisons-Alfort (Seine), France. Ln Dr. J. B. Lyon, Department of Biochemistry, Kon UniversitÃ¤t Konstanz, Fachbereich Biologic, Emory University, Atlanta, Georgia 30322. 775 Konstanz, Postfach 733, Germany (Dr. Berenice Kindred). Lo Los Alamos Scientific Laboratory, P.O. Box 1663, Los Alamos, New Mexico 87544 (Dr. Kp Dr. Hilary Koprowski, The Wistar Institute, J.F.Spalding). 36th at Spruce, Philadelphia, Pennsylvania 19104. I.s Dr. Edwin P. Las, The Jackson Laboratory, Bar Harbor, Maine 04609. Kr Prof. L. Kreyberg, Universitetets Institutt for Patologi, Rikshospitalet, Oslo, Norway. Lw Dr. L. W. Law, National Cancer Institute, Bethesda, Maryland 20014. Ks Dr. N. Kaliss, The Jackson Laboratory, Bar Harbor, Maine 04609. Ly Dr. Clara Lynch (retired), Rockefeller Institute, 66th St. and York Ave., New York, New York 10021. Kt Karold Kalter, Ph.D., Children's Hospital Research Foundation, Elland Ave. and M Memorial Hospital and Sloan-Kettering Bethesda, Cincinnati, Ohio 45229. Institute for Cancer Research, 410 E. 68th Street, New York, New York 10021. Kun Katholieke Universiteit, Central Animal Laboratory, Nijmegen (Dr. J. C. J. Van Ma Dr. E. A. Mirand, Roswell Park Memorial Vliet). Institute, Buffalo, New York, 14203.

Kw Department of Animal Genetics and Organic Mac Massey University of Manawatu and Evolu tion , Jagiellonian University, Palmerston North General Hospital, Krupnicza 50, Krakow 2, Poland (Dr. llama Palmerston North, New Zealand (Dr. R. E. Krzanowska). Munford).

L Lilly Research Laboratories, Eli Lilly & Co., Mai Microbiological Associates, Inc., 4813 Indianapolis, Indiana 46206 (Dr. Terence T. Bethesda Ave., P. 0. Box 5970, Washington, T.Yen). D.C.20014.

La Dr. A. Lacassagne (deceased). Man Stanley J. Mann, Ph.D., Temple University Health Sciences Center, The Skin and Cancer Lac Laboratory Animals Centre, M.R.C. Hospital of Philadelphia, 3322 North Broad La b o r a t ones, Woodmansterne Road, Street, Philadelphia, Pennsylvania 19140. Carshalton, Surrey, England. Mas University of Massachusetts, Department of 14 J. Russell Lindsey, D.V.M., University of Zoology, Amherst, Massachusetts 01002 Alabama in Birmingham, Department of (Dr. H. Rauch). Comparative Medicine, 1919 Seventh Ave. South, Birmingham, Alabama 35233. Mc Dr. W. B. Mcintosh, Box 96A, Rt. 1, Darlington, Maryland. La Mrs. Priscilla W. Lane, The Jackson Laboratory, Bar Harbor, Maine 04609. Md Dr. Anne McLaren, Institute of Animal Genetics, West Mains Road, Edinburgh 9, Lai W. Hijmans, M.D., Research Laboratories, Scotland. Department of Rheumatology, University Hospital, Leiden, The Netherlands. Md Dr. E. C. MacDowell (retired).

Lhm The London Hospital Medical College, Me Prof. P. B. Medawar, Department of

AUGUST 1972 164!

Zoology, University College London, Gower Ciencias Medicas, Universidad Nacional de Street, W.C. 1., England. Cuyo, Hospital Central, 6Â°piso Mendoza, Argentina. Mg Prof. Walter Morgan, South Dakota State College, Brookings, South Dakota. N Genetics Research Unit, Laboratory Aids Branch, National Institutes of Health, Mi Dr. D. Michie, Department of Surgical Bethesda, Maryland 20014 (Carl Hansen). Science, University New Buildings, Teviot Place, Edinburgh 8, Scotland. Nga Nagoya University School of Agriculture, Department of Animal Genetics, Furo-cho, Mib Genetic Laboratory of the Institute of Chikusa-Ku, Nagoya-shi, Japan (Dr. Kyoji Experimental Biology, Academy of Medical Kondo). Sciences of the USSR, Baltiskaya 8, Moscow A-3l 5 (Dr. B. V. Konyukhov). Nimr National Institute for Medical Research, Mill Hill, London, N. W. 7, England (Dr. Marjorie Mk Dr. Sajiro Makino, Zoological Institute, Dinsley). Hokkaido University, Sapporo, Japan. Nmg Mouse Research Group, Genetics Labora Ml Dr. James R. Miller, Department of tory, Driehuizerweg 200, Nijmegen, The Neurological Research, University of British Netherlands (Dr. P. H. W. van der Kroon). Columbia, Vancouver, British Columbia, Canada. No Dr. D. J. Nolte, University of the Witwatersrand, Genetics Laboratory, Milner Mn Prof. Wallace McNutt, University of Park, Johannesburg, South Africa. Texasâ€”Medical Branch, Department of Anatomy, Galveston, Texas 77550. Not Cancer Research Laboratory, The University, University Park, Nottingham, Mo Dr. R. H. Mole, Radiobiology Unit, Harwel!, England (Dr. R. W. Baldwin). Didcot, Berks., England. Nvs Nevis Biological Station, Columbia Mq Dr. Jacqueline Mouriquand, Centre University, Irvington, New York (Dr. L. C. d'Etudes Nuc!Ã©aires de Grenoble, Boite Dunn). Postale 269, Grenoble, France. 0 Universitetets Institutt for Generell og Mr Dr. E. W. Miller, Cancer Research Eksperimental Patologi, Oslo, Norway (Dr. Laboratory, Department of Pathology, K. Arnesen). Royal Victoria Infirmary, Newcastle upon Tyne I,England. Oci Ontario Cancer Institute, University of Toronto, 500 Sherbourne Street, Toronto 5, Ms National Institute of Genetics, Yata 1111, Ontario, Canada. Misima, Sizuoka-ken, Japan (Dr. Tosihide H. Yoshida). Orl Centre de Selection et d'Elevage d'Animaux de Laboratoire , 45 Orleans-la-Source, Mt Dr. Balfour M. Mount, Royal Victoria France. Hospital, Department of Urology, 687 Pine Ave. West, Montreal 112, Quebec, Canada. Os Osaka University, Institute for Cancer Mu Dr. Irving Mauer, Willowbrook State School, Research, DOjima-HamadOri, Fukushima-ku, Neuro-Endocrine Research Unit, Staten Osaka, Japan (Dr. Yasuyuki Akamatsu). Island, New York 10014. Osb Osaka University, Department of Mv Dr. N. N. Medvedev, Gamaleya Institute of Experimental Chemotherapy, Research Epidemiology and Microbiology, Schukin Institute for Microbiol Diseases, Yamada skaya 33, Moscow D-98, USSR. kami, Suita, Osaka-fu, Japan (Dr. Jun-ichi Kawamata). My Dr. W. S. Murray (deceased). Ott Genetics Section, Animal Research Institute, Mza Dr. J. Echave Uanos, Instituto de Patologia Central Experimental Farm, Ottawa, Canada General y Experimental, Facultad de (Dr. R. S. Gowe).

1642 CANCER RESEARCH VOL. 32

P Pondville Hospital, Walpole, Massachusetts Rap Breeding Farm Rappolova, Laboratory of 02081. Inbred Animals, Academy of Medical Science, Solyanka 14, Moscow USSR (Dr. N. Pat Paterson Laboratories, Christie Hospital and N. Medvedev). Holt Radium Institute, Manchester 20, England (Drs. A. Howard and D. D. Rb Dr. R. G. Busnel, Institut National de la Porteous). Recherche Agronomique, Laboratoire de Physiologie Acoustique, Jouy-en-Josas (S & Pe Dr. P. R. Peacock, Royal Beatson Memorial 0), France. Hospital, 132â€”138 Hill Street, Glasgow C.3, Scotland. Rd Dr. G. Rudali, Fondation Curie, 26 rue d'Ulm, Paris (ye), France. Per Division of Cancer Research, University of Perugia, Perugia, Italy (Prof. Lucio Seven). Re Dr. Elizabeth S. Russell, The Jackson Laboratory, Bar Harbor, Maine 04609. Pgi Population Genetics Institute, Life Science Building, G-117, Purdue University, Rg University of Reading, Department of Lafayette, Indiana 47907 (Drs. W. H. Kyle Physiology and Biochemistry, Reading, and T. G. Martin). Berks., England (R. Batt, Lacturer).

Ph Czechoslovak Academy of Science, Institute Rho Laboratoire de Recherches de la SociÃ©td of Experimental Biology and Genetics, Rhone-Poulenc, 13 Quai Jules Guesde, Vitry Budejovicka 1083, Prague 4, Czechoslovakia sur Seine (Seine), France (Prof. R. Paul). (Doc. MÃ¼Dr.MilanHa@ek,D. Sc.). Rij Radiobiological Institute T.N.O., Lange .Pi Dr. H. I. Pilgrim, University of Utah College Kleiweg 15 1, Rijswijk (Z.H.), Netherlands of Medicine, Department of Surgery, Salt (Dr. D. W. Van Bekkum). Lake City, Utah 84112. Rjb Mr. Robert J. Burns, Supervisor, Animal Pk B. S. Parker, Meat Research Laboratory, Colony, Wistar Institute of Anatomy and Sydney University Farms, Camden, N. S. W., Biology, 36th at Spruce, Philadelphia, Australia. Pennsylvania 19104.

P1 Mr. Samuel M. Poiley, Mammalian Genetics Rk Dr. Thomas H. Roderick, The Jackson and Animal Production Section, Drug Laboratory, Bar Harbor, Maine 04609. Evaluation Branch, CCNSC, National Cancer Institute, Bethesda, Maryland 20014. RI Drs. W. L. and L. B. Russell, Biology Division, Oak Ridge National Laboratory, P. Pm Dr. Joy Palm, The Wistar Institute, 36th at 0. Box Y, Oak Ridge, Tennessee 37830. Spruce, Philadelphia, Pennsylvania 19104. Ro Dr. U. Roth, Zoo!ogisches Institut, Po Dr. E. E. Pogosianz, Institute of Jungiusstr. 6, Hamburg 36, Germany. Experimental and Clinical Oncology, Kashirskoje sh. 6, Moscow M-478, USSR. Rr Dr. M. N. Runner, University of Colorado, Department of Biology, Boulder, Colorado Pr Dr. Louis J. Pierro, University of 80304. Connecticut, Department of Animal Genetics, Storrs, Connecticut 06268. 5 Dr. Kurt Stern, Department of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel. Pu Dr. B. D. Pullinger, Institute for Medical Research, Copewood Street, Camden, New Sa Research Institute for Tuberculosis, Leprosy Jersey 08103. and Cancer, Cancer Research Laboratory, Tohoku University, Sendai, Japan (Dr. R Rand Development Corporation, Cleveland, Haruo Sato). Ohio 44110.

Ra Dr. Harold Rauch, Zoology Department, Sb Dr. Arthur G. Steinberg, Biological University of Massachusetts, Amherst, Laboratory, Western Reserve University@ Massachusetts 01002. Cleveland, Ohio 44106.

AUGUST 1972 1643

Sbh Department of Serology and Bacteriology, Sp Dr. William L. Simpson, Detroit Institute of University of Helsinki, Helsinki, Finland Cancer Research, 48 11 John R Street, (Prof. 0. MÃ¤kelÃ¤)(Mrs.Maria Virkki). Detroit, Michigan 48201.

Sc Dr. J. P. Scott, Bowling Green State Sr Dr. Howard A. Schneider, Institute of University, Department of Psychology, Nutrition, University of North Carolina Bowling Green, Ohio 43402. School of Medicine, Chapel Hill, North Carolina 27514. 5cr Scripps Clinic and Research Foundation, Department of Experimental Pathology, 476 Sri Stanford Research Institute, Department of Prospect Street, La Jolla, California 92037 Experimental Therapeutics, Menlo Park, (Mr. Harold L. Spencer). California 94025.

Sda Tohoku University, Laboratory of Animal Ss Dr. Willys K. Silvers, Department of Medical Breeding, Department of Animal Husbandry, Genetics, University of Pennsylvania School Faculty of Agriculture, 210 Kita-6-bancho, of Medicine, Philadelphia, Pennsylvania Sendai, Japan (Dr. Shusaku Nishida). 19104.

Se Prof. Lucio Seven, Istituto di Anatomia e St Dr. L. C. Strong, Leonell C. Strong Research Istologia Patologica dell'Universita degli Foundation, Inc., Del Mar, California. Studi di Perugia, Italy. Sth State Serum Institute, Helsinki, Finland (Dr. Se! Laboratorio Bioterapico Milanese, Selvi & M. Jahkola). C., Milan, Italy (Dr. W. Murmann). Sto Breeding Farm Stolbovaya, Laboratory of Sf Dr. Donald C. Shreffler, University of Inbred Animals, Academy of Medical Michigan, Department of Human Genetics, Science, Solyanka 14, Moscow USSR. 1133 E. Catherine Street, Ann Arbor, Michigan 48104. Sv Dr. L. C. Stevens, The Jackson Laboratory, Bar Harbor, Maine 04609. Sfd Stanford University School of Medicine, Department of Anatomy, Palo Alto, Sy Dr. A. Symeonidis, Cancer Institute, California 94304 (Dr. Elizabeth M. Center). Theagenion Memorial, Thessaloniki, Greece.

Sg Dr. Jack Stimpfling, The McLaughlin T Department of Zoology, University of Research Institute, Columbus Hospital, Toronto, Toronto 5, Ontario, Canada (Dr. L. Great Falls, Montana. Butler).

Shi Shionogi & Co., Ltd., Research Laboratory, Ta Takatsuki Animal Farm, Takeda Chemical Sagisu-KamidOri, Fukushima-ku, Osaka, Industries, Kyoto, Japan. Japan (Dr. Yasunao Ogawa). Tb Dr. S. A. Barnett, Australian National Si Dr. Morten Simonsen, Queen Victoria University, Dept. Zoology, Canberra ACT Hospital, East Grinstead, Sussex, United 2600, Australia. Kingdom. Tbr Dr. Yoshthiko Tsubura, 2nd Department of 5k Dr. H. E. Skipper, Southern Research Pathology, Nara Medical College, Kathihara Institute, Birmingham, Alabama 35205. shi, Nara-ken, Japan.

Sm Dr. David Steinmuller, Department of Th Dr. Karl Theiler, Anatomisches Institut, der Pathology and Surgery, University of Utah, UniversitÃ¤t, Gloriastr. 19, 8006 Zurich, Salt Lake City, Utah 841 12. Switzerland.

Tif Tierfarm AG, 4334 Sisseln, Switzerland (Dr. Sn Dr. G. D. Snell, The Jackson Laboratory, H. Hurni). Bar Harbor, Maine 04609. Tn Dr. A. Tannenbaum, Medical Research So Miss Janice L. Southard, The Jackson Institute, Michael Reese Hospital, 29th and Laboratory, Bar Harbor, Maine 04609. Ellis Ayes., Chicago, Illinois 60616.

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Tr Dr. John J. Trentin, Division of Department of Zoology, Lawrence, Kansas Experimental Biology, Baylor University 66044. College of Medicine, Houston, Texas 77025. Wm Dr. Wffliam H. Murphy, University of Michigan, Department of Microbiology, East Tu Dr. F. C. Turner (deceased). Medical Building, Ann Arbor, Michigan 48104. Tw Noboru Takasugi, Dr. Sci., Zoological Institute, Faculty of Science, University of Wmr Dr. Willie M. Reams, Jr., Department of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan. Biology , University of Richmond, Richmond, Virginia 23173. Umc University of Minnesota Medical School, Department of Physiology, Minneapolis, Wn Weizmann Institute of Science, Laboratory Minnesota 55455. (Miss June Smith). Animals Breeding Centre, Rehovoth, Israel. Un Dr. A. C. Upton, Biology Division, Oak Wq Dr. Walter C. Quevedo, Jr., Brown Ridge National Laboratory, P. 0. Box Y, University, Division of Biological and Oak Ridge, Tennessee 37831. Medical Sciences, Providence, Rhode Island 02912. Up Miss Delta E. Uphoff, National Cancer Institute, Bethesda, Md. 20014. Wr University of Wisconsin Medical Center, Department of Radiology, 1300 University W Instytut Onkologii, im. Marii Sldowdo Ave., Madison, Wisconsin (Dr. Kelly H. wskiej-Curie, Zaklad Biologii Nowotworow, Clifton). Warszawa, ul. Wawe!ska 15, Poland (Dr. Kazimierz Dux, Dr. Alma Czarnomska). Ws! H. Bazin, D.V.M., Dr. Sci., UniversitÃ© Catholique de Louvain, Ecole de Sante Wak Wakayama Medical College, Department of Publique, Avenue Chapelle aux Champs 4, Physiology, Wakayama, Japan (Dr. H. 1200 Bruxelles, Belgium. Matsushita). Wt Dr. Wesley K. Whitten, The Jackson We Dr. J. A. Weir, University of Kansas, Laboratory, Bar Harbor, Maine 04609. Department of Zoology, Lawrence, Kansas 66044. Ww Mrs. E. F. Woodworth, The Jackson Laboratory, Bar Harbor, Maine 04609. Wehi Walter and Eliza Hall Institute of Medical Research, Melbourne 3050, Australia (Dr. G. J.V.Nossal). Wy Dr. G. W. Woolley, Division of Genera! Medical Sciences, National Institutes of Wf Dr. George L. Wolff, Institute for Cancer Health, Bethesda, Maryland 20014. Research, Fox Chase, Philadelphia, Pennsylvania19111. Y Yurlovo, Department of Genetics, Laboratory of Experimental Animals, Wg Dr. H. E. Walburg, Jr., Oak Ridge National Yurlovo Post Office, Khimki Town, Moscow Laboratory, Gnotobiotics Group, P. 0. Box Region, USSR. Y, Oak Ridge, Tennessee 37831. Yok Department of Veterinary Science, National Institute of Health (Yoken) Kamiohsaki, Wh Dr. Abraham White, Department of Shinagawa-ku, Tokyo, Japan (Dr. Kiyoshi Biochemistry, Albert Einstein College of Imaizumi). Medicine, 1300 Morris Park Ave., Bronx, New York 10461. APPENDIX 3 Wi Dr. J. W. Wilson (deceased). The Committee recommends the use of the following Wis Wistar Institute of Anatomy and Biology, abbreviations for the names of inbred strains in compound 36th Street at Spruce, Philadelphia, symbols and in other situations where brevity is desired. In all Pennsylvania 19104. cases, the full strain designations should always be given in either the Materials and Methods or Introduction section of Wl Dr. H. G. Wolfe, University of Kansas, any paper; e.g. , â€œ... AKR/J X DBA/2J F1 (hereafter called

AUGUST 1972 1645

AKD2F1 . . . .â€œIn hybrid designations, the female parent C57BL B should be the first listed. C57BL/6 B6 C57BL/lO BlO STRAIN ABBREVIATION C57BR BR CS7L L AKR AK DBA/1 Dl BALB/c C DBA/2 D2 C3H C3 RIII R3

1646 CANCER RESEARCH VOL. 32

Joan Staats

Cancer Res 1972;32:1609-1646.

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