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The major subtypes of human B‐cell lymphomas lack mutations in BCL‐2 family member BAD
Author(s) -
Schmitz Roland,
Thomas Roman K.,
Harttrampf Anne C.,
Wickenhauser Claudia,
Schultze Joachim L.,
Hansmann MartinLeo,
Wolf Jürgen,
Küppers Ralf
Publication year - 2006
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.22010
Subject(s) - lymphoma , chronic lymphocytic leukemia , b cell , biology , mantle cell lymphoma , cancer research , pathogenesis , gene , follicular lymphoma , bcl10 , leukemia , genetics , immunology , antibody
Members of the BCL‐2 gene family are well known for their role in the pathogenesis of B‐cell lymphomas in humans and in mouse models. A recent report that knockout mice deficient for the proapoptotic BCL‐2 family member gene BAD frequently develop B‐cell lymphomas prompted us to analyze a large collection of human B‐cell lymphomas for inactivating mutations in the BAD gene. All 3 exons of the BAD gene were amplified and directly sequenced. The 81 lymphomas analyzed included 16 cases of B‐cell chronic lymphocytic leukemia, 11 mantle‐cell lymphomas, 10 follicular lymphomas, 7 MALT lymphomas, 8 Burkitt's lymphoma cell lines, 3 cell lines of multiple myeloma, 15 cases and 4 cell lines of diffuse large B‐cell lymphoma and 7 Hodgkin's lymphoma lines. No mutations were found in any of the cases. We conclude that mutations in the BAD gene do not play a role in the pathogenesis of the major subtypes of human B‐cell lymphomas. © 2006 Wiley‐Liss, Inc.