Medical Research: What are the main findings of the study?
Dr. Brinckerhoff: The genetic mutation BRAFV600E , frequently found in metastatic melanoma, not only secretes a protein that promotes the growth of melanoma tumor cells, but can also modify the network of normal cells around the tumor to support the disease’s progression. Targeting this mutation with Vemurafenib reduces this interaction, and suggests possible new treatment options for melanoma therapy.
Medical Research: What should clinicians and patients take away from your report?
Dr. Brinckerhoff: This work supports the importance of the tumor cells “talking” with the normal cells present in the tumor microenvironment. Targeting the tumor cells with specific therapy to reduce the secreted proteins can reduce the aggressive behavior of the tumor and inhibit disease progression.
Medical Research: What recommendations do you have for future research as a result of this study?
Dr. Brinckerhoff: Given that the data show that Vemurafenib is able to reduce the expression of several proteins that are essential for activating the tumor microenvironment (TME), a next step would be to ask whether Vemurafenib normalizes the tumor microenvironment , or keeps it from becoming activated, and if so, does it create a window of time where we could target the tumor microenvironment , normalize it, and enhance the patient’s therapeutic response.
BRAFV600E melanoma cells secrete factors that activate stromal fibroblasts and enhance tumourigenicity
C A Whipple and C E Brinckerhoff
British Journal of Cancer , (12 August 2014) | doi:10.1038/bjc.2014.452