As advances in diagnosis and therapy have improved survival for breast cancer and gynecologic cancer, therapy-related myeloid neoplasms (t-MN) become one of the worst long-term consequences of previous therapy for female-specific cancer. T-MN is characterized by greater biological complexity than de novo disease; the main risk factors involved in t-MN pathogenesis can be subgrouped into patient-specific, inherited, and acquired predispositions. Existing literature and clinical reports consistently indicate that its pathogenesis results from the combined effects of multiple factors, including prior treatment exposure, germline mutations, somatic mutations, clonal hematopoiesis, molecular methylation, and alterations in the bone marrow microenvironment. Increased adverse cytogenetic burden in t-MN may correlate with poorer treatment efficacy and shortened survival. The standard 7+3 regimen, CPX-351, and allogeneic hematopoietic stem cell transplantation are primary therapeutic modalities with measurable but limited efficacy, which highlights the urgency of prospective monitoring aimed at reducing the incidence of t-MN. We underscore practical implications for genetic testing for female-specific cancer patients, individualizing regimens and balancing expected benefit against t-MN risk, and propose female-focused prevention strategies, including early risk recognition, tailored treatment intensity, and strengthened longitudinal surveillance.
Qin et al. (Thu,) studied this question.