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Researchers detail possible resistance mechanisms of colorectal cancer to bevacizumab (Avastin)
Date:10/28/2013

ood vessel growth in the absence of VEGF-A, blocked by bevacizumab," Lieu says.

Then the researchers also took a snapshot of levels in 403 colorectal cancer patients, at one time during treatment. Because this group included patients who were and were not being treated with chemotherapy along with bevacizumab, they could show that the rise in VEGF levels was, in fact, due to bevacizumab and not to some interaction with the chemotherapy.

"It's too early to say with certainty that VEGF-C, VEGF-D, and placental growth factor are the cause of colorectal cancer resistance to bevacizumab, but the correlation we saw in this study is compelling," Lieu says.

Current studies are exploring the use of drugs that block more blood-vessel-growth-promoting factors than VEGF-A. For example, Lieu points to the example of aflibercept (Zaltrap), which was given FDA approval in August, 2013 for the treatment of metastatic colorectal cancer, along with the chemotherapy regimen known as FOLFIRI. The drug inhibits placental growth factor along with VEGF-A.

"It's an attractive strategy, and also proof of concept that by targeting not only the primary mechanism of tumor growth but also one or more of these 'workarounds,' this drug or other future drugs could stall growth longer than blocking any one of these growth factors, individually," Lieu says.

Lieu points out that in addition to targeting these additional growth factors, the fact that spikes in VEGF-C and placental growth factor presage tumor progression could give doctors and researchers a clue that bevacizumab has lost its efficacy. Though more work is needed, Lieu can imagine using spikes in VEGF-C or prenatal growth factor to recommend evaluating new treatment options.


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Contact: Garth Sundem
garth.sundem@ucdenver.edu
University of Colorado Denver
Source:Eurekalert

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