Acute promyelocytic leukemia pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Acute promyelocytic leukemia is characterized by chromosomal translocation involving the retinoic acid receptor-alpha gene on chromosome 17 (''RARα''). In 95% of cases of APL, retinoic acid receptor-alpha (''RARα'') gene on chromosome 17 is involved in a reciprocal translocation with the promyelocytic leukemia gene (''PML'') on chromosome 15, a translocation denoted as t(15;17)(q22;q12). | Acute promyelocytic leukemia is characterized by chromosomal translocation involving the retinoic acid receptor-alpha gene on chromosome 17 (''RARα''). In 95% of cases of APL, retinoic acid receptor-alpha (''RARα'') gene on chromosome 17 is involved in a reciprocal translocation with the promyelocytic leukemia gene (''PML'') on chromosome 15, a translocation denoted as t(15;17)(q22;q12). | ||
Revision as of 20:51, 13 August 2015
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
Acute promyelocytic leukemia is characterized by chromosomal translocation involving the retinoic acid receptor-alpha gene on chromosome 17 (RARα). In 95% of cases of APL, retinoic acid receptor-alpha (RARα) gene on chromosome 17 is involved in a reciprocal translocation with the promyelocytic leukemia gene (PML) on chromosome 15, a translocation denoted as t(15;17)(q22;q12).
Four other gene rearrangements have been described in APL fusing RARα to promyelocytic leukemia zinc finger (PLZF), nucleophosmin (NPM), nuclear matrix associated (NUMA), or signal transducer and activator of transcription 5b (STAT5B) genes.
The resultant fusion proteins disrupt the function of RARα which blocks the normal maturation of granulocytes. Although the chromosomal translocation involving RARα is believed to be the initiating event, additional mutations are required for the development of leukemia.