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Deletions and Losses in Chromosomes 5 Or 7 in Adult Acute Leukemia (1999) 13, 869–872 1999 Stockton Press All rights reserved 0887-6924/99 $12.00 http://www.stockton-press.co.uk/leu Deletions and losses in chromosomes 5 or 7 in adult acute lymphocytic leukemia: incidence, associations and implications BS Dabaja1, S Faderl1, D Thomas1, J Cortes1, S O’Brien1, F Nasr1, S Pierce1, K Hayes2, A Glassman2, M Keating1 and HM Kantarjian1 Departments of 1Leukemia and 2Hematopathology, Section of Cytogenetics, The University of Texas, MD Anderson Cancer Center, Houston, Texas, USA Deletions or losses in chromosomes 5 or 7 are recurrent non- Table 1 Characteristics of the study group random abnormalities in acute myeloid leukemia (AML), and are associated with prior exposure to carcinogens or leukem- Characteristic Category No. of patients (%) ogenic agents, and with poor prognosis. Their occurrence and significance in adult acute lymphocytic leukemia (ALL) is not well described. The aim of the study was to evaluate the inci- Chromosome 5 or P value dence, associations and implications of chromosome 5 or 7 7 abnormality abnormalities in adult ALL. Patients with newly diagnosed ALL referred to MD Anderson Cancer Center between 1980 and 1996 Present Absent were analyzed. Characteristics and outcome of patients with or without chromosome 5 or 7 abnormalities were compared by Number 31 437 standard statistical methods. Thirty-one of 468 patients (6.6%) Age (years) у60 9 (29) 80 (18) 0.14 had chromosome 5 or 7 abnormalities. Loss of chromosome 5 Performance (Zubrod) у3 1 (3) 36 (8) 0.33 occurred in six cases, three of them had both chromosome 5 Hepatomegaly yes 3 (10) 96 (22) 0.1 and 7 abnormalities. Deletion or loss of chromosome 7 Splenomegaly yes 9 (29) 141 (32) 0.71 occurred as a single abnormality in three patients; in 28 Hemoglobin (g/dl) Ͻ10 18 (58) 289 (66) 0.36 patients it was associated with other abnormalities. The most Platelets (×109/dl) Ͻ50 12 (39) 212 (48) 0.29 significant cytogenetic association was with the Philadelphia WBC (×109/dl) Ͼ50 22 (71) 357 (82) 0.14 chromosome (Ph) abnormality occurring in nine patients (29%). Marrow blasts % Ͼ50 30 (97) 427 (92) 0.38 Compared with patients without the abnormalities, patients with chromosome 5 or 7 abnormalities tended to express CD34 more frequently (74% vs 54% P = 0.07), to be older (age Ͼ60 years 29% vs 18% P = 0.14), and to be associated with Ph (29% vs 11% P = 0.004). With therapy, the complete response (CR) rate with chromosome 5 or 7 abnormalities was lower (64% vs Table 2 Immunophenotypic characteristics of patients with or 79% P = 0.038) but the survival rate was similar (3-year survival without chromosome 5 or 7 abnormalities rate 32% vs 36% P = 0.14). When the 22 patients without Ph were considered separately, the CR and survival rates were No. of patient/Total analyzed (%) similar among patients with or without chromosome 5 or 7 abnormalities. Abnormalities in chromosome 5 or 7 are not spe- Chromosome 5 or 7 P value cific for AML, and may occur in ALL. Unlike in AML, chromo- abnormalities some 5 or 7 abnormalities in ALL were not predictive of worse prognosis, which is accounted for mostly by the association Present Absent with Ph. Keywords: acute lymphocytic leukemia; cytogenetic abnormalities; chromosomes 5 and 7 (A) Specific marker CD 10 (CALLA) 17/24 (70) 209/305 (68) 0.81 CD 19 15/20 (75) 215/280 (76) 0.85 CD 34 17/23 (74) 152/280 (54) 0.07 Introduction T cell markers 5/24 (21) 73/347 (21) 0.98 Myeloid markers 12/23 (52) 131/289 (45) 0.52 Cytogenetic studies in de novo acute leukemia have identified nonrandom chromosomal abnormalities to be associated with (B) Immunophenotype significant differences in patient prognosis. Deletions or losses Mature B cell 1/24 (4) 41/347 (12) 0.25 Pre B 3/24 (12) 29/347 (8) 0.41 in chromosomes 5 or 7, alone or with other changes, have CALLA-positive 13/24 (54) 179/347 (52) 0.73 been found in a variety of hematological disorders, including T cell 5/24 (21) 73/347 (21) 0.98 acute myelogenous leukemia (AML) and myelodysplastic Null 2/24 (8) 25/347 (7) 0.84 syndromes (MDS), and are associated with prior exposure to carcinogens and with poor prognosis.1–6 Little is known about the prognostic significance of chromo- the incidence and implications of chromosome 5 or 7 some 5 or 7 abnormalities in ALL. Their presence may intuit- abnormalities in adult ALL. ively imply poor prognosis, as suggested by their prognostic effect in AML and MDS. However, such prognostic associ- ations have not been described in ALL. Herein, we report on Materials and methods Study group Correspondence: HM Kantarjian, MD Anderson Cancer Center, Department of Leukemia, Box 61, 1515 Holcombe Blvd, Houston, TX Four hundred and sixty-eight patients with newly diagnosed 77030, USA; Fax: 1 713 792 2031 untreated ALL, 15 years and older, who were referred to our Received 18 November 1998; accepted 23 February 1999 institution between 1980 and 1996, were reviewed. The Insti- Chromosome 5 or 7 abnormalities in ALL BS Dabaja et al 870 Table 3 Detailed karyotypic analysis in the study group Patient No. Karyotype 1 47,XX,−7,t(9;22)(q34;q11), +17,−21,+der(22)t(9;22),+mar[13] 47,XX,del(7)(q11),t(9;22)(q34;q11),−21,+der(22)t(9;22),+2mar[7] 46,XX[2] 2 46,XX,inv(7)(p21q23),t(9;22)(q34;q11)[21] 46,XX,inv(7)(p23q23)[4] 3 67–69,XY,−3,−5,−5,−6,−7,+8,+8,+8,+9,−10,+12,−13,−14,−15,−16,−17,+18,−19,+21, +21,−22,+2−6mar[cp5] 46,XY[15] 4 45,XY,−7,add(16)(p13.3)[21] 45,X,−Y,−7,add(16)(p13.3),+mar[2] 5 45,XX,−7,t(9;22)(q34;q11)[25] 6 47,Y,−X,−5,−7,+13,−14,−15,+5−6mar[8] 84–91,YY,−X,−X,−4,−4,−5,−5,−7,−7,i(8)(q10),−14,−14,−15,del(22)(q13),+8,−10mar[cp11] 46,XY[1] 7 47,XY,−7,−15,+19,add(22)(p11),+2mar[10] 47,XY,−7,add(9)(p13),−15,+19,add(22)(p11),+2mar[2] 46–47,XY,−4,−6,−7,−15,+19,add(22)(p11),+2–3mar[cp7] 46,XY[1] 8 45,XX,−7[4] 46,XX[21] 9 45,XX,add(6)(p25),−7,dup(7)(q21q32),t(9;22)(q34;q11)[25] 10 46,XY,del(9)(p23)[25] 46,XY,−5,−7,der(7)t(7;?)(p22;?)del(7)(q31.3),+mar[19] 46,XY[15] 11 43–45,XX,−7,der(9)inv(9)(p11q12)c t(9;22)(q34;q11),add(19)(p13.3)[cp7] 12 45,XY,−7[11] 46,XY [14] 13 79–81,XXYY,−2,add(2)(q24)×2,−4,−5,−6,−7×2,−8,−9×2,−11x2,−12,−13,−15,−16,−17,−20×2,+22,+3−6mar[cp5] 46,XY[7] 14 47,XY,inv(7)(p13p22),−7,der(9)del(9)(p13)t(9;22)(q34;q11),−19,+3mar[22] 46,XY[3] 15 37,X,−Y,−2,−3,−4,−7,−9,−12,−13,−17[5] 46,XY[13] 16 41,XY,del(3)(p13),−5,−7,−16,−17,−20[12] 46,XY[13] 17 45,XY,−7,add(13)(p10)[17] 46,XY[2] 18 45,XX,−7[8] 46,XX[2] 19 46,X,−Y,add(1)(p36),del(9)(q12),del(7)(q32),−13,−13,add(14)(q32), add(16)(p13.3),−17,+add(22)(q13),+3mar[3] 46,XY[22] 20 46,XX,add(1)(p36),add(5)(q35),del(7)(q11.23),del(8)(q13),del(9)(p13), t(10;?)(p15;?),del(11)(q21),del(12)(p12),−13,add(15)(q26),add(19)(p13.3),+mar[9] 46,XX[41] 21 78,XXX,+X,+1,+2,−3,+4,+5,+6,−7,+8,del(9)(p13),+11,+12,+13,+14,−15,−16,−17,−19,+21,+22,+2mar[19] 22 46,XY,del(3)(q21),del(7)(q31),−9,del(9)(p21),del(12)(p11),add(20)(q13),+mar[25] 23 46,XX,+3,−5,−8,−10,t(14;18)(q32;q21),t(17;?)(p13;?),+2mar,ෂ42dmin[34] 24 46,XXYc,del(7)(q22),t(19;?)(p13;?),−20[19] 47,XXYc[2] 25 45,XY,−7,t(7;?)(q36;?),t(9;22)(q34;q11),del(20)(q13)[5] 46,XY[12] 26 39,XX,−3,−7,−13,−14,−15,−16,−17[18] 35–40,XX,−3,−7,−13,−14,−15,−16,−17,−18, +mar[cp6] 46,XX[1] 27 45,XY,−7,t(9;22)(q34;q11)[25] 28 43–44,XX,add(4)(p16),−5,t(10;11)(p15;q13),del(17)(p11.2),−19,+mar[cp27] 46,XX[6] 29 46,XX,−7,t(9;22)(q34;q11),−22,+2mar[18] 46–50,XX,−7,t(9;22)(q34;q11),−22,+2mar[cp7] 30 46,XX,del(7)(q21)[25] 31 44–46,XX,−5,+mar[cp4] 46,XX[3] tutional Review Board approved the studies at MD Anderson evaluated using cytochemical staining procedures including Cancer Center. Samples were obtained with the informed myeloperoxidase (MPO), terminal deoxynucleotidyl transfer- consent of patients. ase (TdT), non-specific esterase, and periodic-acid schiff The diagnosis was based on morphological analysis of bone (PAS). The diagnostic evaluations were complemented by marrow aspirates and biopsies according to the French–Amer- immunophenotypic and flow cytometric studies. The cut-off ican–British (FAB) guidelines.7 Bone marrow specimens were point for positivity was at 20%.
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