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Researchers Report the EGFR Gene Found in Mesothelioma Silences Tumor Suppression Leading to Uncontrolled Growth


The pulmonologist is checking the radiographic film of mesothelioma patient

The epidermal growth factor receptor (EGFR) gene has been the focus of researchers for finding new, effective treatments for both lung cancer and mesothelioma patients. The gene, that is overexpressed in more than 50% of pleural mesothelioma patients, and in approximately 15% of lung cancer patients, is one of the primary targets for bringing personalized care to the cancer patients. Now, researchers report they understand just how the gene impacts cancer growth.

Researchers from Yale are referring to the EGFR gene as the “silencer” gene, because, they say, it “silences genes that typically suppress tumors.” The team, led by Narendra Wajapayee, assistant professor of pathology and a member of Yale Cancer Center, report in a June 23 press release, that this critical finding “may lead to the development of more effective, individualized treatment for patients with lung cancer and other cancer types.”

Wajapayee and the team found that EGFR negatively regulated the TET1 protein, important for controlling gene expression and required to suppress tumors, allowing the cancer cells continue to grow and divide.

“EGFR can target multiple unrelated tumor suppressor genes in different cancer types using a common mechanism,” said Wajapayee.

Approximately 2,500 to 3,000 Americans are diagnosed with mesothelioma, an asbestos-caused cancer, each year. Most people diagnosed with mesothelioma are retired workers and veterans who were exposed to asbestos in a workplace or during military service decades ago. The most common form of the cancer is malignant pleural mesothelioma, affecting the lining of the lungs. Disease symptoms can take between 15 and 60 years to appear.

Mesothelioma often resists standard treatments and can build up a resistance to the powerful chemotherapy drugs used to attack the aggressive cancer. Although even targeted EGFR inhibitors can eventually become ineffective, personalized cancer treatment targeted to the unique characteristics of the patient optimizes the potential for success of the treatment.

“The finding informs the future direction of research and treatment of patients who don’t respond or develop resistance to drugs that inhibit EGFR,” said Wajapayee . “It will also help determine how effective cancer therapies will be against different EGFR mutations.”

The results of the study can be found in the June 23 issue of Cell Reports.

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