The combination of cytogenetic analysis, interphase FISH, and CGH has identified genetic abnormalities in over 80 percent of cases of CLL. The incidence of abnormalities is highest in patients with advanced disease, whereas deletion of chromosome 13q14 is the only consistent abnormality in patients with a stable mild lymphocytosis, a condition analogous to a monoclonal gammopathy of undetermined significance.

Deletions of chromosome 17p and 11q occur mainly in patients with unmutated VH genes and are independent adverse prognostic factors. Deletions of chromosome 13q and trisomy 12 do not have independent prognostic significance, and the apparently poorer survival of patients with trisomy 12 reflects the association between trisomy 12 and unmutated VH genes. Despite intensive study, the genetic consequences of the common cytogenetic deletions and of trisomy 12 in CLL remain unknown. Although translocations involving chromosome 13q14 are common, they are accompanied by large genetic deletions, which complicate their molecular analysis. Translocations involving the immunoglobulin gene loci are rare in CLL and result in overexpression of the BCL2, BCL3, and BCL11 genes.

Concurrently with the investigation of genetic abnormalities, there has been enormous recent progress in elucidating the pathways responsible for apoptosis, cell cycle control, and signal transduction in both normal and malignant B cells. Based on current progress of the human genome sequencing project and of global gene expression analysis, it is reasonable to anticipate that both the key genetic abnormalities and their role in the pathogenesis of CLL will soon be discovered.

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