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'Star Trek'-type scanning may reveal genetic activity of tumors, Stanford study shows

Peering into the body and visualizing its molecular secrets, once the stuff of science fiction, is one step closer to reality with a study from researchers at the Stanford University School of Medicine and the University of California, San Diego School of Medicine.

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Keywords: star, trek, -type, scanning, reveal, genetic, activity, tumors, stanford, study, shows, type, tumor, show

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1. Analysis of breast and colon cancer genes finds many areas of differences between tumors
   10-11-2007 · EurekAlert!
   Researchers from University Hospitals Ireland Cancer Center and Case Western Reserve University School of Medicine are part of a new national study that has analyzed more than 18,000 genes, including 5,000 previously unmapped genes, from breast and colorectal tumors. The study shows a great number of genetic differences between breast and colon cancer tumors, leading the researchers to conclude that new drugs must be developed that can hit these newly identified genetic targets in a manner specific to each different individual's tumor.
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2. 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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3. One Wwox isn't enough (to protect against cancer)
   03-15-2007 · EurekAlert!
   A new study shows that the loss of even one of the two copies of a particular tumor-suppressor gene greatly increases the risk that lung cancer will develop in experimental animals. The study examined the Wwox gene, a suspected tumor-suppressor gene, and showed that even when mice have one working copy of the gene, they nonetheless develop five times more lung tumors than do mice with both copies of the gene.
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4. Innovative movies show real-time immune-cell activity within tumors
   11-20-2006 · EurekAlert!
   Using advanced new microscopy techniques in concert with sophisticated transgenic technologies, scientists have for the first time created three-dimensional, time-lapse movies showing immune cells targeting cancer cells in live tumor tissues. Immune cells called T cells can be seen actively migrating though tissues, making direct contact with tumor cells, and killing them. Insights from this new view of the body's on-board defenses against cancer may open the way for improved immunotherapies to treat the disease.
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5. Therapeutic peptide frees the protein p73 to kill tumor cells
   03-08-2007 · EurekAlert!
   p53 suppresses tumor development by inducing tumor cell death. However, targeting p53 for the treatment of cancer is confounded by the fact that genetic mutations cause loss or inactivation of p53 in approximately 50 percent of human cancers. Now, a new study indicates that targeting the p53-related protein p73 in mice induces the regression of established tumors of human origin, leading to the suggestion that p73 might be a viable target for developing anticancer therapeutics.
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6. Identifying the mechanism behind a genetic susceptibility to type 2 diabetes
   08-01-2007 · EurekAlert!
   Type 2 diabetes is reaching epidemic proportions in the developed world. Determining if and how certain genes predispose individuals to type 2 diabetes is likely to lead to the development of new treatment strategies for individuals with the disease. A new study now shows that certain variants of the gene TCF7L2 make individuals more susceptible to type 2 diabetes and provides a mechanism by which these genetic variants might cause susceptibility to the disease.
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7. Jefferson oncologists show focused radiation is effective as surgery against nerve tumor
   10-30-2007 · EurekAlert!
   Specifically aimed, "stereotactic" radiation may be as good as surgery -- and in some cases, even better -- in treating benign but potentially devastating brain tumors called nonacoustic schwannomas, according to a study by rradiation oncologists at the Kimmel Cancer Center at Thomas Jefferson University and Thomas Jefferson University Hospital in Philadelphia.
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8. Jefferson oncologists show breast cancers to be more aggressive in African-American women
   07-09-2007 · EurekAlert!
   A study of more than 2,200 women shows that African-Americans have more advanced breast cancer at the time of diagnosis than Caucasians. African-American women tend to have breast cancer tumor types that are more aggressive and have poorer prognoses. The findings are in line with other recent studies, and provide more evidence of the continuing need for early breast cancer screening for African-American women and the development of individual treatment strategies.
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9. ChemGenex reports successful personalized dosing of Quinamed at ASCO
   06-04-2007 · EurekAlert!
   Data from a phase 1/2a dose-escalation study of Quinamed, an anti-cancer compound under development by ChemGenex Pharmaceuticals against a variety of solid tumors was presented at ASCO. The key outcomes from this study were: demonstration that dose level could be optimized according to patient genotype; the drug was well tolerated, with predictable and manageable side effects; and there was evidence of anti-cancer activity in several solid tumor types.
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10. New study reveals gender disparity in anti-TNF treatment for rheumatoid arthritis
    06-14-2007 · EurekAlert!
    Findings reported today at EULAR 2007, the Annual European Congress of Rheumatology in Barcelona, Spain, reveal a treatment disparity between female and male patients with rheumatoid arthritis. Data from a study at the Karolinska Institute, Sweden, show that women receive anti-TNFs -- very effective but expensive modern medications against this disease -- at a higher perceived level of disease activity, and when they are reporting more severe pain than their male counterparts.
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