There exist some cancer stem cells, which help cancer cells avoid being destroied completely by drugs, further it seems that cancer cells become drug resistance.

Dear Dipon DAS,

Different mechanisms have been described: perhaps the oldest and well known is activation of MDR genes in some cancer cells (multi-drug resistance) , that increase synthesis of a membran protein that accelarates the exit of drug by cells.

But specialist could described us the different mechanisms actually known ?

Regards

Didier JAMBOU

There exist some cancer stem cells, which help cancer cells avoid being destroied completely by drugs, further it seems that cancer cells become drug resistance.

I agree with Dr Jambou that the MDR efflux pump is a very common mechanism of drug resistance in cancer and a very important one so my comments here are restricted to genotoxic drugs ,-antifolates like methotrexate and halogenated pyrimidines like 5-FU. Very old drugs but still used as frontline agents. In many cases resistance to these two classes of chemotherapeutic drugs is mediated by amplification of the target gene ie in this case dihydrofolate reductase (dhfr) and thymidylate sythetase (tyms) respectively. Increased enzyme levels of the target gene product then mediate drug resistance. One of the problems with these drugs that negatively affect clinical outcomes is that they are clastogenic (chromosome breaking) they tend to induce resistance to themselves by causing the formation of dicentric chromosomes, extra-chromosomal elements like circular episomes and large palindromes. All of these structures are common in cancer cells and are well-known vehicles of gene amplification.