Table 1.
Common resistance mechanisms observed with different chemotherapeutics. Molecular aberrations leading to resistance to the various classes of chemotherapeutics are classified as either influencing drug influx/efflux, metabolism, or mutations of target.
| Drug | Resistance Mechanism | References |
|---|---|---|
| Anti-metabolites | ||
| 5-FU | Aberrant expression of: | [13,15] |
| Gemcitabine |
Thymidylate synthase Thymidine phosphorylase Dihydropyrimide dehydrogenase Human equilibrative nucleoside transporter 1 |
|
| Platins | ||
| Cisplatin | Aberrant expression of: | [23] |
| Carboplatin |
Copper transporter (CTR1) ATPase copper transporting alpha (ATP7A) ATPase copper transporting beta (ATP7B) ATP binding cassette subfamily C member 2 (ABCC2) Excision repair cross-complementing-1 (ERCC1) mutL homolog 1(MLH1) |
|
| Taxanes | ||
| Paclitaxel | Increased P-glycoprotein (P-gp) expression | [58] |
| Docetaxel | Altered microtubule dynamics and binding of drug to target | |
| TKIs | ||
| Gefitinib | Mutations in target | [37,59,60,61] |
| Erlotinib | Induced expression of MET and/or HGF | |
| Sunitinib | Aberrant drug influx/efflux (OCT1 and/or ABCB1) | |