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Clinical Cancer Research 15, 30, January 1, 2009. doi: 10.1158/1078-0432.CCR-08-1808
© 2009 American Association for Cancer Research

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Human Cancer Biology

Array Comparative Genomic Hybridization Analysis of PTCL-U Reveals a Distinct Subgroup with Genetic Alterations Similar to Lymphoma-Type Adult T-Cell Leukemia/Lymphoma

Masao Nakagawa1, Aya Nakagawa-Oshiro1, Sivasundaram Karnan1, Hiroyuki Tagawa1, Atae Utsunomiya4, Shigeo Nakamura2, Ichiro Takeuchi3, Koichi Ohshima5 and Masao Seto1

Authors' Affiliations: 1 Division of Molecular Medicine, Aichi Cancer Center Research Institute; 2 Pathology/Clinical Laboratories, Nagoya University Hospital; 3 Department of Computer Science, Scientific and Engineering Simulation, Nagoya Institute of Technology (Tsukuri-College), Nagoya, Japan; 4 Department of Hematology, Imamura Bun-in Hospital, Kagoshima, Japan; and 5 Department of Pathology, School of Medicine, Kurume University, Kurume, Japan

Requests for reprints: Masao Seto, Division of Molecular Medicine, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya 464-8681, Japan. Phone: 81-52-762-6111, ext. 7080/7082; Fax: 81-52-764-2982; E-mail: mseto{at}aichi-cc.jp.

Purpose: Peripheral T-cell lymphoma, unspecified (PTCL-U) comprises histopathologically and clinically heterogeneous groups. The purpose of this study was to identify subgroups with distinct genetic, histopathologic, and prognostic features.

Experimental Design: We used array comparative genomic hybridization (CGH) for high-resolution analysis of 51 PTCL-U patients and the array data for examining possible correlations of histopathologic and clinical features. Moreover, we compared the genetic, histopathologic, and prognostic features of the PTCL-U cases with those of 59 cases of lymphoma-type adult T-cell leukemia/lymphoma (ATLL).

Results: We identified 32 regions with frequent genomic imbalance, 1 region with high copy number gain at 14q32.2, and 1 region with homozygous loss at 9p21.3. Gains of 7p and 7q and loss of 9p21.3 showed a significant association with poor prognosis. PTCL-U cases with genomic imbalance showed distinct histopathologic and prognostic features compared with such cases without alteration and a marked genetic, histopathologic, and prognostic resemblance to lymphoma-type ATLL.

Conclusions: The array CGH enabled us to identify the frequently altered genomic regions with strong prognostic power among PTCL-U cases. A correlative analysis using the array CGH data disclosed a subgroup in PTCL-U with genomic alterations and with histopathologic and clinical relevance. In addition to histopathologic similarity, the strong genetic and prognostic resemblance between PTCL-U cases with genomic imbalance detected by array CGH and lymphoma-type ATLL seems to support the notion that the former may constitute a distinct PTCL-U subgroup.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2009 by the American Association for Cancer Research.