Most cases of leukemia are sporadic with no identifiable cause. Certainly, exposure to ionizing radiation and other carcinogens such as certain chemotherapeutic agents can be implicated in some cases. Many recurring genetic lesions have been described that result in the disruption of normal regulatory pathways. Autonomous proliferation may occur as a result of activating mutations. Increased self-renewal, loss of cell-cycle control, escape from apoptosis, and a block of cellular differentiation have all been reported (8). Acute promyelocytic leukemia (AML M3), which frequently presents with a low white blood cell (WBC) count and evidence, either laboratory, clinical, or both, of disseminated intravascular coagulation (DIC), is associated with the t(15;17) in most cases. The resulting fusion transcript promyelocytic leukemia-retioic acid receptor alpha (PML-RARa) predicts responsiveness to all-trans retinoic acid (ATRA), which has been used along with chemotherapy to manage this disorder successfully.

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