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Genomewide array‐based comparative genomic hybridization analysis of acute promyelocytic leukemia
Author(s) -
Karnan Sivasundaram,
Tsuzuki Shinobu,
Kiyoi Hitoshi,
Tagawa Hiroyuki,
Ueda Ryozo,
Seto Masao,
Naoe Tomoki
Publication year - 2006
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.20309
Subject(s) - comparative genomic hybridization , acute promyelocytic leukemia , biology , fusion gene , gene , chromosomal translocation , genetics , promyelocytic leukemia protein , mutation , leukemia , cancer research , copy number variation , microbiology and biotechnology , genome , retinoic acid
Acute promyelocytic leukemia (APL) is typically associated with the t(15;17) that generates the PML–RARA fusion protein. Animal models have shown that although the fusion protein is necessary, it is insufficient for the development of APL, implying that additional mechanisms are responsible for full‐blown leukemia. The mutation of specific genes has been implicated in leukemogenesis; however, alterations in gene copy number have not been well investigated. Here, we applied the genomewide array‐comparative genomic hybridization technique to 30 APL clinical samples and 2 APL cell lines. It was found that (1) approximately half the clinical samples (14 of 30 APL cases) had no detectable chromosomal imbalances; and (2) the remaining 16 cases, including the cell lines, exhibited recurrent chromosomal imbalances, such as loss of 1p36, 2p11, 16p, and 17p, and gain of 8p, 8q, and 13q. These results suggest that chromosomal imbalances are largely absent in APL, although some nonrandom chromosomal imbalances could be linked to the development of APL in a limited number of cases. © 2006 Wiley‐Liss, Inc.