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Blood, 1 June 2006, Vol. 107, No. 11, pp. 4500-4507.
Prepublished online as a Blood First Edition Paper on February 16, 2006; DOI 10.1182/blood-2005-09-3801.
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Submitted September 22, 2005
Accepted January 10, 2006
Identification of subtype-specific genomic alterations in aggressive adult T-cell leukemia/lymphoma
Aya Oshiro, Hiroyuki Tagawa, Koichi Ohshima, Kennosuke Karube, Naokuni Uike, Yukie Tashiro, Atae Utsunomiya, Masato Masuda, Nobuyuki Takasu, Shigeo Nakamura, Yasuo Morishima, and Masao Seto*
Division of Molecular Medicine, Aichi Cancer Center Institute, Nagoya, Aichi, Japan; Second Department of Internal Medicine, University Hospital of the Ryukyus, Nishihara, Okinawa, Japan
Division of Molecular Medicine, Aichi Cancer Center Institute, Nagoya, Aichi, Japan
Department of Pathology, Kurume University School of Medicine, Kurume, Fukuoka, Japan
Department of Hematology, National Kyushu Cancer Center, Fukuoka, Japan
Department of Pathology, Imakiire General Hospital, Kagoshima, Japan
Department of Hematology, Imamura Bun-in Hospital, Kagoshima, Japan
Second Department of Internal Medicine, University Hospital of the Ryukyus, Nishihara, Okinawa, Japan
Pathology/Clinical Laboratories, Nagoya University Hospital, Nagoya, Aichi, Japan
Division of Hematology and Cell Therapy, Aichi Cancer Center Hospital, Nagoya, Aichi, Japan
* Corresponding author; email: mseto{at}aichi-cc.jp.
Aggressive adult T-cell leukemia/lymphoma (ATLL) such as acute and lymphoma types are fatal diseases with poor prognosis. Although these two subtypes feature different clinicopathological characteristics, no detailed comparative analyses of genomic/genetic alterations have been reported. We performed array-based comparative genomic hybridization for 17 acute and 49 lymphoma cases as well as real-time quantitative PCR to identify the target genes of recurrently amplified regions. Comparison of the genome profiles of acute and lymphoma types revealed that the lymphoma type had significantly more frequent gains at 1q, 2p, 4q, 7p and 7q, and losses of 10p, 13q, 16q and 18p, whereas the acute type showed a gain of 3/3p. Of the recurrent high-level amplifications found at 1p36, 6p25, 7p22, 7q and 14q32 in the lymphoma type, we were able to demonstrate that CARMA1 is a possible target gene of the 7p22 amplification for the lymphoma type but not for the acute type. Furthermore, we found BCL11B overexpression in acute type irrespective of the 14q32 gain/amplification, while no or low expression of the gene in the lymphoma type. These results suggest that acute and lymphoma types are genomically distinct subtypes, and thus may develop tumors via distinct genetic pathways.
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