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University of Washington-led team discovers a gene that causes familial pancreatic cancer

An international group of researchers has discovered that the mutated form of a gene called Palladin causes familial pancreatic cancer. The findings, published online today, Dec. 12, in the peer-reviewed journal PLoS-Medicine, may help explain why the disease is so deadly. The research project was led by Dr. Teri Brentnall, University of Washington associate professor of medicine, and supported by the Lustgarten Foundation, Canary Foundation and other private sources.

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1. University of Washington-led team discovers a gene
   12-12-2006 · EurekAlert!
   An international group of researchers has discovered that the mutated form of a gene called Palladin causes familial pancreatic cancer. The findings, published online today, Dec. 12, in the peer-reviewed journal PLoS-Medicine, may help explain why the disease is so deadly. The research project was led by Dr. Teri Brentnall, University of Washington associate professor of medicine, and supported by the Lustgarten Foundation, Canary Foundation and other private sources.
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2. First familial pancreatic cancer gene identified
   12-11-2006 · EurekAlert!
   At least 10 percent of pancreatic cancers are thought to be familial, i.e., caused by inherited genetic mutations. The responsible genes have so far remained elusive, but one of the research teams that had been on a pancreatic cancer gene hunt for years now reports success: Teri Brentnall (University of Washington), David Whitcomb (University of Pittsburgh), and colleagues publish the identification of the palladin gene as the one mutated in a large family they had been studying for a while.
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3. New study reveals for first time how BRCA1 mutations cause breast cancer
   12-09-2007 · EurekAlert!
   An international team of researchers led by Columbia University Medical Center's Herbert Irving Comprehensive Cancer Center and Sweden's Lund University has, for the first time, revealed how mutations in the BRCA1 gene lead to breast cancer. Findings show that one way BRCA1 mutations cause cancer is by knocking out a powerful tumor suppressor gene known as PTEN.
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4. Gene analysis might explain ethnic differences in sensitivity to chemotherapy in lung cancer
   04-23-2007 · UT Southwestern Medical Center
   Analysis of three genetic mechanisms that cause non-small cell lung cancer might explain why East Asians respond better than other ethnic groups to a certain type of chemotherapy, a team led by UT Southwestern Medical Center researchers has found.
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5. Biologists at Tufts University discover 1 reason why chromosomes break, often leading to cancer
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   In the past 10 years, researchers in genome stability have observed that many kinds of cancer are associated with areas where human chromosomes break. They have hypothesized -- but never proven -- that slow or altered replication led to the chromosomes breaking. A new Tufts University study proves the hypothesis after molecular biologists used yeast artificial chromosomes to find a highly flexible DNA sequence that increases fragility and stalls replication, which then causes the chromosome to break.
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6. Early Phase II results show bosutinib safe, effective for CML
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   A new drug for chronic myelogenous leukemia works for patients who have developed resistance to frontline therapy and causes fewer side effects than other medications in its class, a research team led by scientists at the University of Texas M. D. Anderson Cancer Center reports at the 49th annual meeting of the American Society of Hematology.
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7. If air gets scarce -- new gene causes asthma in children
   08-20-2007 · EurekAlert!
   Usually harmless external stimuli like animal hair, pollen and house dust cause a life-endangering narrowing of the bronchi in asthma patients. An international team of scientists headed by researchers from the Ludwig-Maximilians University, Munich, and Oxford University, UK, have now been able to identify a gene that clearly increases the risk for asthma in childhood.
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8. Gene analysis might explain ethnic differences in sensitivity to chemotherapy in lung cancer
   04-23-2007 · EurekAlert!
   Analysis of three genetic mechanisms that cause nonsmall cell lung cancer might explain why East Asians respond better than other ethnic groups to a certain type of chemotherapy, a team led by UT Southwestern Medical Center researchers has found.
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9. Advance in understanding of blood pressure gene could lead to new treatments
   02-04-2007 · EurekAlert!
   Research by scientists at UCL (University College London) has clearly demonstrated for the first time the structure and function of a gene crucial to the regulation of blood pressure. The discovery could be important in the search for new treatments for illnesses such as heart disease, the UK's biggest killer. In a paper published online today in Nature Medicine, the team, led by Professor Patrick Vallance and Dr James Leiper, UCL Department of Medicine, reveal the role of the human gene dimethylarginine dimethylaminohydrolase (DDAH), showing that loss of DDAH activity disrupts nitric oxide (NO) production. NO is critical in the regulation of blood pressure, nervous system functions and the immune system. The role of DDAH is to break down modified amino acids (Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA)) that are produced by the body and have been shown to inhibit NO synthase. These molecules accumulate in various disease states including diabetes, renal failure and pulmonary and systemic hypertension, and their concentration in plasma (the fluid component of blood) is strongly predicative of cardiovascular disease and death. In a healthy human body, the majority of ADMA is eliminated through active metabolism by DDAH. Scientists have hypothesised that if DDAH function is impaired, NO production is reduced, and that this could be an important feature of increased cardiovascular risk. To examine this pathway in more detail, the researchers deleted the DDAH gene in mice. These mice went on to develop hypertension, or high blood pressure. They also designed specific inhibitors (small molecules) which bind to the active site of human DDAH. These small molecule inhibitors also induced hypertension in mice, confirming the importance of DDAH in the regulation of blood pressure. Dr Leiper, UCL Medicine, said: “These genetic and chemical approaches to disrupt DDAH showed remarkably consistent results, and provide compelling evidence that loss of DDAH function increases the concentration of ADMA and thereby disrupts vascular NO signalling. “There has been considerable scientific interest in this pathway and the role of ADMA as a novel risk factor, but so far there's been little evidence to support the idea that it's a cause of disease, rather than just a marker. Genes and their pathways are crucial to our understanding of cardiovascular disease and a better understanding of DDAH-1 could lead to important new treatments. “It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity. “Our research also shows that this pathway could be harnessed therapeutically to limit production of NO in certain situations where too much nitric oxide is a bad thing; for example, hypotension and septic shock. These are some of the biggest problems in intensive care medicine and there is a huge unmet need for drug treatments.” The study, which was carried out at UCL's Rayne Institute, was funded by grants from the British Heart Foundation, the Wellcome Trust and the Medical Research Council. Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, said: "The unexpected finding in the 1980s that a simple gas, nitric oxide (NO), is made by cells in the blood vessel wall and is a powerful control of blood vessel relaxation led to the award of the Nobel Prize in 1998 to its discoverers. "More recently, there has been increasing evidence that impairment of NO production is likely to be an important factor in the development of heart and circulatory disease, but the mechanisms responsible are not fully understood. "This study suggests for the first time that the loss of the activity of the enzyme DDAH-1 leads to reduced NO production and may cause heart and circulatory disease. These findings are likely to be important in the search for new ways to optimise the health of our blood vessels." ### Notes for Editors 1. For more information, please contact Ruth Metcalfe in the UCL Media Relations Office on tel: +44 (0)20 7679 9739, mobile: +44 (0)7990 675 947, out of hours: +44 (0)7917 271 364, e-mail: r.metcalfe@ucl.ac.uk2. 'Disruption of methylarginine metabolism impairs vascular homeostasis' is published in the February issue of the journal Nature Medicine. Advance online publication is embargoed to 18.00 GMT (13.00 US Eastern) Sunday 4 February 2007. Journalists can obtain copies of the paper by contacting the UCL Media Relations Office.3. The study was funded by the British Heart Foundation, the Wellcome Trust and the Medical Research Council. About UCL Founded in 1826, UCL was the first English university established after Oxford and Cambridge, the first to admit students regardless of race, class, religion or gender, and the first to provide systematic teaching of law, architecture and medicine. In the government's most recent Research Assessment Exercise, 59 UCL departments achieved top ratings of 5* and 5, indicating research quality of international excellence. UCL is the fourth-ranked UK university in the 2006 league table of the top 500 world universities produced by the Shanghai Jiao Tong University. UCL alumni include Mahatma Gandhi (Laws 1889, Indian political and spiritual leader); Jonathan Dimbleby (Philosophy 1969, writer and television presenter); Junichiro Koizumi (Economics 1969, Prime Minister of Japan); Lord Woolf (Laws 1954, Lord Chief Justice of England & Wales); Alexander Graham Bell (Phonetics 1860s, inventor of the telephone), and members of the band Coldplay.
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10. UCSD researchers discover cause of rosacea
    08-05-2007 · EurekAlert!
    A team of researchers, led by Richard L. Gallo, M.D., Ph.D., professor of medicine and chief of the Division of Dermatology at the University of California, San Diego School of Medicine and the dermatology section of the Veterans Affairs San Diego Healthcare System, has determined that it is not one, but a combination of two abnormal factors, that result in rosacea.
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