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At The University of Texas Health Science Center at Houston(UTHealth) Medical School, scientists have made a key discovery incell signaling that is relevant to the fight against melanoma skincancer and certain other fast-spreading tumors. The scientists report that they have discovered why a class of drugcalled BRaf inhibitors that are widely used to treat melanomas donot always work and most importantly how these drugs maypotentially accelerate cancer growth in certain patients. Melanoma,according to the American Cancer Society, accounts for almost 9,000deaths each year. The scientists' research was published onlineahead of the June 5 print issue of Current Biology , which is published by Cell Press. "This information may aid the development of more effectiveanti-cancer drugs and better inform the choice of new combinationsof drugs," said John Hancock, M.B, B.Chir, Ph.D., the study'ssenior author, John S. Dunn Distinguished University Chair inPhysiology and Medicine, chairman of the Department of IntegrativeBiology and Pharmacology and interim director of the BrownFoundation Institute of Molecular Medicine for the Prevention ofHuman Diseases at the UTHealth Medical School. Growth signals are transmitted from a cell's surface to the nucleusby a chain of proteins that form a signaling pathway. The commandfor cells to divide to generate new cells is relayed by a chain offour proteins (Ras → BRaf → MEK → ERK). All cellshave this pathway and it does an effective job of generating newcells most of time. Problems happen when a mutation occurs in one of the first twoproteins in the chain -- both of which lock the signaling pathwayin the "on" position. The good news is that doctors havedrugs that block signaling from the second protein known as BRaf.These are the BRaf inhibitors, which are successful at treatingmelanomas with mutant BRaf proteins. The not-so-good news is that doctors cannot block the signal fromthe first protein called Ras. Researchers therefore studied in vivo what happens when BRaf inhibitors are applied to human cancertissues with Ras mutations. "Surprisingly recent studies found that BRaf inhibitors do notblock signaling in melanoma cells with Ras mutations. In fact, thedrugs actually enhance the abnormal signaling activity. Our worknow describes the mechanism for this seemingly paradoxical enhancedsignaling activity," said Kwang-jin Cho, Ph.D., the study'slead author and research fellow at the UTHealth Medical School. Most melanomas isolated from patients turn out to have either aBRaf or Ras mutation but rarely have both. Ras mutations cause anotherwise normal BRaf protein to stay switched on. "Our study also emphasizes the importance of genetic testingof melanomas before using BRaf inhibitors. Our study may also helpdesign a better drug," Cho said. The study was supported by the Cancer Prevention & ResearchInstitute of Texas. Hancock and Cho's co-authors from the UTHealth Medical School are:Jin-Hee Park, senior research assistant; Sravanthi Chigurupati,senior research assistant; Dharini van der Hoeven, Ph.D., researchfellow; and Sarah J. Plowman, Ph.D., assistant professor. Other collaborators include: Rinshi S. Kasai, Ph.D., and AkihiroKusumi, Ph.D., Kyoto University, Japan; and Sonja J. Heidorn,Ph.D., and Richard Marais, Ph.D., Institute for Cancer Research,London. I am an expert from digital-metaldetector.com, while we provides the quality product, such as China Under Vehicle Inspection Mirror , Wireless Signal Jammer, Walk Through Metal Detector,and more.
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