News Feature | April 23, 2014

Biomarker Leads To Cancer Drug Resistance And Tumor Formation

By Estel Grace Masangkay

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Researchers from the University of California, San Diego School of Medicine have identified CD61, a biomarker present on the surface of drug-resistant tumors, which they believe could shed light on why many drugs used in the treatment of lung, breast, and pancreatic cancer also encourage drug resistance and eventually lead to tumor formation in patients.

Dr. David Cheresh, Distinguished Professor of Pathology at the UCSD School of Medicine, said, “There are a number of drugs that patients respond to during their initial cancer treatment, but relapse occurs when cancer cells become drug-resistant. We looked at the cells before and after they became resistant and asked, ‘What has changed in the cells?’”

To answer the question, Dr. Cheresh and colleagues analyzed how tumor cells become resistant to tyrosine kinase inhibitors often used in standard cancer treatment programs. They found that concurrent to the development of drug resistance, tumor cells acquired stem cell like properties. CD61, it turned out, induced tumor metastasis by enhancing the stem-cell-like properties of cancer cells.

Dr. Hatim Husain, an assistant professor who also treats lung and brain cancer patients at Moores Cancer Center, said, “Resistance builds to targeted therapies against cancer, and we have furthered our understanding of the mechanisms by which that happens. Based on these research findings we now better understand how to exploit the ‘Achilles heel’ of these drug-resistant tumors. Treatments will evolve into combinational therapies where one may keep the disease under control and delay resistance mechanisms from occurring for extended periods of time.”

The discovery could lead to the development of methods to reverse drug resistance in different cancer types, the researchers said. Dr. Husain plans to launch a clinical trial set to begin in the next 12 months that will explore CD61 as a target in lung cancer patients who have become resistant to erlotinib.

The researchers’ work was published online in the April 20 edition of Nature Cell Biology.

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