The rising number of cases of secondary acute myelogenous leukemia and related clonal cytopenias and holoblastic (subacute) myelogenous leukemia (myelodysplastic syndromes) has complemented the advances in the therapy of malignancy. A high-dose acute ionizing radiation exposure, alkylating agents, topoisomerase II inhibitors, possibly other DNA-damaging therapeutic agents, heavy, prolonged cigarette smoking, and high dose-time contact with benzene can cause a rise in the occurrence of acute myelogenous leukemia. Countless major types of chromosome damage can be the cause of acute myelogenous leukemia and myelodysplastic syndromes. A precise break-in chromosome bands 9q34 and 22q11 must take place to result in the causal fusion oncogene (BCR-ABL), which in turn can cause chronic myelogenous leukemia. The researchers revised 11 studies of the chromosomal abnormalities found in presumptive cases of cytotoxic therapy-induced leukemia. They also reviewed 40 studies of the subtypes of leukemia that happen following cytotoxic therapy for other cancers. Yet, they have not found sufficient evidence to suggest an augmented risk for chemically induced BCR-ABL–positive chronic myelogenous leukemia. In addition, they have looked into studies that detail the effects of alkylating agents, topoisomerase inhibitors, and benzene on chromosomes of hematopoietic cells in vitro. Together with the previously mentioned studies, there is no indication that there is any relationship between chemical exposure, injury to chromosome bands 9q34 and 22q11, and an increased risk for BCR-ABL–positive chronic myelogenous leukemia.
Link:theoncologist.onlinelibrary.wiley.com/doi/10.1634/theoncologist.2008-0057
