Molecular biology of chronic lymphocytic leukemia.
Chronic lymphocytic leukemia (CLL) represents the quintessential example of a human malignancy which is caused principally by defects that prevent cell turnover due to programmed cell death (PCD) rather than by alternations in cell cycle regulation. In the vast majority of patients, CLL cells are predominantly G0 quiescent cells that gradually accumulate in the patient's body, not because they are dividing more rapidly than normal, but because they are surviving too long. As such, the genetics of CLL seem likely to teach us much about the molecular mechanisms that regulate PCD. Moreover, since defects in the pathway for PCD can render neoplastic cells resistant to the cytotoxic effects of chemotherapeutic drugs and radiation, investigations of the molecular biology of CLL may also prove informative for gaining a better understanding of drug- and radiation-resistance mechanisms. In this article, I review some of the current knowledge about the molecular biology of CLL with a particular emphasis on cytogenetic abnormalities associated with these leukemias and the role of deregulated cell death in the pathogenesis of these neoplastic disorders of mature B and occasionally T lymphocytes.
Reed
J C
JC
Burnham Institute, La Jolla, CA 92037, USA.
D017209:Apoptosis; D002869:Chromosome Aberrations; D019940:Genes, bcl-1; D019254:Genes, bcl-2; D016158:Genes, p53; D006801:Humans; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology