A new complex translocation (15;20;17)(q22;p13;q21) in acute promyelocytic leukemia

被引：21
作者：
Yamamoto, K
Hamaguchi, H
Nagata, K
Kobayashi, M
Takashima, T
Taniwaki, M
机构：
[1] Musashino Red Cross Hosp, Dept Hematol, Tokyo 180, Japan
[2] SRL Inc, Tokyo, Japan
[3] Kyoto Prefectural Univ Med, Dept Internal Med 3, Kyoto 602, Japan
来源：
CANCER GENETICS AND CYTOGENETICS | 1998年 / 101卷 / 02期
关键词：
D O I：
10.1016/S0165-4608(97)00251-3
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
We describe here a 39-year-old male with acute promyelocytic leukemia (APL) carrying a new complex translocation (15;20;17). A chromosomal analysis of the bone marrow cells showed 46,XI: t(15;20;17)(q22;p13;q21). Fluorescence in situ hybridization (FISH) analysis using plasmid DNA libraries of chromosomes 15, 17, and 20 revealed three derivative chromosomes, der(15)t(15;17), der(17)t(17;20), and der(20)t(15;20). Fluorescence in situ hybridization with cosmid DNA probes flanking the breakpoints of t(15;17) did not show the retinoic acid receptor alpha (RAR alpha)/PML fusion signal usually generated on the der(17)t(15;17). However, rearrangement of the RAR alpha gene and expression of the PML/RAR alpha chimeric transcript were identified by Southern blot and reverse-transcriptase polymerase chain reaction (RT-PCR) analyses, respectively. Our results confirmed that the PML/RAR alpha gene on the der(15)t(15;17), not the RAR alpha/PML gene, must be essential to leukemogenesis In APL. Furthermore, considering another reported case with a 20p13 aberration, it is possible that 20p13 is a nonrandom breakpoint in APL with a complex translocation. (C) Elsevier Science Inc., 1998.
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页码：89 / 94
页数：6
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