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Study reveals how some molecules inhibit growth of lung cancer cells

By mapping the interlocking structures of small molecules and mutated protein "receptors" in non-small cell lung cancer (NSCLC) cells, scientists at Dana-Farber Cancer Institute and their colleagues have energized efforts to design molecules that mesh with these receptors, potentially interfering with cancer cell growth and survival.

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Keywords: study, reveals, molecules, inhibit, growth, lung, cancer, cells, reveal, molecule, cell

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1. Vitamin A derivative associated with reduced growth in some lung cells
   10-30-2007 · EurekAlert!
   Treatment with a derivative of vitamin A called retinoic acid was associated with reduced lung cell growth in a group of former heavy smokers, according to a study published online Oct. 30 in the Journal of the National Cancer Institute.
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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. Leukemia drug turns mini-molecules up, cancer genes down
   03-01-2007 · EurekAlert!
   New research shows that a form of vitamin A used to treat acute promyelocytic leukemia induces changes in an unusual class of small molecules called microRNAs (miRNAs) in the leukemic cells. The study also shows that three of these miRNAs inhibit the action of two genes important for cancer development, helping to explain how the drug works.
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4. New protein inhibitor impedes growth of cancerous cells
   02-08-2007 · EurekAlert!
   Researchers have developed a small-molecule inhibitor of a protein that plays key roles in the control of cell division, and they show that the inhibitor can halt the growth of tumors in mice and cancer-derived cells growing in culture.
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5. Study says normal but out-of-control enzyme may be culprit that signals some cells to become cancer
   07-31-2007 · EurekAlert!
   Working with human colorectal cancer cells, a University of Minnesota team, led by cancer biologists Zigang Dong and Ann Bode, has found the potential culprit among a network of enzymes that relay signals inside cells to regulate such functions as cell growth, cancer development and programmed cell death. The work suggests that drugs designed to disable the enzyme, known as TOPK, could have anticancer benefits. The study appears in the July issue of the journal Gastroenterology.
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6. Scripps Research study reveals new function of protein kinase pathway in tumor suppression
   01-25-2007 · EurekAlert!
   Scientists at the Scripps Research Institute have discovered a surprising new function of a well-known signaling pathway that, when activated, can inhibit tumor development. This finding may lead to the development of drugs that can serve as an effective cancer therapy by artificially activating this pathway in cancer cells.
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7. Targeting surgar on blood vessels may inhibit cancer growth
   05-07-2007 · EurekAlert!
   In a study that could point to novel therapies to prevent cancer spread, or metastasis, researchers at the University of California, San Diego, School of Medicine have targeted a sugar that supports blood vessel growth in the tumor. Their findings will be published in the May 7 online issue of Journal of Cell Biology.
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8. Role of TRPM8 in the development of prostate cancer
   05-17-2007 · EurekAlert!
   In normal prostate epithelium, cells coexist in many stages of development-differentiation, and disrupted differentiation and proliferation are major causes of cancer. A new study shows that the endoplasmic reticulum protein TRPM8 (ER-TRPM8) present in human prostate epithelial luminal cancer cells retains it’s function as a calcium release channel, independent of the differentiation state of the cell, and may be an important factor in controlling the growth of prostate cancer cells.
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9. Targeting sugar on blood vessels may inhibit cancer growth
   05-07-2007 · EurekAlert!
   In a study that could point to novel therapies to prevent cancer spread, or metastasis, researchers at the University of California, San Diego, School of Medicine have targeted a sugar that supports blood vessel growth in the tumor. Their findings will be published in the May 7 online issue of Journal of Cell Biology.
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10. White blood cell booster may help cancer patients avoid deadly complications
    07-25-2007 · EurekAlert!
    Cancer patients who receive a drug that stimulates the growth of infection-fighting white blood cells may be significantly less likely to die from a chemotherapy-related complication characterized by fever and low white blood cell levels, according to a multi-institutional study led by researchers from the University of Rochester School of Medicine and Dentistry and the Duke University Comprehensive Cancer Center.
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