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t(1;3)(p36;p21) is a recurring therapy‐related translocation
Author(s) -
Sato Yuko,
Izumi Tohru,
Kanamori Hirakazu,
Davis Elizabeth M.,
Miura Yasusada,
Larson Richard A.,
Le Beau Michelle M.,
Ozawa Keiya,
Rowley Janet D.
Publication year - 2002
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.10055
Subject(s) - chromosomal translocation , cosmid , breakpoint , karyotype , leukemia , biology , chronic myelogenous leukemia , cytogenetics , chemotherapy , medicine , chromosome , cancer research , genetics , dna , gene
Chromosome bands 1p36 and 3p21 are known to be recurring breakpoints in therapy‐related (t‐) leukemia. We identified a recurring translocation, t(1;3)(p36;p21), in eight patients with various hematologic malignancies: three patients with ALL, one with chronic myelogenous leukemia (CML) in accelerated phase (AP), two with MDS, and two with AML(M3). Five of the eight patients had a history of chemotherapy, including alkylating agents in three, before the translocation was detected. In two of these five patients, the t(1;3)(p36;p21) emerged only at relapse or in the accelerated phase of CML. The karyotypes of the patients were complex, including −7 and structural abnormalities of 5q, 6q, 7q, 9p, and 11q23. Survival time varied among patients (25 days to more than 16 years). Using FISH with 13 1p35–36 cosmid probes (tel—FB12–CA5–G7–FD2–CB1–ED8–FD9–G32–AE3–G50–AD8–GG4–G43—cen), we delineated the 1p36 breakpoint in two patients with MDS and ALL as lying between FB12 and FD2 (between BAC47P3 and PAC963K15), with a small deletion near the breakpoint in both cases. In the patient with MDS, there was also a deletion at 3p21.3, as detected with the cosmid probe cosNRL9. The results of the present study suggest that t(1;3)(p36;p21) in hematologic diseases is associated with prior exposure to mutagens, including alkylating agents. © 2002 Wiley‐Liss, Inc.