A copy of this work was available on the public web and has been preserved in the Wayback Machine. The capture dates from 2019; you can also visit the original URL.
The file type is
HGF/c-Met Acts as an Alternative Angiogenic Pathway in Sunitinib-Resistant Tumors
Molecular and cellular mechanisms underlying resistance/low responsiveness to antiangiogenic compounds are under extensive investigations. Both populations of tumor and stroma (nontumor compartment) seem to contribute in inherent/acquired resistance to antiangiogenic therapy. Here, investigating in vivo efficacy of sunitinib in experimental models resulted in the identification of tumors that were resistant/ sensitive to the therapy. Analysis of tumor protein lysates indicated a greaterdoi:10.1158/0008-5472.can-10-0489 pmid:20952508 fatcat:o7y7dry235fdlinhakb7srhfbi