Many believe that a simultaneous combination of two or more treatments targeted to the same pathway could overwhelm the cancer cells' evasive abilities. Researchers haven't given up hope, though. As a result, many patients who at first respond successfully to treatment can face the heartbreak of a relapse within months or a few years. Unfortunately, the pinpoint specificity of such treatments can make it easier for a rapidly mutating cancer cell to develop resistance. On paper, it's a sure-fire win-win - when it works. Current examples of targeted therapies include some well-known drugs: Herceptin, Gleevec, Rituxan and Avastin, to name a few. When successful, targeted treatments reduce the overall toxicity to the patient compared with chemotherapy, and also can be more effective. They generally do so by inhibiting specific signaling relays that are abnormally active in cancer cells, by tagging cancer cells with antibodies that recognize certain molecular configurations found only on the surface of diseased cells, or by blocking cancer cell-stimulated growth of new blood vessels to tumor sites. Unlike traditional chemotherapy and most radiation treatments, targeted cancer treatments are meant to kill only cancer cells and leave others unscathed. Former graduate student Katherine Jameson, PhD, and postdoctoral scholar Pawel Mazur, PhD, share lead authorship. Khavari, who is also a member of the Stanford Cancer Institute and chief of the dermatology service at the Veterans Affairs Palo Alto Health Care System, is the senior author of the study, which was published online April 21 in Nature Medicine. By doing so, this blocks growth of even cancer cells that have already become resistant to other targeted treatments." This new approach takes away the table so those cancer-promoting actions never happen. "It's as if the cancer-causing proteins are convening around a conference table to implement tumor-forming discussions. Herzog Professor and chair of the Department of Dermatology. "This could be a new type of tool for clinicians," said Paul Khavari, MD, PhD, the Carl J. The versatility of the technique, as well as its apparent ability to tackle drug-resistant cancers, indicates that targeting scaffold proteins may lead to a new class of cancer therapies in humans. It also significantly slowed the growth in laboratory culture of human melanoma cells that had become resistant to a new, targeted cancer treatment called vemurafenib (marketed as Zelboraf).
#Scaffold protein skin
They've done so by disrupting the function of a mediator, or scaffold, protein that brings together key members of the pathway and promotes their interaction to stimulate cell growth and division.īlocking the function of the scaffold protein, or even removing it entirely, impeded the development of chemically induced skin cancers in laboratory mice and extended the life span of mice with established pancreatic tumors, the researchers say. Researchers at the Stanford University School of Medicine have devised an entirely novel way to block biological signaling pathways that, when overactive, lead to many types of cancers.
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