Secondary chromosomal changes in 34 Philadelphia-chromosome-positive chronic myelocytic leukemia patients from the Mexican West

被引:4
作者
Espinoza, JPM
Cárdenas, VJP
Gutiérrez-Angulo, M
García, JRG
机构
[1] Inst Mexicano Seguro Social, CIBO, Ctr Med Nacl Occidente, Lab Citogenet,Div Genet, Guadalajara, Jalisco, Mexico
[2] Univ Guadalajara, Doctorado Genet Humana, Guadalajara, Jalisco, Mexico
关键词
D O I
10.1016/S0165-4608(03)00283-8
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The clonal evolution in t(9;22)-positive chronic myelocytic leukemia (CML) is well established. Four major changes occur in more than 70% of patients: +8, i(17q), +19, and an extra Philadelphia chromosome. The frequencies of secondary chromosomal changes in 34 patients from the states of Jalisco, Nayarit, Michoacan, and Colima (the Mexican West) with Philadelphia-chromosome-positive CML were assessed. The most frequent abnormalities were tetraploidy (12 cases); +8, inv(3)(q21q26), and octoploidy (3 cases each); and +der(22)(2 cases). Some translocations not previously associated with CML were observed, such as t(2;7)(p12;q36), t(3;6)(q26;p25), t(3;17)(q26;p13), and t(6;17)(q21;q23similar toq25). Significant differences were found for +8 with respect to population results from Japan and from southern, eastern, and western Europe; for i(17)(q10) from eastern Europe; for +19 from Japan and western Europe; and for +der(22) from Japan, southern Europe, and western Europe. Although polyploidy could result from endomitosis, there is no direct evidence that the BCR/ABL protein influences such a process; however, protein kinases such as MAPK, which are involved in endomitosis, are activated by the BCR/ABL protein, and so the BCRIABL protein could promote endomitosis through the MAPK pathway. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:166 / 169
页数:4
相关论文
共 39 条
[1]  
ALIMENA G, 1982, SCAND J HAEMATOL, V28, P103
[2]   Multicolor COBRA-FISH analysis of chronic myeloid leukemia reveals novel cryptic balanced translocations during disease progression [J].
Barbouti, A ;
Johansson, B ;
Höglund, M ;
Mauritzson, N ;
Strömbeck, B ;
Nilsson, PG ;
Tanke, HJ ;
Hagemeijer, A ;
Mitelman, F ;
Fioretos, T .
GENES CHROMOSOMES & CANCER, 2002, 35 (02) :127-137
[3]   Regulation of CDC6, geminin, and CDT1 in human cells that undergo polyploidization [J].
Bermejo, R ;
Vilaboa, N ;
Calés, C .
MOLECULAR BIOLOGY OF THE CELL, 2002, 13 (11) :3989-4000
[4]  
BERNSTEIN R, 1988, SEMIN HEMATOL, V25, P20
[5]   KARYOTYPE ANALYSIS IN ACUTE NONLYMPHOCYTIC LEUKEMIA (ANLL) - COMPARISON WITH ETHNIC-GROUP, AGE, MORPHOLOGY, AND SURVIVAL [J].
BERNSTEIN, R ;
PINTO, MR ;
MORCOM, G ;
MACDOUGALL, LG ;
BEZWODA, W ;
DUKES, I ;
PENFOLD, G ;
MENDELOW, B .
CANCER GENETICS AND CYTOGENETICS, 1982, 6 (03) :187-199
[6]   The Bcr-Abl tyrosine kinase activates mitogenic signaling pathways and stimulates G1-to-S phase transition in hematopoietic cells [J].
Cortez, D ;
Reuther, G ;
Pendergast, AM .
ONCOGENE, 1997, 15 (19) :2333-2342
[7]  
Drexler HG, 1999, LEUKEMIA RES, V23, P207
[8]   Endoreplication cell cycles: More for less [J].
Edgar, BA ;
Orr-Weaver, TL .
CELL, 2001, 105 (03) :297-306
[9]   Mechanisms of disease - The biology of chronic myeloid leukemia [J].
Faderl, S ;
Talpaz, M ;
Estrov, Z ;
O'Brien, S ;
Kurzrock, R ;
Kantarjian, HM .
NEW ENGLAND JOURNAL OF MEDICINE, 1999, 341 (03) :164-172
[10]   Secondary leukemias induced by topoisomerase-targeted drugs [J].
Felix, CA .
BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION, 1998, 1400 (1-3) :233-255