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Dr. Venook on Immunotherapy Potential in Colorectal Cancer

Alan P. Venook, MD
Published: Wednesday, Dec 14, 2016



Alan P. Venook, MD, The Madden Family Distinguished Professor of Medical Oncology and Translational Research at the University of California, San Francisco Helen Diller Family Comprehensive Cancer Center, discusses the potential that immunotherapy may have in the treatment of patients with colorectal cancer (CRC).

Venook describes a subtype of CRC, referred to as subtype 4, which tends to have tumors with heavy lymphocytic infiltrate, and could therefore derive benefit from immunotherapy agents. However, evidence suggests that microsatellite instability (MSI)­–high patients with metastatic disease can benefit from checkpoint inhibitors. Moreover, this is only about 3% to 4% of patients with metastatic disease, says Venook.

In terms of the future that checkpoint inhibitors may have in this treatment landscape, Venook mentions some recent data that suggest the possibility to “fake” cancers out, and make them behave as if they are MSI-high. A randomized study is looking at the combination of a MEK inhibitor plus a checkpoint inhibitor to see whether that treatment could flip the cancer to behave similar to MSI-high, though those results remain to be seen.


Alan P. Venook, MD, The Madden Family Distinguished Professor of Medical Oncology and Translational Research at the University of California, San Francisco Helen Diller Family Comprehensive Cancer Center, discusses the potential that immunotherapy may have in the treatment of patients with colorectal cancer (CRC).

Venook describes a subtype of CRC, referred to as subtype 4, which tends to have tumors with heavy lymphocytic infiltrate, and could therefore derive benefit from immunotherapy agents. However, evidence suggests that microsatellite instability (MSI)­–high patients with metastatic disease can benefit from checkpoint inhibitors. Moreover, this is only about 3% to 4% of patients with metastatic disease, says Venook.

In terms of the future that checkpoint inhibitors may have in this treatment landscape, Venook mentions some recent data that suggest the possibility to “fake” cancers out, and make them behave as if they are MSI-high. A randomized study is looking at the combination of a MEK inhibitor plus a checkpoint inhibitor to see whether that treatment could flip the cancer to behave similar to MSI-high, though those results remain to be seen.



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