Identification of a potential role for POU2AF1 and BTG4 in the deletion of 11q23 in chronic lymphocytic leukemia

• Published in: Genes chromosomes & cancer 2005-05, Vol.43 (1), p.1-10
• Main Authors: Auer, Rebecca L., Starczynski, Jane, McElwaine, Suzanne, Bertoni, Francesco, Newland, Adrian C., Fegan, Chris D., Cotter, Finbarr E.
• Format: Article
• Language: English
• Subjects: Base Sequence; Cell Cycle Proteins - genetics; Chromosome Deletion; Chromosome Mapping; Chromosomes, Human, Pair 11; Cloning, Molecular; Consensus Sequence; DNA Primers; DNA, Neoplasm - blood; DNA, Neoplasm - genetics; DNA, Neoplasm - isolation & purification; DNA-Binding Proteins - genetics; Humans; Immunoglobulin Heavy Chains - genetics; Molecular Sequence Data; Octamer Transcription Factor-1; Polymerase Chain Reaction; Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics; RNA, Messenger - genetics; Transcription Factors - genetics
• ISSN: 1045-2257; 1098-2264
• DOI: 10.1002/gcc.20159

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.