Dear Professor Joachim Pimiskern

really, you gave a nice web link to download the papers.

Thankyou very much.

Thanks Joachim and William, appreciate that.

ABC B1 transporter and MRP-5 transporter are pesponsible most frequently for the gemcitabine resistance of pancreatic cancer. CD44 pos cells have important role in gemcitabine resistance as well. Joseph Molnar

Couldn't agree more. We published on this - see attachments

Here come the pdf

Thanks Mr. Joseph Molnar will surely look into CD44+ cells i was thinking of targeting MDR (as u you and Mr. Matthias said MRP5 & may be MDR1) genes using SiRNA for decreasing gemcitabine efflux.

Mr. Matthias Löhr thank you for your kind link i went through it and found it very interesting and informative. Appreciate your help.

This paper is a little old, but it discusses how gemcitabine works and mechanisms of resistance.

http://www.sciencedirect.com/science/article/pii/S136876460200002X

Actually our research does not give any evidence that gemcitabine is a substrate for any of the ABC pumps. Actually we showed that MDR cells are more sensitive to gemcitabine (Bergman BJC 2003). A paper (submitted) shows no that evidence that MRP4 and MRP5 use gemcitabine or gemcitabine monophosphate are substrates. Only ara-CMP is. An update of the 2002 review is added.

here the BJC paper

And another with similar evidence

Thank you all for the kind help! Actually i was considering ABC transporters & gemcitabine resistance for PhD research and was wondering what points should i consider while writing hypothesis (keeping molecular biology background)?

Resistance is not only made up by the tumor cell itself but its microenvironment. There are several papers out there describing this desmoplasia and that "breaching the stromal fortress" is the name of the game

With verapamil we have shown an increased sensitivity to gemcitabine! See the Bergman paper.