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Friday, Mar. 17, 2017, 8:00 AM
by Meredith Jackson
In a new study published in the journal Oncogene, Dana Hardbower, Ph.D., Keith Wilson, M.D., and colleagues demonstrated that epidermal growth factor receptor (EGFR) signaling in macrophages is associated with increased colitis-associated colon cancer development.
While inflammatory bowel disease and colitis can increase risk of colon cancer, the mechanisms behind this connection are poorly understood.
The current study showed that in models of colitis-associated cancer, EGFR was highly activated (phosphorylated) in macrophages. When the researchers specifically deleted the EGFR gene in myeloid cells, they were able to reduce colitis and additionally decrease tumor burden in mice.
They also found that upon deleting EGFR, they were able to decrease the signals that normally increase blood vessel growth around tumors, indicating a potential mechanism for the decreased tumor burden.
These findings indicate that phosphorylated EGFR could be used as a biomarker for potential cancer development in colitis or a potential target for therapies preventing cancer development for patients with inflammatory bowel disease.
This research was funded by grants from the National Institutes of Health (DK053620, AT004821, CA190612, CA116087, CA028842), a Veterans Affairs Merit Review grant, the Thomas F. Frist Sr. Endowment, and the Vanderbilt Center for Mucosal Inflammation and Cancer.
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Health and Medicine, Reporter, Research Aliquots, colorectal cancer, Department of Medicine, Department of Veterans Affairs, EGF, EGFR, Epidermal growth factor, Keith Wilson, NCCIH, NCI, NIDDK, NIH, Oncogene, Reporter March 17 2017, Vanderbilt Center for Mucosal Inflammation and Cancer
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