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Demand for Spanish-language cancer Web materials quadruples

Contact: Beth Bukata
bethb@astro.org
703-431-2332
American Society for Therapeutic Radiology and Oncology

Internet resources and access remain scarce

Although Spanish-speaking cancer patients are rapidly increasing their search for patient education resources on the Internet, there are very few Spanish-language Web sites available to provide this information, according to a study presented October 28, 2007, at the American Society for Therapeutic Radiology and Oncology’s 49th Annual Meeting in Los Angeles.

Spanish-speaking cancer patients were also shown to have more limited access to the Internet compared to English-speaking users of cancer information Web sites, based on the user patterns of the two groups.

“There is an urgent need for more Web-based information to be more available to Spanish-speaking patients with cancer, and Internet access needs to be more widely available,” said Charles Simone II, M.D., lead author of the study and a radiation oncologist at the Hospital of the University of Pennsylvania in Philadelphia. “The increased knowledge gained among these patients will help to eliminate healthcare disparities and lead to improved medical outcomes.”

The Spanish-language cancer information Web site, OncoLink en español, quadrupled their number of unique visitors last year, from 7,000 visitors per month in January 2006 to nearly 29,000 monthly visitors by the end of the year. More than 200,000 users visited the Web site in 2006.

In contrast, the English-language version of the site, OncoLink, had nearly 2 million visitors last year, although their number of unique visitors did not increase throughout the year. OncoLink en espanõl was launched in 2005 by OncoLink, one of the oldest and largest Internet-based cancer information resources. Both sites are managed by the University of Pennsylvania.

The study shows that OncoLink en español users were less likely to browse the Internet during weekends and morning hours, compared to the users who browsed OncoLink, suggesting that they are accessing the Internet more through work or specialized services.

In addition to when they accessed the Internet, OncoLink en español users also differed on the types of cancers they searched for, as well as the timing and method of their Internet search patterns.

“Awareness of these differences can assist cancer education Web sites to tailor their content to best meet the needs of their Spanish-speaking users,” said Dr. Simone.

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The study was carried out using AWStats, a Web-data analyzing program, to collect and compare statistical data from the secure servers of both language versions of OncoLink.

For more information on radiation therapy in English and in Spanish, visit http://www.rtanswers.org.

The abstract, “The Utilization of Radiation Oncology Web-based Resources in Spanish-speaking Oncology Patients,” will be presented for poster viewing starting at 10:00 a.m, Sunday, October 28, 2007. To speak to the study author, Charles Simone, II, M.D, please call Beth Bukata or Nicole Napoli October 28-31, 2007, in the ASTRO Press Room at the Los Angeles Convention Center at 213-743-6222 or 213-743-6223. You may also e-mail them at bethb@astro.org or nicolen@astro.org.

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October 29, 2007 Posted by | Cancer, Cancer Information In Spanish, FMS Global News, Global, Global Health Vision, Global News, London, London UK Feed, Lung Cancer, News, Oncology, Ottawa, Ottawa City Feed, Research, RSS Feed, Spanish, Toronto, Toronto City Feed, Washington DC City Feed | , , , | 7 Comments

Multicenter study nets new lung tumor-suppressor gene

BOSTON–Collaborating scientists in Boston and North Carolina have found that a particular gene can block key steps of the lung cancer process in mice. The researchers report in the journal Nature that LKB1 is not only a “tumor-suppressor” gene for non-small cell lung cancer in mice, it also may be more powerful than other, better-known suppressors. The study will be published on the journal’s Web site on Aug. 5 and later in a print version.

If further research shows LKB1 has a similar effect in human lung cells, it could influence the way non-small cell lung cancer is diagnosed and treated, says the study’s senior author, Kwok-Kin Wong, MD, PhD, of Dana-Farber, one of three institutions, along with Massachusetts General Hospital and the University of North Carolina School of Medicine, leading the work. If tumors with LKB1 mutations are found to be especially fast-growing, for example, patients with such tumors might be candidates for more aggressive therapy.

People born with defective versions of LKB1 often develop Peutz-Jeghers syndrome, which is marked by intestinal growths and an increased risk for certain cancers. Non-inherited mutations of the gene have been found in some lung cancers. This suggested that LKB1 normally thwarts tumors from forming. Mutated versions may be unable to act as a brake on cancer.

To find out, the investigators ran a series of experiments in mice with a defective form of a gene called Kras, which drives the formation and growth of lung cancer. They tracked the development of lung cancer in animals with mutated LKB1 and compared it to the experience of animals with abnormalities in either of two well-known tumor-suppressor genes.

They found that while Kras “cooperated” with the mutated tumor-suppressor genes to produce lung cancer, it cooperated even more strongly with mutated LKB1. “The LKB1-deficient tumors grew more rapidly and spread more frequently than the others, and comprised all three types of non-small cell lung cancer — squamous cell carcinoma, large-cell carcinoma, and adenocarcinoma — rather than just one or two,” Wong says. “This suggests that LKB1 plays a role at major stages of the tumors’ development: initiation, differentiation of normal lung cells into cancer cells, and metastasis.”

An examination of human non-small-cell lung tissue suggests LKB1 mutations play a role there as well. Of 144 samples analyzed, 34 percent of the lung adenocarcinomas and 19 percent of the squamous cell carcinomas contained abnormal versions of the gene, researchers report.

“We were surprised at how significant a role LKB1 mutations play in non-small cell lung cancer development in mice,” say Wong, who is also an assistant professor of medicine at Harvard Medical School. “This suggests there may be additional lung tumor-suppressor genes yet to be discovered. We’re currently examining whether these results apply to human lung cancers as well and, if so, how such information can improve treatment.”

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The lead author of the study was Hongbin Ji, PhD, of Dana-Farber. Other Dana-Farber co-authors include Dongpo Cai, PhD, Liang Chen, PhD, Pasi Janne, MD, PhD, Bruce Johnson, MD, Jussi Koivunen, MD, PhD, Danan Li, Mei-Chih Liang, PhD, Kate McNamara, Matthew Meyerson, MD, PhD, Samanthi Perera, PhD, Geoffrey Shapiro, MD, PhD, and Takeshi Shimamura, PhD. Other authors were based at Children’s Hospital Boston, Brigham and Women’s Hospital, Broad Institute of Harvard University and Massachusetts Institute of Technology, University of Tennessee Health Science Center, and the University of Texas Southwestern Medical Center.

The research was supported by the National Institutes of Health, the Sidney Kimmel Foundation for Cancer Research, the American Federation of Aging, the Joan Scarangello Foundation to Conquer Lung Cancer, the Flight Attendant Medical Research Institute, the Waxman Foundation, the Harvard Stem Cell Institute, and the Linda Verville Foundation.

Dana-Farber Cancer Institute (www.dana-farber.org) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute.

Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute

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August 5, 2007 Posted by | Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Cancer, Cancer Biology, France, Genes, Genetic, Genetic Link, Genetics, Genome, Genomic, Germany, Global, Global Health Vision, Global News, Health Canada, Human Genome, LKB1, Lung Cancer, Medical History, Medical Journals, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, NIH, Peutz-Jeghers syndrome, University of North Carolina, World News | 2 Comments

U-M researchers find family of ‘on switches’ that cause prostate cancer

Gene fusions trigger cancer growth, could impact treatment choices

ANN ARBOR, Mich. — Researchers at the University of Michigan Comprehensive Cancer Center have discovered how genes turn on the switch that leads to prostate cancer.

The team discovered that pieces of two chromosomes can trade places with each other and cause two genes to fuse together. The fused genes then override the “off” switch that keeps cells from growing uncontrollably, causing prostate cancer to develop.

By testing these gene fusions in mice and in cell cultures, the researchers showed that the fusions are what cause prostate cancer to develop. But it’s not just one set of genes that fuse. The researchers found that any one of several in a family of genes can become scrambled and fuse. Results of the study appear in the Aug. 2 issue of Nature.

“Each of these switches, or gene fusions, represent different molecular subtypes. This tells us there’s not just one type of prostate cancer. It’s a more complex disease and potentially needs to be treated differently in each patient,” says lead study author Arul Chinnaiyan, M.D., Ph.D., director of the Michigan Center for Translational Pathology, a new U-M center whose goal is to translate research into real world practice.

The gene fusion research is the centerpiece project of the new center. In the current study, researchers found one of several abnormal gene fusions in the prostate cancer tissue samples they tested. In 2005, the researchers identified a prostate-specific gene called TMPRSS2, which fuses with either ERG or ETV1, two genes known to be involved in several types of cancer.

The Nature paper reports on five additional genes that fuse with ERG or ETV1 to cause prostate cancer. Gene fusions were involved in 60 percent to 70 percent of the prostate cancer cell lines the researchers looked at. The genes involved are all controlled by a different mechanism. For example, four of the genes are regulated by androgen, a male sex hormone known to fuel prostate cancer. Androgen deprivation is a common therapy for prostate cancer.

Knowing which gene fusion is involved in an individual patient’s tumor could impact treatment options. If an androgen-regulated gene is involved, androgen therapy would be appropriate. But if the gene fusion involves a gene that represses androgen, the anti-androgen therapy could encourage the cancer’s growth. This may also explain why androgen treatment is not effective for some prostate cancers.

“Typing someone’s prostate cancer by gene fusion can affect the treatment given. We would not want to give androgen to someone whose prostate cancer gene fusion is not regulated by androgen,” says Chinnaiyan, who is the S.P. Hicks Collegiate Professor of Pathology at the U-M Medical School.

Rearrangements in chromosomes and fused genes are known to play a role in blood cell cancers like leukemia and lymphoma, and in Ewing’s sarcoma. A fused gene combination that plays a role in chronic myelogenous leukemia led researchers to develop the drug Gleevec, which has dramatically improved survival rates for that disease.

Chinnaiyan believes the prostate gene fusions will eventually lead to similar treatments for prostate cancer.

“More immediately, we hope to develop tests for diagnosis or prognosis. But long-term, we hope this will lead to better therapies to treat prostate cancer. The key challenge is to find a drug that would go after this gene fusion,” Chinnaiyan says.

The gene fusion technology has been licensed to San Diego-based Gen-Probe Inc., which is working on a screening tool to detect gene fusions in urine. The tool could one day supplement or replace the prostate specific antigen, or PSA, test currently used to screen for prostate cancer.

The idea of translating laboratory research findings into a test or treatment that will impact patients is central to the new Michigan Center for Translational Pathology. The center brings together experts in genomics, proteomics and bioinformatics to look at common patterns and potential targets in cancer and other diseases. This is the first center of its kind in the nation in that it is associated with one of 39 National Cancer Institute-designated “comprehensive” cancer centers, a premier medical school and a large health system with both clinicians and patients.

The center’s goal is to study the genes, proteins and other markers on cells to develop new diagnostic tests or screening tools as well as targeted treatments for cancer and other diseases, with the key being to translate these laboratory discoveries into clinical applications.

Chinnaiyan and his team have received numerous awards and honors, including the American Association for Cancer Research Team Science Award for their previously published work on gene fusions, and the Specialized Program of Research Excellence Outstanding Investigator award. The new Center for Translational Pathology supported in part by the Prostate Cancer Foundation, which has offered to match up to $1 million dollars in donations to support work related to developing therapies against prostate cancer gene fusions at the university.

“Mapping of the human genome was only the beginning. Equipped with the comprehensive analysis of the human genome, we can now systematically examine the blueprint of disease at the molecular level. This essential knowledge may lead to better diagnostic tests and promising new treatments for cancer, cardiovascular disease, diabetes and other illnesses,” Chinnaiyan says.

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For information about the Michigan Center for Translational Pathology, go to http://www.med.umich.edu/mctp.

About 218,890 men will be diagnosed with prostate cancer this year, and 27,050 will die from the disease, according to the American Cancer Society. The gene fusion work is not currently available for treatment or diagnosis, and no clinical trials are currently recruiting. For information about prostate cancer and currently available treatments, go to http://www.mcancer.org or call the U-M Cancer AnswerLine at 800-865-1125.

In addition to Chinnaiyan, U-M study authors were Scott Tomlins; Saravana Dhanasekaran, Ph.D.; Bharathi Laxman; Qi Cao; Beth Helgeson; Xuhong Cao; David Morris, M.D.; Anjana Menon; Xiaojun Jing; Bo Han; James Montie, M.D.; Kenneth Pienta, M.D.; Diane Roulston; Rajal Shah, M.D.; Sooryanarayana Varambally, Ph.D.; and Rohit Mehra, M.D. Mark Rubin, M.D., from Brigham and Women’s Hospital, Dana-Farber Cancer Institute and Harvard Medical School is also a study author.

Funding for the study came from the U.S. Department of Defense, the National Institutes of Health, the Early Detection Research Network, the Prostate Cancer Foundation and Gen-Probe Inc.

The University of Michigan has filed for a patent on the detection of gene fusions in prostate cancer, on which Tomlins, Mehra, Rubin and Chinnaiyan are co-inventors. The diagnostic field of use has been licensed to Gen-Probe Inc. Chinnaiyan also has a sponsored research agreement with Gen-Probe; however, GenProbe has had no role in the design or experimentation of this study, nor has it participated in the writing of the manuscript.

Reference: Nature, Vol. 448, No. 7153, Aug. 2, 2007

Contact: Nicole Fawcett
nfawcett@umich.edu
734-764-2220
University of Michigan Health System

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August 1, 2007 Posted by | acute lymphoblastic leukemia, Alberta, Baltimore, Barcelona, Bethesda, Calgary, Canada, Cancer, Cancer Biology, Cancer Biology and Therapy, Chemotherapy, Childhood Lukemia, France, Genes, Genetic, Genetic Link, Genetics, Genome, Genomic, Germany, Global, Global Health Vision, Global News, Health Canada, Human Genome, Irvine, Italy, Japan, journal Nature Genetics, Leukemia, Lung Cancer, Medical Journals, Nature Genetics, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, non-Hodgkin's lymphoma, Nova Scotia, Oncology, Osaka, Ottawa, Prince Edward Island, Public Health, Quebec, Research, RSS, RSS Feed, Slovakia, Spain, Toronto, UK, University of Michigan, US, Virginia, Washington DC, Washington DC City Feed, World News | 3 Comments

Tobacco industry efforts to derail effective anti-smoking campaigns

Anti-smoking ads that reveal the tobacco industry’s deceptive practices have been aggressively quashed through various methods found Temple University Assistant Professor Jennifer K. Ibrahim, co-author of an analysis in the August issue of the American Journal of Public Health.

In the article, Ibrahim tracks the rise and fall of state and national efforts to curb smoking for the past 40 years. She chronicles industry strategies to prevent a campaign’s creation, steer messages to smaller audiences, limit the content of the message, limit or eliminate the campaign’s funding, and pursue litigation against the campaign. Ibrahim looks at campaigns in Minnesota, California, Arizona, Oregon, Florida, and a national campaign from the American Legacy Foundation.


This billboard was part of a weak media campaign in Michigan after Gov. John Engler’s political staff took control of the campaign, excluding the state health department’s staff from any…

“It tells the story behind the smoke. People often judge these ads and now you know what the tobacco industry was doing trying to undermine them,” Ibrahim said.

Research has found ads that reveal the deceptive practices of the tobacco industry are the most effective media campaigns that reduce smoking rates, she said.


This billboard ad from California in 2001 is considered a more effective message to reduce smoking rates.

For example, one billboard in California read “Tobacco is legal, profitable, and kills people” featuring an alligator labeled big tobacco with a smirk saying “Two out of three’s not bad.”

However, these messages aren’t always getting out there because of the money spent by the tobacco industry to eliminate them, said Ibrahim, an assistant professor of public health.

State health departments face an uphill battle when dealing with the political clout of the industry with its lobbying, campaign contributions and specials events, Ibrahim said.

One tactic also involves the industry producing its own ineffective campaigns in order to portray state programs as duplicative and a waste of public dollars. Campaigns designed by the tobacco companies patronize youth in their early teen years, with messages like “Think, Don’t smoke”, Ibrahim said.

In contrast, Florida’s “truth” anti-smoking campaign empowered them by giving them information about how the tobacco industry tried to manipulate by marketing.

The tobacco industry has spent more money in advertising in light of successful media campaigns that target large audiences.

From 1975 to 2003, tobacco industry expenditures in advertising and promotion grew from $491 million to $15.5 billion. During this period, the percentage of smokers in the United States fell from about 37 percent to 22 percent, according to the Behavioral Risk Factor Surveillance System.

Attitudes are changing as the public is becoming more aware about the dangers of smoking, secondhand smoke, and the deceptive practices of the industry, Ibrahim said.

While the numbers offer some promise, more initiatives are needed to keep anti-smoking efforts alive.

“It’s naïve to think the industry is still not following these practices and preparing tactics to respond,” Ibrahim said.

The Master Settlement Agreement in 1998 marked an important step when seven tobacco companies agreed to change the way tobacco products are marketed, release previously secret industry documents, dispand trade groups, and pay the states an estimated $206 billion. The tobacco companies also agreed to finance a $1.5 billion public anti-smoking campaign.

States’ attorney generals continue to enforce the provisions of the agreement, Ibrahim said.

A recent product that has created uproar is Camel’s No. 9s pink cigarettes that public health advocates say target teenage girls not women. In June, congress sent a letter to the editors of 11 major magazines, from Glamour to Cosmopolitan, requesting them to stop running the ads for the cigarettes.

Aggressive efforts to battle current marketing efforts and litigation from the tobacco industry are vital to keep the best media campaigns from disappearing, Ibrahim said.

“The efforts put forth by California and the American Legacy Foundation as they pursued legal battles with tobacco companies provide a good example of the tenacity needed to successfully defend and promote tobacco control campaigns,” said Ibrahim. “Persistence can pay off. We need to go with campaigns that work,”

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The research was funded by the National Cancer Institute. For the article, Ibrahim collected the data, conducted the analysis, and drafted the article. Co-author Stanton A. Glantz from the Center for Tobacco Control Research and Education at the University of California, San Francisco, supervised the data collection, edited and revised the article.

Contact: Anna Nguyen
anna.nguyen@temple.edu
215-707-1731
Temple University

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July 11, 2007 Posted by | Alberta, American Journal of Public Health, American Legacy Foundation, Baltimore, Barcelona, Bethesda, Calgary, Cancer, COPD, Global, Global Health Vision, Global News, Italy, Japan, Lung Cancer, Medical Journals, National Cancer Institute, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, Osaka, Ottawa, Pennsylvania, RSS, RSS Feed, Slovakia, Spain, Temple University, Toronto, Uncategorized, Virginia, WASHINGTON, Washington DC, Washington DC City Feed, World News | Leave a comment

Gene variations directly link inflammation to an increased risk for lung cancer

Contact: Greg Lester
lester@aacr.org
267-646-0554
American Association for Cancer Research

Variations in two genes related to inflammation may be a major risk factor for developing lung cancer, according to a team of scientists from the National Cancer Institute and the University of Texas M. D. Anderson Cancer Center. The effect of these genes is especially strong among heavy smokers, suggesting that the inflammatory response is important in modulating the damage caused by tobacco smoke.

Their study, published in the July 1 issue of Cancer Research, a publication of the American Association for Cancer Research, is the first to pinpoint the mechanism by which damage to the lung might trigger an overzealous inflammatory response by the immune system, leading to lung cancer. The variants, or polymorphisms, were found in genes for interleukin 1A and interleukin 1B, two signaling molecules that immune system cells secrete in response to infection or tissue damage.

“Our findings help explain how heavy smoking, for example, combines with a genetic predisposition to create a besieged environment within the lungs,” said lead author Eric Engels, M.D., MPH, researcher at the Viral Epidemiology Branch of the NCI’s Division of Cancer Epidemiology and Genetics. “Essentially, sustained inflammation alters the microenvironment of the lung tissue, damaging cells and altering DNA.”

Inflammation is part of the immune system’s arsenal to combat the effects of infection and cell damage. However, prolonged or intense inflammation could lead to conditions within the lung environment that foster cancer, Engels said. Previous studies have shown that diseases associated with lung damage, such as tuberculosis and asthma, increase the risk of developing lung cancer. Likewise, exposure to tissue-damaging substances like silica and asbestos, inhaled into the lungs, has also been shown to increases lung cancer risk.

“Inflammation has long been thought to be a factor in many cancers, including lung cancer, and could provide an explanation how damage to lung tissue leads to cancer,” Engels said. “Knowing more about the downstream effects of these polymorphisms, and discovering others like them, will increase our understanding of how some people are predisposed to developing cancer.”

To examine the relationship between inflammation and lung cancer risk, the researchers compared differences in genes related to inflammation between more than 1,500 lung cancer patients and 1,700 controls at M. D. Anderson Cancer Center in Houston, Texas. More than 80 percent of the cancer patients in the study were current or former smokers. Among the 59 variations in 37 inflammation-related genes studied, the researchers discovered that some variants in the genes for interleukin (IL) 1A and 1B, are found more frequently in patients with lung cancer — and especially among heavy smokers. The effect was most profound in polymorphisms in IL1B, which is central to the inflammation process, the researchers said.

According to Engels, the IL1B protein is an integral part of the chemical cascade by which cell signals moderate the response to inflammation. Variations in the gene may lead to greater expression of the protein, which is more likely to turn on the cascade and sustain the damaging effects of inflammation. Over time, the constant damage of inflammation could lead to genetic damage and cancer, Engels said.

The researchers believe their findings will provide the basis for further lung cancer research as well as a model for examining the nature of inflammation in other types of cancer.

“While smoking is still the greatest risk factor, we still do not understand how other factors play a role,” Engels said. “A better understanding of the risks involving inflammation will lead to a better understanding of cancer prevention.”

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July 4, 2007 Posted by | Alberta, American Association for Cancer Research, Baltimore, Barcelona, Bethesda, Calgary, Cancer, Global, Global Health Vision, Global News, Lung Cancer, Medical Journals, News, News Australia, News Canada, News Israel, News Jerusalem, News UK, News US, News USA, Research, Slovakia, Spain, Virginia, WASHINGTON, Washington DC, World News | Leave a comment