Resistance Gene | Key Molecular Function | Mechanism of Gene Expression | References |
---|---|---|---|
ABC Transporters (e.g., ABCB1, ABCG2) | Efflux of chemotherapeutic drugs | Overexpression or altered expression due to genetic mutations, epigenetic modifications (e.g., DNA methylation, histone modifications), or transcriptional regulation by signaling pathways (e.g., Notch, Wnt) | |
DNA Repair Genes (e.g., BRCA1, BRCA2, ATM) | Repair of DNA damage caused by chemotherapy or radiation | Overexpression or enhanced activity due to genetic mutations, epigenetic modifications, or transcriptional regulation by signaling pathways (e.g., PI3K/AKT, NF-κB) | |
Anti-Apoptotic Genes (e.g., Bcl-2, Bcl-xL) | Inhibition of apoptosis | Overexpression or altered expression due to genetic mutations, epigenetic modifications, or transcriptional regulation by signaling pathways (e.g., PI3K/AKT, NF-κB) | |
Stem Cell Markers (e.g., CD44, CD133, ALDH1) | Maintenance of stem cell phenotype and self-renewal | Overexpression or altered expression due to genetic mutations, epigenetic modifications, or transcriptional regulation by signaling pathways (e.g., Notch, Wnt, Hedgehog) | |
Epithelial–Mesenchymal Transition (EMT) Markers (e.g., vimentin, N-cadherin, Twist) | Acquisition of migratory and invasive properties | Overexpression or altered expression due to genetic mutations, epigenetic modifications, or transcriptional regulation by signaling pathways (e.g., TGF-β, Wnt, Notch) | |
Metabolic Enzymes (e.g., GLUT1, LDHA) | Altered metabolism to support survival and proliferation under stress conditions | Overexpression or altered expression due to genetic mutations, epigenetic modifications, or transcriptional regulation by signaling pathways (e.g., HIF-1α, MYC) |