Cediranib resistance pathways research article
Posted: Wed Nov 20, 2013 1:26 pm
Very interesting article became available in full text in the Cancer Research J.
Corresponding Author:
Rakesh K. Jain, Steele Laboratory, COX-734, Massachusetts General Hospital
Glioblastoma Recurrence after Cediranib Therapy in Patients: Lack of “Rebound” Revascularization as Mode of Escape
http://cancerres.aacrjournals.org/conte ... 9.abstract
they were looking into what happens to the Glioblastoma (brain tumor) after it escapes the cediranib treatment, becomes resistant to it and regrows.
They found that cediranib-treated GBMs showed high levels of PDGF-C (platelet-derived growth factor C) and c-Met expression and infiltration by myeloid cells, which may potentially contribute to resistance to anti-VEGF therapy. The treated tumors switch their growth pattern after anti-VEGF therapy—characterized by lower tumor cellularity in the central area, decreased pseudopalisading necrosis, and blood vessels with normal molecular expression and morphology—without a second wave of angiogenesis.
The data for the article is not fresh - it is from Nov. 2010 and I was wondering if there is something new avail. from the same lab by now. Our organization has established ties with the Harvard university and Dana Farber hospital. What if the pathways of resistance are the same regardless of the type of primary and is just caused by the treatment itself so then it would open some possibilities to explore for the ASPS patients who's tumors escaped cediranib such as c-Met or PDGF-C inhibitors (I do not even know if there are any avail. off label)?
Corresponding Author:
Rakesh K. Jain, Steele Laboratory, COX-734, Massachusetts General Hospital
Glioblastoma Recurrence after Cediranib Therapy in Patients: Lack of “Rebound” Revascularization as Mode of Escape
http://cancerres.aacrjournals.org/conte ... 9.abstract
they were looking into what happens to the Glioblastoma (brain tumor) after it escapes the cediranib treatment, becomes resistant to it and regrows.
They found that cediranib-treated GBMs showed high levels of PDGF-C (platelet-derived growth factor C) and c-Met expression and infiltration by myeloid cells, which may potentially contribute to resistance to anti-VEGF therapy. The treated tumors switch their growth pattern after anti-VEGF therapy—characterized by lower tumor cellularity in the central area, decreased pseudopalisading necrosis, and blood vessels with normal molecular expression and morphology—without a second wave of angiogenesis.
The data for the article is not fresh - it is from Nov. 2010 and I was wondering if there is something new avail. from the same lab by now. Our organization has established ties with the Harvard university and Dana Farber hospital. What if the pathways of resistance are the same regardless of the type of primary and is just caused by the treatment itself so then it would open some possibilities to explore for the ASPS patients who's tumors escaped cediranib such as c-Met or PDGF-C inhibitors (I do not even know if there are any avail. off label)?