Daily non-political popular news in brief.

Study suggests newer breast cancer drug may protect heart

06-08-2007 · EurekAlert!

By uncovering how one breast cancer drug protects the heart and another does not, Duke University Medical Center researchers believe they may have opened up a new way to screen drugs for possible heart-related side effects and to develop new drugs.

Keywords: study, suggests, newer, breast, cancer, drug, protect, heart, suggest

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Study: Fountain of youth for your heart?
11-02-2007 · EurekAlert!
University of Alberta professor Jason Dyck's findings suggest that the protein responsible for transporting fat into the contractile cells of the heart may be a candidate for drug inhibition and that this drug could protect the heart from aging. This research holds great promise for human beings. Dyck hopes it will lead to the development of medications that inhibit the uptake of fatty acids into the heart and prevent and/or reverse the effects of aging on the heart muscle.
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Latest drugs improve survival for metastatic breast cancer
07-23-2007 · EurekAlert!
Newer drug therapies available since the 1990s, in particular aromatase inhibitors, improve the survival of women with metastatic breast cancer in the general population, according to a new study.
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USC-led study suggests exercise reduces risk of developing invasive breast cancer
02-26-2007 · EurekAlert!
Significant findings have emerged from the California Teachers Study (CTS) that suggest long-term recreational physical activity plays a protective role against invasive and in situ breast cancer.
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Study: Re-engineered Gleevec reduces heart risks
12-03-2007 · EurekAlert!
Using a new bottom-up approach for rational drug design, researchers at Rice University and the University of Texas M. D. Anderson Cancer Center have reengineered the powerful anticancer drug imatinib -- best known by its brand name Gleevec -- to more specifically target one type of cancer while potentially curbing a rare life-threatening cardiotoxic side effect. The re-design strategy employed in the study is broadly applicable to reducing side effects in other drugs.
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Study suggests estrogen deficiency can lead to obesity-induced high blood pressure after menopause
08-08-2007 · EurekAlert!
At menopause, women lose hormone protection against heart and kidney diseases, and are likely to become obese. A research team has tested the idea that estrogen deficiency in aged females may trigger the development of high blood pressure and obesity. The results of their study, using an animal model, suggest that estrogen depletion can have these effects.
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Diet and exercise key to surviving breast cancer, regardless of obesity, new UCSD study says
06-08-2007 · EurekAlert!
Breast cancer survivors who eat a healthy diet and exercise moderately can reduce their risk of dying from breast cancer by half, regardless of their weight, suggests a new longitudinal study from the Moores Cancer Center at the University of California, San Diego.
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Dietary vitamin B6, B12 and folate, may decrease pancreatic cancer risk among lean people
06-01-2007 · EurekAlert!
Researchers exploring the notion that certain nutrients might protect against pancreatic cancer found that lean individuals who got most of these nutrients from food were protected against developing cancer. The study also suggests this protective effect does not hold true if the nutrients come from vitamin supplements.
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New weapon to fight leukemia
08-23-2007 · EurekAlert!
A new study indicates that the drug FTY720 prevents disease in a mouse model of two leukemias -- blast crisis chronic myeloid leukemia and acute lymphocytic leukemia -- caused by the cancer protein BCR-ABL. As the drug also induced cell lines from humans with these leukemias to die in vitro the authors suggest that FTY720 should be considered by researchers and clinicians developing new approaches to treat CML-BC and ALL.
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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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A black and white look at breast cancer mortality
02-21-2007 · EurekAlert!
Researchers suggest a reason for racial disparity in breast cancer survival rates. African and African American women are much less likely to survive breast cancer surgery than their white counterparts and far more likely to get the disease before the menopause. Previous research suggests that those who undergo surgery for the disease before the menopause are more prone to relapse.
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