Acute promyelocytic leukemia is a specific type of acute myeloid leukemia with specific fusion genes and altered chromosomal karyotype. The etiology of primary acute promyelocytic leukemia is unclear and is associated with multiple factors. Secondary cases are commonly seen in patients with tumors treated with chemotherapy and/or radiotherapy, and APL has also been reported to be caused by the application of alkylating agents and topoisomerase II inhibitors. The prognosis of secondary APL is better, with response to therapy and long-term survival similar to that of the primary, but significantly different from chemotherapy-associated AML.
The t(15;17) translocation is seen in the vast majority of patients with acute promyelocytic leukemia, where the vincristine receptor α gene forms a PML-RARα fusion gene with the promyelocytic leukemia (PML) gene on chromosome 15, which encodes a protein with a function different from that of the wild-type vincristine receptor encoded by the normal RARα allele. the RARα gene is located on The RARα gene is located in the 2l region of the long arm of chromosome 17 and functions as a nuclear hormone receptor. In acute promyelocytic leukemia, RARα on chromosome 17 and PML on chromosome 15 translocate to each other, i.e., t(15; 17)(q22; q21) occurs.