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.
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页码:166 / 169
页数:4
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