Therapy-Related Acute Myeloid Leukemia with KMT2A-SNX9 gene fusion associated with a hyperdiploid karyotype after Hemophagocytic Lymphohistiocytosis

Therapy-related acute myeloid leukemia (t-AML) following treatment with topoisomerase-II (topo-II) inhibitors has been increasingly reported and accounts for about 6.8% of AML [1]. The t-AML is a causal effect of somatic alterations after cytotoxic chemotherapy and/or radiotherapy, or even exposure to agents, such as anthracyclines and topo-II inhibitors (e.g. epipodophyllotoxins). Etoposide – a podophyllotoxin derivative – induces DNA strand breaks by inhibiting the action of topo-II and it is used in combination with other chemotherapeutic agents as first-line treatment of a variety of malignancies as well as in hemophagocytic lymphohistiocytosis (HLH).
Source: Cancer Genetics and Cytogenetics - Category: Genetics & Stem Cells Authors: Tags: Short Communication Source Type: research