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Archive - Apr 13, 2015

Mayo Develops Profile of Those at Greatest Risk of Pancreatic Cancer

When people find out, usually from a diagnostic scan looking at something else, that they have a lesion in their pancreas that could morph into pancreatic cancer, they often panic. They insist on having frequent CT scans and biopsies to monitor the lesion, or they ask for surgery. Physicians also don't know if these abnormalities are dangerous, so the patients end up in surgery having part of their pancreas removed. Often, the lesion is nothing to worry about. But an international team of physicians, led by researchers at the Mayo Clinic campus in Jacksonville, Florida, has now developed a profile of the patient s who would be most at risk of developing lesions that are most likely to develop into cancer. The Mayo analysis was published online on April 10, 2015 in the journal Digestive and Liver Diseases. The article is titled “Risk Factors for Malignant Progression of Intraductal Papillary Mucinous Neoplasms.” "The factors we found that increase risk of pancreatic cancer now allow us to separate patients as either low or high risk," says the study's senior author, Michael B. Wallace, M.D., M.P.H., a gastroenterologist at the Mayo Clinic. "High-risk patients can then be scanned and biopsied more frequently or can opt for surgery, but low-risk patients don't need such surveillance. They can be watched much less intensively. Pancreatic cancer is difficult to detect early -- most patients are diagnosed at later stages when its 95 percent fatal -- so we're seeking ways to understand who is at risk," Dr. Wallace says. "Our study offers valuable insight into the problem." The lesions evaluated in this study that can become cancerous are known as intraductal papillary mucinous neoplasms. They are common. "Between 10 and 40 percent of people have them," Dr. Wallace says.

Two Cancer-Suppressing Proteins Identified in Lab of Israeli Nobel Laureate in Chemistry

A new study by researchers at the Technion-Israel Institute of Technology in Haifa, Israel could hold a key to control cancer cell growth and development. In a paper publishedin the April 9, 2015 issue of Cell, the team reports on the discovery of two cancer-suppressing proteins (KPC-1 and p50). The article is titled “KPC1-Mediated Ubiquitination and Proteasomal Processing of NF-κB1 p105 to p50 Restricts Tumor Growth.” The research was conducted in the laboratory of Distinguished Professor Aaron Ciechanover (photo), of the Technion Rappaport Faculty of Medicine. Dr. Ciechanover shared the 2004 Nobel Prize in Chemistry for the “discovery of ubiquitin-mediated protein degradation.” The team was led by Research Associate Dr. Yelena Kravtsova-Ivantsiv and included additional research students and colleagues, as well as physicians from the Rambam, Carmel, and Hadassah Medical Centers, who are studying tumors and their treatment. KPC1 (Kip1 ubiquitylation-promoting complex 1) is the catalytic subunit of the ubiquitin ligase KPC, which regulates the degradation of the cyclin-dependent kinase inhibitor p27(kip1) at the G1 phase of the cell cycle. The KPC1 pathway is vital in the life of the cell, which is responsible for the degradation of defective proteins that could damage the cell if not removed. The ubiquitin system tags these proteins and sends them for destruction in the cellular complex known as the proteasome. The system also removes functional and healthy proteins that are not needed anymore, thereby regulating the processes that these proteins control. Usually, the proteins that reach the proteasome are completely broken down, but there are some exceptions, and the current line of research examined p105, a long precursor of a key regulator in the cell called NF-kB.