http://www.tobacco.org/newsfeed/category/genes.rss Latest top tobacco news headlines en-us http://news.bbc.co.uk/2/hi/health/7396814.stm http://tobacco.org/news/265291.html A key mechanism by which smoking triggers genetic changes that cause lung cancer has been unravelled. Researchers have shown exposure to cigarette smoke slows production of a protein called FANCD2 in lung cells. This protein plays a key role in repairing damage to DNA, and causing faulty cells to commit suicide before they go on to become cancerous. The study, led by Oregon Health and Science University, appears in the British Journal of Cancer. BBC Online UK Wed, 14 May 2008 04:00:00 GMT http://www.sciencedaily.com/releases/2008/05/080513130635.htm http://tobacco.org/news/265253.html Oregon Health & Science University Cancer Institute researchers have pinpointed the protein that can lead to genetic changes that cause lung cancer. Researchers discovered that the production of a protein called FANCD2 is slowed when lung cells are exposed to cigarette smoke. Low levels of FANCD2 leads to DNA damage, triggering cancer. Cigarette smoke curbs the production of 'caretaker' proteins, like FANCD2, which normally prevent cancer by fixing damages in DNA and causing faulty cells to commit suicide. Research has shown that smoking is strongly linked to lung cancer, but this discovery may help scientists improve treatments for lung disease in the future. "These findings show the important role FANCD2 plays in protecting lung cells against cigarette smoke, and may explain why cigarette smoke is so toxic to these cells," said lead author Laura Hays, Ph.D., research assistant professor of medicine (hematology/medical oncology) and member of the OHSU Cancer Institute. . . . Journal reference: * Hays et al. Cigarette smoke induces genetic instability in airway epithelial cells by suppressing FANCD2 expression. British Journal of Cancer. May 12, 2008. ScienceDaily Magazine editor@sciencedaily.com Tue, 13 May 2008 04:00:00 GMT http://www.washingtonpost.com/wp-dyn/content/article/2008/05/09/AR2008050902546.html http://tobacco.org/news/265028.html The company 23andMe promises to "unlock the secrets of your own DNA." Navigenics wants you to be tested to "do everything you can to stay healthy." And deCODEme hopes that genetic testing will "prompt people to do the right thing." It all sounds so good. If you have a couple of thousand dollars to part with (along with some saliva), why not have one of these companies scan your genome? The primary caution about genetic testing has usually been that you will learn that you are destined to develop some dreadful disease (such as Huntington's disease, a degenerative neurological disorder) for which there is no known therapy. A positive test only allows you to start worrying about your demise earlier. Do you really want to know? . . . (These uncertainties, combined with the absence of increased lung-cancer risk, may tempt you to keep smoking.) What's the right thing to do? With the exception of quitting smoking, the truth is: No one knows. The Washington Post Sun, 11 May 2008 04:00:00 GMT http://www.eurekalert.org/pub_releases/2008-05/uotm-cpa043008.php http://tobacco.org/news/264819.html Whole-organ maps that superimpose genetic information over the terrain of cancerous bladders chart the molecular journey from normal cell to invasive cancer, an international research team led by scientists at The University of Texas M. D. Anderson Cancer Center reports online at the journal Laboratory Investigation, a member of the Nature Publishing Group. By geographically relating an organ's varied tissues - normal, precancerous and malignant - to their underlying genetic variation or regulation, the team also identified a crucial new category of genes that launches the process of cancer development. . . . A gene known as P2RY5 located inside a portion of the RB1 gene was affected by a number of single-nucleotide changes. A case-control study of one of the gene's variant forms was conducted using blood DNA from 790 bladder cancer patients and 712 controls matched for age and gender. The specific variation was present in 2.78 percent of patients and every patient with the variation who also smoked developed bladder cancer. EurekAlert smerville@mdanderson.org (geographically relating an organ) Mon, 05 May 2008 04:00:00 GMT http://english.people.com.cn/90001/90782/6403396.html http://tobacco.org/news/264764.html Genes could play an important role in determining a person's smoking habit, Finnish researchers reported in a study published on Sunday. Researchers from Helsinki University came to the conclusion after surveying 9,000 twins and their families, and checking their genetic samples. People's Daily Mon, 05 May 2008 04:00:00 GMT http://www.medwire-news.md/46/74652/Oncology/Genotype-cigarette_smoke_interaction_shown_in_breast_cancer.html http://tobacco.org/news/264483.html Cigarette smoke exposure substantially increases the risk for developing breast cancer among premenopausal women with certain polymorphisms in interleukin 6 (IL6) and estrogen receptor alpha (ESR1), results of a case-control study demonstrate. The findings add to a growing body of evidence suggesting that genotype and cigarette smoke can interact to increase the risk for breast cancer. One study recently reported by MedWire News found that smokers with the slow-metabolizing N-acetyltransferase 2 genotype face an increased risk for the disease compared with non-smokers. For the present study, Martha Slattery (University of Utah, Salt Lake City, USA) and colleagues enrolled 3128 non-Hispanic White women, including 1527 with breast cancer and 1601 controls, along with 798 cases and 924 controls of Hispanic/American Indian ethnicity. . . . Notably, exposure to more than 10 hours of passive smoke per week was associated with a 3.0- and 4.4-fold increased breast cancer risk in Hispanic/American Indian and non-Hispanic White premenopausal GG rs2069832 carriers, respectively, compared with women with the wild-type genotype who reported less than 1 hour of exposure. In addition women of either ethnicity group who smoked more than 15 cigarette pack-years and had the ESR1 Xba1 AA genotype faced a 3-fold increased risk for breast cancer compared with nonsmokers with the wild-type allele. "Our data suggest that this risk may be influenced by underlying genetic susceptibility and that mechanisms involving both estrogen and inflammation may be important in defining risk," Slattery and colleagues conclude in the journal Breast Cancer Research and Treatment. MedWire News Tue, 29 Apr 2008 04:00:00 GMT http://www.nih.gov/news/health/apr2008/nida-02.htm http://tobacco.org/news/263390.html Scientists have identified a genetic variant that not only makes smokers more susceptible to nicotine addiction but also increases their risk of developing two smoking-related diseases, lung cancer and peripheral arterial disease. The research was supported by the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health (NIH). The study, published in the April 3 issue of the journal Nature, "highlights the advances that are being made in genetics research, which can now identify gene variants that increase the risk of complex bio-behavioral disorders," says NIH Director Dr. Elias Zerhouni. "This finding will help us in our efforts to further reduce the scope and devastating consequences of cigarette smoking." National Institutes of Health media@nida.nih.gov Wed, 02 Apr 2008 04:00:00 GMT http://www.medicalnewstoday.com/articles/104048.php http://tobacco.org/news/263298.html According to research from a team of Mayo Clinic scientists, smoking puts older women at significant risk for loss of DNA repair proteins that are critical for defending against development of some colorectal cancers. In a study being presented at the annual meeting of the American Association for Cancer Research (AACR), the researchers found that women who smoked were at increased risk of developing colorectal tumors that lacked some or all of four proteins, known as DNA mismatch repair (MMR) proteins. These proteins keep cells lining the colon and rectum healthy because they recognize and repair genetic damage as well as mistakes that occur during cell division. Researchers believe that, in this study population, few if any of the four proteins were absent because of an inherited genetic alteration. "We think that smoking induces a condition within intestinal cells that does not allow MMR genes to express their associated proteins, and this loss leads to formation of tumors in some women." Medical News TODAY Tue, 15 Apr 2008 04:00:00 GMT http://www.eurekalert.org/pub_releases/2008-04/mc-msf041008.php http://tobacco.org/news/263244.html Smoking puts older women at significant risk for loss of DNA repair proteins that are critical for defending against development of some colorectal cancers, according to research from a team led by Mayo Clinic scientists. In a study being presented at the annual meeting of the American Association for Cancer Research (AACR), the researchers found that women who smoked were at increased risk for developing colorectal tumors that lacked some or all of four proteins, known as DNA mismatch repair (MMR) proteins. These proteins keep cells lining the colon and rectum healthy because they recognize and repair genetic damage as well as mistakes that occur during cell division. Researchers believe that, in this study population, few if any of the four proteins were absent because of an inherited genetic alteration. "We think that smoking induces a condition within intestinal cells that does not allow MMR genes to express their associated proteins, and this loss leads to formation of tumors in some women," says the study's lead author, Mayo gastroenterologist Paul Limburg, M.D. EurekAlert newsbureau@mayo.edu Sun, 13 Apr 2008 04:00:00 GMT http://www.sciencedaily.com/releases/2008/04/080413183701.htm http://tobacco.org/news/263216.html Cells lining the mouth reflect the molecular damage that smoking does to the lining of the lungs, researchers at The University of Texas M. D. Anderson Cancer Center report today at the annual meeting of the American Association for Cancer Research. Examining oral tissue lining the mouth to gauge cancer-inducing molecular alterations in the lungs could spare patients and those at risk of lung cancer from more invasive, uncomfortable procedures used now, said senior researcher Li Mao, M.D., professor in M. D. Anderson's Department of Thoracic/Head and Neck Medical Oncology. "We are talking about just a brushing inside of the cheek to get the same information we would from lung brushings obtained through bronchoscopy . . . The researchers tracked whether either p16, FHIT or both had been silenced by methylation - the attachment of a chemical methyl group to crucial spots in a gene that shut down its function. Patterns of methylation were compared between the tissues. The baseline tissue comparison showed methylation of p16 in the lungs of 23 percent of study participants, of FHIT in 17 percent and of either of the two genes in 35 percent. The percentages were similar in oral tissue, with p16 methylated in 19 percent, FHIT in 15 percent and one of the two in 31 percent. Strong correlations were observed between methylation patterns in both tissues. ScienceDaily Magazine editor@sciencedaily.com Sun, 13 Apr 2008 04:00:00 GMT http://www.newswise.com/articles/view/539694/ http://tobacco.org/news/263210.html Smoking puts older women at significant risk for loss of DNA repair proteins that are critical for defending against development of some colorectal cancers, according to research from a team led by Mayo Clinic scientists. In a study being presented at the annual meeting of the American Association for Cancer Research (AACR), the researchers found that women who smoked were at increased risk for developing colorectal tumors that lacked some or all of four proteins, known as DNA mismatch repair (MMR) proteins. These proteins keep cells lining the colon and rectum healthy because they recognize and repair genetic damage as well as mistakes that occur during cell division. Researchers believe that, in this study population, few if any of the four proteins were absent because of an inherited genetic alteration. “We think that smoking induces a condition within intestinal cells that does not allow MMR genes to express their associated proteins, and this loss leads to formation of tumors in some women,” says the study’s lead author, Mayo gastroenterologist Paul Limburg, M.D. Newswise Sun, 13 Apr 2008 04:00:00 GMT http://www.eurekalert.org/pub_releases/2008-04/uotm-gvr033108.php http://tobacco.org/news/262930.html Two common inherited genetic variations are associated with increased risk of lung cancer for smokers and former smokers, a research team led by scientists at The University of Texas M. D. Anderson Cancer Center reports April 2 in the online edition of Nature Genetics. "This is the first study to identify a common genetic variant that influences the risk for developing lung cancer," said lead author Chris Amos, Ph.D., professor in M. D. Anderson's Department of Epidemiology. The variants are present in about half of the Caucasian population studied. The paper is one of three published by Nature this week from three unique teams that have identified the same genetic locus as associated with increased lung cancer risk. The findings are a major step forward in identifying those at high risk for non-small cell lung cancer and for understanding how smoking and genetic factors interact to cause the disease. EurekAlert smerville@mdanderson.org Wed, 02 Apr 2008 04:00:00 GMT http://www.westwoodone.com/pg/jsp/osgood/transcript.jsp?pid=21538 http://tobacco.org/news/262821.html "What this finding means is that some individuals --- who are unfortunately at higher risk for getting lung cancer if they carry the genetic factor --- also may find it more difficult to quit." The gene variations in these new studies could help explain some of the anomalies we all know about: 90-year-old smokers who don't get cancer, for example ... and why some people get hooked on nicotine and some don't. All of these new studies link the variations on Chromosome 15 to lung cancer, says CBS News Medical Correspondent Dr. Emily Senay ... but they disagree as to how it works. The Osgood File Thu, 03 Apr 2008 04:00:00 GMT http://www.timesonline.co.uk/tol/life_and_style/health/article3682615.ece http://tobacco.org/news/262815.html the link was found by three independent teams. These groups, however, differed in their explanations. One attributed the gene's impact to its effect on smoking behaviour, finding that people with the risky version become addicted more easily and smoke more. Another came to the opposite conclusion, finding that the raised risk was independent of tobacco consumption, and applied even to people who have never smoked. Either way, this gene is important. But before it can contribute much to medical research, we are going to have to establish who is right. Locating the gene is a big step forward, but it is only the first of many. It is understanding how it works that will open new approaches to treating lung cancer, or to helping smokers to give up. As a commentary in the journal Nature said this week, our expectations of genetic research need to be managed in the manner of Winston Churchill. The wonderful fruits of whole-genome association studies are not the beginning of the end of the struggle to understand genetic diseases. It is better to think of them as the end of the beginning. Times Of London Fri, 04 Apr 2008 04:00:00 GMT http://www.medicalnewstoday.com/articles/103040.php http://tobacco.org/news/262751.html US researchers report that exposure to cigarette smoke inhibits innate gene expression and impairs alveolar growth in neonatal mice. Sharon McGrath-Morrow from John Hopkin Medical Institute wrote in the American Journal of Respiratory Cell and Molecular Biology that their findings may in part explain the increased incidence of respiratory symptoms in infants and children exposed to cigarette smoke. Infants exposed to cigarette smoke are at higher risk for sudden infant death syndrome, lower respiratory tract infections, and small airway disease, compared with infants not exposed to cigarette smoke, suggesting that perinatal life represents a period of vulnerability during which exposure to cigarette smoke may impair lung immunity and lung growth. To investigate the effects of cigarette smoke exposure on the neonatal lung, the researchers exposed neonatal mice to cigarette smoke for the first 2 weeks of life. Medical News TODAY Mon, 07 Apr 2008 04:00:00 GMT