Targeting CD44s May Make Glioblastoma More Sensitive To Clinical Treatment

MedicalResearch.com Interview with:

Chonghui Cheng, M.D., Ph.D. Associate Professor Department of Molecular & Human Genetics Lester & Sue Smith Breast Center Baylor College of Medicine Houston, TX77030

Dr. Cheng

Chonghui Cheng, M.D., Ph.D.
Associate Professor
Department of Molecular & Human Genetics
Lester & Sue Smith Breast Center
Baylor College of Medicine
Houston, TX77030

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Understanding the mechanisms that give cancer cells the ability to survive and grow opens the possibility of developing improved treatments to control or cure disease. In the case of glioblastoma multiforme, the deadliest type of brain cancer, abnormal EGFR signaling is frequently observed.

Treatment with the EGFR inhibitor erlotinib attempts to kill cancer cells. However, the clinical benefit of treatment with this and other EGFR inhibitors has been limited by the development of drug resistance.

Scientists at Baylor College of Medicine discovered that the molecule CD44s seems to give cancer cells a survival advantage. Eliminating this advantage by reducing the amount of CD44s resulted in cancer cells being more sensitive to the deadly effects of the drug erlotinib.

MedicalResearch.com: What should clinicians and patients take away from your report?

Response: The scientists found that CD44s holds a strategic place from which it can influence not only EGFR, but also a number of other signaling cascades that are important for cancer cell survival in glioblastoma.

My colleagues and I anticipate that CD44s might also play a similar role in other types of cancer in which EGFR signaling is involved. This opens the possibility that targeting CD44s could potentially reduce the growth of many types of cancer, not just glioblastoma.

MedicalResearch.com: What recommendations do you have for future research as a result of this study?

Response: Researchers have been focused on developing inhibitors of EGRF and related pathways. Instead, we want to find novel approaches to boost the activity of inhibitors already available, and removing CD44s is a good example of how this could be done. Our work suggests that in the future, physicians and scientists might approach cancer treatment in a different way. For example, instead of deciding on a treatment based on the type of breast cancer a patient has, they might choose a treatment according to the type of mechanism that helps this particular cancer grow, regardless of the type of cancer it is.

Disclosures: No conflict of interest

MedicalResearch.com: Thank you for your contribution to the MedicalResearch.com community.

Citation:

Wei Wang, Honghong Zhang, Sali Liu, Chung Kwon Kim, Yilin Xu, Lisa A. Hurley, Ryo Nishikawa, Motoo Nagane, Bo Hu, Alexander H. Stegh, Shi-Yuan Cheng, Chonghui Cheng. Internalized CD44s splice isoform attenuates EGFR degradation by targeting Rab7A. Proceedings of the National Academy of Sciences, 2017; 201701289 DOI: 10.1073/pnas.1701289114

Note: Content is Not intended as medical advice. Please consult your health care provider regarding your specific medical condition and questions.

 

 

 

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