Review highlights drug resistance mechanisms in breast cancer and acute leukemia, suggesting critical implications for treatment outcomes.
Drug resistance compromises targeted therapy across all types of breast cancer and threatens patient survival through mechanisms such as overexpression of P-gp efflux pumps, reactivation of the Phosphatidylinositol 3-kinase (PI3K) or Mitogen-Activated Protein Kinase (MAPK) signal transduction pathways, epithelial-to-mesenchymal transition (EMT), and changes in the tumor microenvironment. Critical findings described in this review include resistance to Human Epidermal Growth Factor Receptor 2 (HER2) inhibitors due to loss of Phosphatase and Tensin Homolog (PTEN) and PIK3 alterations, resistance to endocrine therapy due to alterations of Estrogen Receptor-1 (ESR1) genes, and recurrence with Cyclin-Dependent Kinase (CDK4/6) or Poly ADP-Ribose Polymerase inhibitors (PARPi) inhibitors due to Retinoblastoma 1 (RB1) mutations. An additional 60% of cases may be predicted to be non-responsive due to the EMT mechanism. This review article presents a research gap in polyclonal drug resistance development, tumor-immune system interactions, and changes in multi-omics data to explore the transition from primary tumor to metastasis.
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Saraswat et al. (2026) studied this question.
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