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International Symposium on Pancreatic Disease Headed Up by Hadassah Specialist

Earlier this month, Jerusalem hosted an international symposium dealing with inherited diseases of the pancreas. The symposium was organized by Prof. Michael Wilschanski, Director of Hadassah’s Pediatric Gastroenterology Unit, along with Prof. Markus M. Lerch of Greifswald University Hospital, Germany, and Prof. David C. Whitcomb of the University of Pittsburgh, PA.

Among the presenters from Canada, France, Germany, Israel, Norway, Spain, and the United States were physicians who specialize in identifying genes that are related to chronic diseases of the pancreas. Several presentations addressed aspects of the CFTR gene (Cystic Fibrosis Transmembrane Conductance Regulator), which provides instructions for making a protein called the cystic fibrosis transmembrane conductance regulator. This protein functions as a channel across the membrane of cells that produce mucus, sweat, saliva, tears, and digestive enzymes. Disease-causing mutations in the CFTR gene alter the production, structure or stability of this channel and prevent the channel from functioning properly. They impair the transport of chloride ions and the movement of water into and out of cells so that the cells that line the passageways of the lungs, pancreas, and other organs produce mucus that is abnormally thick and sticky. The abnormal mucus, in turn, obstructs the airways and glands.

Symposium topics included “25 Years of the CFTR Discovery”; Compound CFTR and other Mutations in Children”; “Genotype, Phenotype, and Functional Correlations of CFTR Mutations”; and “The Role of CFTR Mutations in Pancreatitis.”

Prof. Wilschanski, in his presentation, presented his recent research findings regarding “Therapeutic Approaches to Correct CFTR Dysfunction,” which were published in the May 14 issue of Lancet Respiratory Medicine.The article, coauthored with Prof. Eitan Kerem, head of Hadassah’s Pediatrics Division, and other global colleagues, describes a study conducted over a number of years with patients from 36 sites in 11 countries in North America and Europe, which explored the safety and efficacy of the drug, ataluren, in cystic fibrosis patients who have “nonsense mutations.” This category of mutation refers to a change in the DNA that prematurely stops the reading of messenger RNA (mRNA), resulting in a polypeptide chain that ends prematurely and a protein product that is incomplete and usually nonfunctional. Ataluren was developed to restore functional protein production in genetic disorders caused by nonsense mutations—which, in turn, are the cause of cystic fibrosis in 10 percent of patients. The authors note that their research indicates ataluren “might be beneficial for patients who are not taking chronic inhaled tobramycin.”

Others aspects of pancreatic disease discussed at the symposium were the genetics of pancreatic pain, genetic predispositions to pancreatic cancer, and molecular genetics in pancreatic cancer.

Date: 6/25/2014

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