Genetic Variants Involved in Intracellular Mechanisms of Chemoresistance to Anticancer Drugs Due to Changes in the Effect on Their Molecular Targets

摘要: Modern anticancer pharmacological treatment is challenged by the important limitation of refractoriness many tumours to drugs. This due different combinations a complex and yet poorly understood variety mechanisms chemoresistance, which account for reduction in intracellular concentrations active agents or poor response their action. The present article focusses on changes expression appearance genetic variants affecting genes involved weaker activity agents, may be accounted by: (1) molecular targets these drugs, either directly reducing enhancing target modifying its ability respond drug; (2) enhanced repair drug-induced deoxyribonucleic acid damage; finally, because activation apoptosis final goal regimes; (3) stimulation antiapoptotic and/or inhibition proapoptotic ones. Key Concepts: Changes levels strongly determine efficacy drugs. Chemoresistance accounting drugs. Antitumour whose mechanism action based DNA damage, are less efficient tumour cells with DNA-repairing activity. The presence an impaired function favour chemoresistance. The constitutive survival pathways reduces drugs. Keywords: apoptosis; anticancer drug; cancer; mutation; pharmacology; refractoriness; SNP