The research from a study funded by LCRF has assisted researchers at the Translational Genomics Research Institute (TGen) to discover a protein, Mcl-1, that helps enable one of the most common and deadly types of cancer to survive radiation and drug treatments.
News
Tissue analysis near tumors holds promise for earlier detection, new treatments
MD Anderson News Release 03/07/2014
Seemingly healthy cells may in fact hide clues that lung cancer will later develop, according to a study led by researchers at The University of Texas MD Anderson Cancer Center The research is published online in the Journal of the National Cancer Institute.
Examination of gene expression in patients with non-small cell lung cancer (NSCLC) showed the area adjacent to tumors is rich with cancer markers. In addition, researchers discovered the previously unknown role of a cancer-promoting gene in the airways of smokers with lung cancer.
“We believe this study has a “double whammy” application,” said study lead author Humam Kadara, Ph.D., assistant professor, Translational Molecular Pathology at MD Anderson. “These cancer-associated changes that distinguish the airways of smokers with lung cancer and healthy smokers may help us diagnose lung cancer earlier and develop more effective strategies for treatment.”
Field cancerization may yield answers
Lung cancer is the leading cause of cancer death in men and women in the United States. The American Cancer Society estimates more than 224,000 cases are diagnosed each year, and more than 159,000 people die of the disease. Almost 90 percent of lung cancers are NSCLC.
Symptoms of lung cancer usually don’t appear until the disease is advanced and untreatable. Although it’s believed to start as pre-cancerous changes in the lung, little is known about those changes that lead to lung cancer.
Field cancerization (FC) is a phenomenon in which large areas of cells are affected by a cancer-causing event, such as smoking. This is the first effort to comprehensively examine gene expression, known as the transcriptome, of the adjacent airway field cancerization in NSCLC.
Previous research, including pioneering work at MD Anderson by this study’s senior author Ignacio Wistuba, M.D., and others, has shown normal-appearing tissue close to lung premalignant and cancer lesions may have tumor-associated molecular abnormalities. And it’s known cigarette smoke induces widespread cellular changes and premalignant lesions in the lungs of smokers.
Potentially cancer-causing genes discovered
The study included 20 patients with stages I to III NSCLC, including five non-smokers and 15 smokers. Various genetic testing methods were used to examine lung tumors, uninvolved lung tissue and normal-appearing airways located varying distances from the tumors.
Researchers identified 1,661 differentially expressed gene features between tumors and airways compared with normal lung tissue. A subset of these changes was much more prevalent in lung-cancer patients than cancer-free smokers.
In addition, 422 genes, and key cancer-associated signaling pathways, were progressively expressed in airways, with a more intense presence closer to the tumor and tapering at further distances. This gradient site-dependent effect is consistent with NSCLC expression patterns.
Furthermore, higher levels of LAPTM4B, a gene that has been found in liver, lung, breast, ovarian and gastric cancers, were found in airways closer to tumors. It also aids in autophagy, a self-cannibalization mechanism that helps cells survive. LAPTM4B overexpression can cause resistance to certain types of chemotherapy.
“This is the first time the role of this gene in lung cancer has been studied,” Kadara said. “It was highly over-expressed in adjacent normal cells, indicating the possibility of future detection and treatment strategies.”
Larger studies of other lung cancer subtypes planned
The research group plans to move forward with more-advanced technology and larger populations to investigate field cancerization in other lung cancer subtypes, such as small-cell lung cancer, in smokers and in lung cancers that develop in non-smokers.
“We’re just beginning to understand the relevance of airway field cancerization to lung cancer detection and development of treatment and prevention strategies,” Kadara said.
Other MD Anderson researchers included Wistuba, who chairs Translational Molecular Pathology, holds the Anderson Clinical Faculty Chair for Cancer Treatment and Research and has an appointment in Thoracic/Head and Neck Medical Oncology; Junya Fujimoto, M.D., Ph.D., Yuho Maki, M.D. Ph.D., Melinda M. Garcia, Chi-Wan Chow, D.V.M., Zuoming Chu and Gabriella Mendoza, of Translational Molecular Pathology; Mohamed Kabbout, Ph.D., and Waun Ki Hong, M.D., of Thoracic/Head and Neck Medical Oncology; Neda Kalhor, M.D., and Cesar Moran, M.D., of Pathology; Suk-Young Yoo, Ph.D., Li Shen, Jing Wang, Ph.D., and Kevin Coombes, Ph.D., of Bioinformatics.
Also on the team were Adam Gower, Ph.D., and Avrum Spira, M.D., of Computational Medicine at Boston University.
This work was funded in part by grants from the Lung Cancer Research Foundation, the Jimmy Lane Hewlett Lung Cancer Research Fund, National Cancer Institute lung cancer SPORE grant (P50 CA70907), Department of Defense grants and MD Anderson’s NCI Cancer Center Support grant (CA16672).
Reposted from: http://www.mdanderson.org/newsroom/news-releases/2…
CVS/pharmacy will stop selling cigarettes and all tobacco products at its more than 7,600 stores nationwide by October 1, 2014
Ending the sale of cigarettes and tobacco products at CVS/pharmacy is simply the right thing to do for the good of our customers and our company. The sale of tobacco products is inconsistent with our purpose – helping people on their path to better health.
As the delivery of health care evolves with an emphasis on better health outcomes, reducing chronic disease and controlling costs, CVS Caremark is playing an expanded role through our 26,000 pharmacists and nurse practitioners. By removing tobacco products from our retail shelves, we will better serve our patients, clients and health care providers while positioning CVS Caremark for future growth as a health care company. Cigarettes and tobacco products have no place in a setting where health care is delivered. This is the right thing to do.
Watch the videos and learn more: http://www.cvshealth.com/newsroom/message-larry-me…
Fifty years ago today, Dr. Luther Terry released the landmark Surgeon General’s Report – the first of its kind on smoking and health – concluding that smoking causes lung cancer.
In the five decades since, we’ve learned: that smoking damages nearly every organ in the body; it is responsible for an enormous burden of disease, death and economic cost in the United States; and, exposure to secondhand smoke can have devastating health consequences. Yet, since this first report was released, we’ve also shifted the perception of smoking from an accepted national pastime to a discouraged threat to health – and more than halved smoking rates in this country.
Later this month, we will release a new Surgeon General’s Report that will highlight 50 years of progress in tobacco control and prevention, present new data on the health consequences of tobacco use, and detail initiatives that can end the tobacco epidemic in the United States.
While significant progress has been made over the last 50 years, the battle is not yet won. I am extremely proud of the Obama Administration’s tobacco control record – from expanding access to cessation services without cost-sharing through the Affordable Care Act, to giving the Food and Drug Administration comprehensive authority to regulate tobacco products through the Tobacco Control Act. But ending the devastation of tobacco-related illness and death is not in the jurisdiction of any one entity. To end the tobacco epidemic, we must enlist all sectors of society to share in this responsibility. Together we can make the next generation tobacco-free.
To read Acting Surgeon General Dr. Boris D. Lushniak’s statement visit: http://www.hhs.gov/news/press/2014pres/01/20140110c.html
To read CDC Director Dr. Tom Frieden’s statement visit: http://www.hhs.gov/news/press/2014pres/01/20140110d.html
An update of the 2004 U.S. Preventive Services Task Force (USPSTF) recommendation on screening for lung cancer.
Methods: The USPSTF reviewed the evidence on the efficacy of low-dose computed tomography, chest radiography, and sputum cytologic evaluation for lung cancer screening in asymptomatic persons who are at average or high risk for lung cancer (current or former smokers) and the benefits and harms of these screening tests and of surgical resection of early-stage non–small cell lung cancer. The USPSTF also commissioned modeling studies to provide information about the optimum age at which to begin and end screening, the optimum screening interval, and the relative benefits and harms of different screening strategies.
Population: This recommendation applies to asymptomatic adults aged 55 to 80 years who have a 30 pack-year smoking history and currently smoke or have quit within the past 15 years.
Recommendation: The USPSTF recommends annual screening for lung cancer with low-dose computed tomography in adults aged 55 to 80 years who have a 30 pack-year smoking history and currently smoke or have quit within the past 15 years. Screening should be discontinued once a person has not smoked for 15 years or develops a health problem that substantially limits life expectancy or the ability or willingness to have curative lung surgery. (B recommendation)
Learn more: http://annals.org/article.aspx?articleid=1809422#S…
Dr. Donald Kufe was recently awarded a $2.7mm, 5-year NCI grant to further his research on the MUC1-C oncoprotein. LCRF is proud to have supported the pilot studies that made this grant possible.
Read Dr. Kufe’s article about MUC1-C in Molecular Cancer Therapeutics.
Faye Johnson received her bachelor’s degree in biology from the Johns Hopkins University and then her MD from the University of Texas – Houston in 1996. During her graduate work, she studied the role of b (1,4) galaltosyltransferase in cancer metastasis – receiving her PhD in Cancer Biology from the University of Texas Graduate School of Biomedical Sciences in 1996. After completing residency in Internal Medicine at the Baylor College of Medicine she completed a fellowship in Medical Oncology at the University of Texas MD Anderson Cancer Center where she later joined the faculty in 2003.
Dr. Johnson is currently an associate professor and physician-scientist in the department of Thoracic, Head and Neck Medical Oncology. She has integrated laboratory, clinical, and translational work to develop studies of signal transduction in lung and head and neck cancers with the goal to improve therapy for cancer patients. In this regard, she has focused on defining the biological effects of inhibiting therapeutic targets such as Src, Met, Ephrins, and Plk1 and pathways of resistance. She has conducted research projects in the laboratory with complementary clinical trials designed to validate and advance her laboratory findings and improve patient survival.
In the current research, Dr. Johnson’s preliminary data shows that Plk1 inhibitors hold great promise because of a subset of exquisitely sensitive NSCLC cell lines and patients indicating that she will be able to define a subpopulation of sensitive patients and define the underlying molecular mechanisms of sensitivity.