may increase risk of toxicity cyp2d6 tamoxifen breast cancer patients with deficient cyp2d6 activity are at greater risks of relapse egfr anti-egfr therapy colorectal, lung cancer activation of egfr pathways enhances tumor growth, progression, & resistance to therapy kras anti-egfr therapy colorectal, lung cancer kras mutation is associated with resistance to anti-egfr therapy fcgr3a rituximab non-hodgkin's lymphoma fcrg3a 158val/val genotype may be associated with better response brca1/brca2 platinum breast, ovarian cancer brca1/2-mutated cancers are more sensitive to dna damage. secondary intragenic mutations confer acquired resistance genetic approaches to overcome drug resistance mdr proteins are known to be drug-resistance genes, and are highly expressed in various cancers. inhibition of the mdr genes could result in sensitization of cells to therapeutics and a decrease in antineoplastic resistance. reversin 121 (r121) is a high-affinity peptide for mdr, and use of r121 as a treatment for pancreatic cancer cells results in increased chemosensitivity and decreased proliferation. aberrant nf-κb expression is found in many cancers, and nf-κb has been found to be involved in resistance to platinum-based chemotherapies, such as cisplatin. nf-κb inhibition by genistein in various cancer cell lines (prostate, breast, lung and pancreas) showed increased growth inhibition and an increase in chemosensitivity, seen as an increase in apoptosis induced by therapeutic agents. however, targeting the nf-κb pathway can be difficult, as there can be many off-target and non-specific effects. expression of mutated tp53 causes defects in the apoptotic pathway, allowing cancerous cells to avoid death. re-expression of the wild-type gene in cancer cells in vitro has been shown to inhibit cell proliferation, induce cell cycle arrest and apoptosis. in ovarian cancer, the atp7b gene encodes for a copper efflux transporter, found to be upregulated in cisplatin-resistant cell lines and tumors. development of antisense deoxynucleotides against atp7b mrna and treatment of an ovarian cancer cell line shows that inhibition of atp7b increases sensitivity of the cells to cisplatin.