R Center, Department of Oncology, Shanghai Medical College, Fudan University t, Shanghai NVP-BVU972 c-Met Inhibitors 200 032, PR China. 2Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhangjiang Hi Tech Park, Shanghai 201 203, PR China. Authors, Posts GE XZ, SC, CZ, FL, and led the study in the clinical observation and monitoring, KJ, YZ, HG and collected the clinical data for analysis. CL performed KY, FW pharmacokinetic evaluations. JQ coordinated the presentation JL was responsible for the overall development and project design to data interpretation and editing of the manuscript. All authors read and approved the final manuscript. The competing interests of potential conflicts of interest were to Jin Li The other authors report explained Ren, no conflict of interest.
Re U: 16 April 2010 Abstract: 5 October 2010 Ver published on: 5th Health in October 2010. Multiple drug resistance in cancer cells resistant to the cytotoxic effects produced many drugs that are not related structurally and mechanistically, to those antioneoplastic significantly reduced the effectiveness of chemotherapy for cancer. The h Most frequent cause of MDR results from the overexpression Saracatinib SRC inhibitor of cell membrane bound ATP-binding cassette transporters, which actively extrude a variety of chemotherapeutic drugs on cancer cells, thereby easing their cytotoxic effects. Forty-eight ABC proteins Were identified in the human genome and are divided into seven subfamilies on sequence similarities. The subfamily of ABC transporters member B 1, C-subfamily, and a member of the subfamily play G member 2 is an R Important role in the production of MDR in tumor cells.
ABCB1 was found resistant Chinese hamster ovary cells. A variety of antineoplastic drugs such as anthracyclines, vinca alkaloids and taxanes, and epipodophyllotoxins that. ABCG2 was independently Identified ngig of cells c Cancinoma lon, placenta, and a drug selected hlt Human cell line of breast cancer MCF-7. Including ABCG2 can actively efflux a variety of antineoplastic drugs Lich mitoxantrone, indolocarbazole, anthracyclines and topoisomerase I inhbitors and fluorescent dyes such as Hoechst 33342. The side population cells Ph Phenotype in various tumor types, and they express more ABCG2, the inh Pensions products drug resistance. Currently, ABCG2 is considered as a molecular marker of SP cells.
Sun Targeting ABCG2 in these tumor stem cells represents a promising and innovative strategy, the entire Bev Lkerung to eliminate cancer cells. Tyrosine kinase inhibitors, a relatively new class of anti-neoplastic are suspected Ood on their mechanism of action by competing with ATP for the ATP-binding site of the catalytic domain Ne of multiple oncogenic tyrosine kinase exercise. Subsequently End can reduce the downstream TKI Rtigen signaling pathways involved in cancer proliferation, invasion, metastasis and angiogenesis are involved. Previously it was reported that the BCR Abl TKIs nilotinib and imatinib by ABCB1 and ABCG2 transporter and to inhibit significantly interact with their shipments. In addition, epidermal growth factor receptor TKI, gefitinib, erlotinib, VEGFR-TKI vandetanib, and the multi-kinase ITK sunitinib has been shown that significant attenuator Tion or reversal of the ABC transporters mediate MDR in cancer cells. Thus, it is m Possible that TKIs are used as MD nnten k