A complex translocation (9;22;16)(q34;q11.2;p13) in chronic myelocytic leukemia

被引:9
作者
Espinoza, JPM
Cárdenas, VJP
Jiménez, EAV
Angulo, MG
Flores, MAE
García, JRG
机构
[1] Inst Mexicano Seguro Social, Ctr Invest Biomed Occidente, Div Genet, Guadalajara, Jalisco, Mexico
[2] Univ Guadalajara, Doctorado Genet Humana, Guadalajara, Spain
[3] Inst Mexicano Seguro Social, Ctr Med Nacl Occiente, Hosp Pediat, Dept Hematol, Guadalajara, Jalisco, Mexico
关键词
D O I
10.1016/j.cancergencyto.2004.08.009
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The t(9;22) is present in almost all cases with chronic myelocytic leukemia (CML). Around 5% of these patients show complex translocations involving a third chromosome in addition to chromosomes 9 and 22. All chromosomes have participated in these variants and the BCR-ABL1 hybrid gene is always present. We describe a CML case with a new complex t(9;22;16)(q34;q11.2;p13). Seven months after imatinib treatment a karyotype showed the appearance of a clone with a standard t(9;22) in addition to the clone with the complex translocation. The b3a2 transcript of BCR-ABL1 was detected both at diagnosis and 7 months after therapy. In CML, both complex translocations and standard translocations have the same prognosis. However, these complex variants could contribute to the tumoral evolution by conferring selective advantages that, in turn, cause the preferential manifestation at diagnosis of clones with complex translocations. (C) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:175 / 177
页数:3
相关论文
共 24 条
[1]   THE CHRONIC MYELOGENOUS LEUKEMIA SPECIFIC P210-PROTEIN IS THE PRODUCT OF THE BCR/ABL HYBRID GENE [J].
BEN-NERIAH, Y ;
DALEY, GQ ;
MESMASSON, AM ;
WITTE, ON ;
BALTIMORE, D .
SCIENCE, 1986, 233 (4760) :212-214
[2]   THE INCIDENCE, TYPE, AND SUBSEQUENT EVOLUTION OF 14 VARIANT PH1 TRANSLOCATIONS IN 180 SOUTH-AFRICAN PATIENTS WITH PH1-POSITIVE CHRONIC MYELOID-LEUKEMIA [J].
BERNSTEIN, R ;
PINTO, MR ;
WALLACE, C ;
PENFOLD, G ;
MENDELOW, B .
CANCER GENETICS AND CYTOGENETICS, 1984, 12 (03) :225-238
[3]   COMPLEX TRANSLOCATIONS OF THE PH CHROMOSOME AND PH NEGATIVE CML ARISE FROM SIMILAR MECHANISMS, AS EVIDENCED BY FISH ANALYSIS [J].
CALABRESE, G ;
STUPPIA, L ;
FRANCHI, PG ;
PEILA, R ;
MORIZIO, E ;
LIBERATI, AM ;
SPADANO, A ;
DILORENZO, R ;
DONTI, E ;
ANTONUCCI, A ;
PALKA, G .
CANCER GENETICS AND CYTOGENETICS, 1994, 78 (02) :153-159
[4]  
CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1016/0003-2697(87)90021-2
[5]  
DOW LW, 1991, CANCER-AM CANCER SOC, V68, P1678, DOI 10.1002/1097-0142(19911015)68:8<1678::AID-CNCR2820680803>3.0.CO
[6]  
2-J
[7]   LOCATION OF BREAKPOINTS WITHIN THE MAJOR BREAKPOINT CLUSTER REGION (BCR) IN 33 PATIENTS WITH BCR REARRANGEMENT-POSITIVE CHRONIC MYELOID-LEUKEMIA (CML) WITH COMPLEX OR ABSENT PHILADELPHIA CHROMOSOMES [J].
DUBE, I ;
DIXON, J ;
BECKETT, T ;
GROSSMAN, A ;
WEINSTEIN, M ;
BENN, P ;
MCKEITHAN, T ;
NORMAN, C ;
PINKERTON, P .
GENES CHROMOSOMES & CANCER, 1989, 1 (01) :106-111
[8]   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
[9]   IS THE CHROMOSOMAL REGION 9Q34 ALWAYS INVOLVED IN VARIANTS OF THE PH1 TRANSLOCATION [J].
HAGEMEIJER, A ;
BARTRAM, CR ;
SMIT, EME ;
VANAGTHOVEN, AJ ;
BOOTSMA, D .
CANCER GENETICS AND CYTOGENETICS, 1984, 13 (01) :1-16
[10]   LOCALIZATION OF THE C-ABL ONCOGENE ADJACENT TO A TRANSLOCATION BREAK POINT IN CHRONIC MYELOCYTIC-LEUKEMIA [J].
HEISTERKAMP, N ;
STEPHENSON, JR ;
GROFFEN, J ;
HANSEN, PF ;
DEKLEIN, A ;
BARTRAM, CR ;
GROSVELD, G .
NATURE, 1983, 306 (5940) :239-242