A monoclonal antibody targeting a protein known as SFPR2 has been shown by researchers at the University of North Carolina to inhibit tumor growth in pre-clinical models of triple-negative breast breast cancer, according to research published in the April 19 issue of Molecular Cancer Therapeutics,
The UNC lab first discovered the role of SFRP2 in tumor growth while working to develop an alternative to Avastin (bevacizumab), which targets the protein VEGF. Although Avastin is of benefit to some patients with cancer, not all tumors respond to the drug, and of those that respond, some eventually progress. To find a solution for patients whose tumors are resistant to Avastin, researchers began looking at other proteins that could be used as therapeutic targets.  Avastin is not approved by the FDA for use with breast cancer.
“We previously microdissected blood vessels from malignant human breast cancers and compared gene expression to blood vessels microdissected from normal tissue. We found a number of genes that were highly over-expressed in the malignant blood vessels compared to normal. One of those genes was SFRP2,” said research leader Nancy Klauber-DeMore, MD, professor of surgery and a member of UNC Lineberger Comprehensive Cancer Center.
Researchers found that SFRP2 is expressed in a variety of human cancers, including breast, prostate, lung, pancreas, ovarian, colon, kidney tumors, and angiosarcomas. “Demonstrating that a monoclonal antibody to SFRP2 inhibits tumor growth in pre-clinical models opens up a new potential for drug development. This treatment is not presently available for human studies, but our efforts are focused on obtaining funding for further drug development that would lead to a clinical trial” DeMore said.
Read more about TNBC in my book, Surviving Triple-Negative Breast Cancer.
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