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New strategy overcomes tumor resistance to colorectal cancer treatment

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“Identifying the major vulnerabilities of drug-resistant colorectal cancer cells and developing treatment strategies targeting such vulnerabilities is critical to the more effective treatment of the disease,” the development said. Yuesheng Zhang, MD, Ph.D., a research-responsive author who is a member of.Treatment research program at VCU Massey Cancer Center Professor of Pharmacology and Toxicology, VCU School of Medicine.

A class of targeted therapies known as epidermal growth factor receptor (EGFR) inhibitors are clinically effective treatment options for colorectal cancer. Over 80% of colorectal tumors are EGFR positive and over half are overexpressed. These drugs work by targeting the EGFR protein and inhibiting the growth of cancer cells. However, resistance to these treatments is common. The reason for this resistance is not well known scientifically, making it difficult to develop more effective treatment strategies.

Resistance to EGFR inhibitors such as cetuximab and panitumumab was previously thought to be due to mutations in a series of cancer-related genes such as KRAS, BRAF, and PIK3CA. However, according to Zhang’s research, this is not the case.

“Our study unexpectedly shows that colorectal cancer resistance to cetuximab and panitumumab is primarily due to the inability to suppress EGFR,” Zhang said.

In essence, researchers have determined that drugs specifically designed to limit the function of EGFR are not as effective as previously thought.

In search of alternative therapies, Zhang and his collaborators tested the use of recombinant human protein therapy called PEPD-G278D in colorectal tumor cells and mouse tumor models. They found that PEPD-G278D disrupts EGFR activity along with its gene family members and HER2, which affects cancer, by binding to receptors on the outer membrane of colonic rectal cancer cells.

“PEPD-G278D strongly inhibits the growth of cancer cells and tumors that overexpress EGFR and / or HER2,” Zhang said, and PEPD-G278D inhibits EGFR only in protein-rich cancer cells. He added that it was not inhibited by normal cells. There are normal levels of EGFR.

In addition, researchers have found that the use of an oral drug called adervacib in combination with PEPD-G278D allows for a more targeted reduction in tumor growth. Aderbasib itself was not effective in this study, but it enhances target engagement with PEPD-G278D. Researchers also found that the addition of the widely used chemotherapy fluorouracil further improved the antitumor capacity of PEPD.

“These findings suggest that treatment strategies centered around PEPD-G278D are very promising for overcoming drug resistance to colorectal cancer,” Zhang said. “It would be interesting to investigate whether other chemotherapeutic agents used to treat colorectal cancer also enhance tumor suppression when combined with PEPD-based therapies.”

Zhang collaborated on this study with Lu Yang, Ph.D., an assistant professor in the Department of VCU Pharmacology and Toxicology. Arup Bhattacharya, Ph.D., Fengzhi Li, Ph.D., Yun Li, MS, Xiang Ling, Ph.D., and Sandra Sexton, DVM at Roswell Park Comprehensive Cancer Center.

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