Abstract
The pathogenesis of chronic lymphocytic leukemia (CLL) remains incompletely understood.1 Although acquired chromosomal aberrations have been demonstrated to influence CLL biology and clinical behavior, it remains unclear what single gene defects other than p53 or ATM mutations cause or contribute to the CLL phenotype.2 In particular, recurrent gene mutations that are increasingly found in other hematological malignancies have not yet been identified in CLL. One recent CLL gene re-sequencing study reported the analysis of selected exons of 70 tyrosine kinase genes in 95 CLL patients and reported no somatically acquired mutations.3 Given the frequent identification of stereotypical immunoglobulin receptor genes in CLL, it has been suggested that antigen engagement of the B-cell receptor on CLL cells serves a critical role in CLL cell survival and CLL disease etiology. Further, the reduced expression of del(13q)(14)-resident microRNAs has been implicated in early CLL pathogenesis in a subset of cases.4 It is unknown whether CLL is driven by high-frequency recurrent gene mutations in one or a few genes.
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