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Identification of a potential role for POU2AF1 and BTG4 in the deletion of 11q23 in chronic lymphocytic leukemia
Author(s) -
Auer Rebecca L.,
Starczynski Jane,
McElwaine Suzanne,
Bertoni Francesco,
Newland Adrian C.,
Fegan Chris D.,
Cotter Finbarr E.
Publication year - 2005
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.20159
Subject(s) - chronic lymphocytic leukemia , haploinsufficiency , pathogenesis , biology , chromosomal translocation , gene , cancer research , breakpoint , ighv@ , leukemia , genetics , immunology , phenotype
Deletions of 11q in chronic lymphocytic leukemia (CLL) are usually associated with progressive disease and poor prognosis. A novel translocation within the previously identified 11q minimal region has been defined in a patient with CLL. The breakpoint is between genes POU2AF1 and BTG4 . POU2AF1 is a B‐cell‐specific transcriptional coactivator, and BTG4 is a member of the BTG family of negative regulators of the cell cycle, making both of them good candidate genes for the pathogenesis of 11q− CLL. POU2AF1 was observed to be differentially expressed in the cells of patients with CLL compared to its expression in normal B cells in the absence of mutations. This may reflect ongoing stimulation and active accessory signaling in CLL cells. BTG4 could contribute to CLL pathogenesis following inactivation by haploinsufficiency. © 2005 Wiley‐Liss, Inc.