UCLA scientists have identified a new mechanism that delivers a key substance that fuels the growth of pancreatic and prostate cancer cells, a finding that offers new hope in the fight against two of the deadliest forms of the disease. Cancer cells require high amounts of the sugar glucose to survive and grow, and long-standing research has established passive glucose transporters, known as GLUTS, as the primary method the body uses to deliver glucose to tumors. But the results of a three-year study by UCLA researchers, have demonstrated that pancreatic and prostate cancer cells also utilize glucose from sodium-dependent glucose transporters known as SGLTs, specifically SGLT2 (image). The findings in the study, which were published online on July 13, 2015 in PNAS, provide the first promising evidence that positron emission tomography (PET) imaging techniques and SGLT2 inhibitors could be used to better diagnose and treat pancreatic and prostate cancers, said Dr. Ernest Wright, Professor of Physiology in the David Geffen School of Medicine at UCLA and lead author of the three-year study. The PNAS article is titled “Functional Expression of Sodium-Glucose Transporters in Cancer.” “This is exciting because it provides strong evidence that SGLT2 inhibitors, such as those currently approved by the FDA to treat diabetes, could potentially block glucose uptake and reduce tumor growth and increase survival in pancreatic and prostate cancers,” said Dr. Wright, who is also a member of the UCLA Jonsson Comprehensive Cancer Center. Dr. Wright, Dr. Jorge Barrio, Dr. Claudio Scafoglio, and colleagues first mapped the distribution of sodium-dependent glucose transporters in human cancer tumors, then measured glucose uptake in fresh tumors using a glucose analog specifically transported by SGLTs.
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