AI Article Synopsis
- Acute myeloid leukemia (AML) consists of various types that arise from the uncontrolled growth of myeloid precursor cells in the bone marrow.
- Most cases of AML develop spontaneously due to somatic mutations, but some can occur as a secondary cancer after chemotherapy treatment.
- The presented case involves therapy-related AML (t-AML) linked to prior chemotherapy, showcasing a notable genetic change with a balanced translocation at 11q23, which may explain how the cancer developed.
Article Abstract
Acute myeloid leukemia (AML) is a group of diseases resulting from a clonal expansion of myeloid precursor cells in the bone marrow. Each subtype harbors characteristic clinical, morphologic, and molecular features. AML is most often de novo and arises from somatic mutations causing unchecked proliferation of myeloblasts, but it may also present as a secondary malignancy, often as the result of prior cytotoxic exposure. Here we present a case of therapy-related AML (t-AML) following chemotherapy exposure found to have a characteristic balanced translocation involving 11q23 and outline a potential mechanism of oncogenesis.
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