Lung Cancer
Profiling approach to enable right lung cancer treatment match
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Manchester researchers have tested a new way to genetically profile lung cancer samples, potentially allowing doctors to more easily identify the most appropriate treatment for patients.
Non-small cell lung cancer (NSCLC) represents over 85% of lung cancer cases. The recent introduction of targeted therapies has led to improved patient survival, but only patients whose tumours have a specific genetic change are eligible for such treatments.
Identifying individual patients who may benefit from targeted therapy is becoming an essential part of treatment planning, but many current genetic analysis methods such as next generation sequencing require relatively large amounts of tumour material.
Dr Fiona Blackhall, a senior lecturer in The University of Manchester’s Institute of Cancer Sciences and a consultant based at The Christie NHS Foundation Trust - both part of the Manchester Cancer Research Centre - said: “Unfortunately the biopsy samples we take from these patients are generally quite small. In this study we looked at an alternative genetic screen that utilises a much smaller tissue biopsy to see if it can detect a range of changes in 26 key genes.”
Pfizer lung cancer drug beats chemo for previously untreated patients
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Pfizer Inc’s Xalkori delayed progression of lung cancer longer than chemotherapy in patients who had never previously been treated for the disease, according to results of a late-stage study released on Tuesday.
The medicine, which received U.S. approval in 2011 for lung cancer patients who have a specific gene mutation, had shown in a previous Phase III trial that it significantly delayed disease progression among those who have already undergone chemotherapy for non-small-cell lung cancer, the most common form of the illness.
Pfizer said favorable results from the latest trial, combined with those from the earlier big study, establish that Xalkori is appropriate for first-line as well as second-line use, meaning for patients receiving initial treatment as well as for those who have already undergone chemotherapy.
Moffitt Cancer Center Researchers Find Potential New Therapeutic Target for Treating Non-Small Cell Lung Cancer
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Researchers at Moffitt Cancer Center have found a potential targeted therapy for patients with tobacco-associated non-small cell lung cancer. It is based on the newly identified oncogene IKBKE, which helps regulate immune response.
The study appeared in the Feb. 13 online issue of Oncogene.
The IKBKE gene is part of a family of enzyme complexes involved in increasing cellular inflammation. IKBKE overexpression has been associated with breast and prostate cancers. However, it had not been linked to environmental carcinogen, such as tobacco smoke, until now.
Tobacco smoke is the strongest documented initiator and promoter of lung cancer. The traditional model holds that tobacco components promote carcinogenesis through a process that leads to DNA damage.
Genome-wide scan maps mutations in deadly lung cancers; reveals embryonic gene link
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Scientists have completed a comprehensive map of genetic mutations linked to an aggressive and lethal type of lung cancer.
Among the errors found in small cell lung cancers, the team of scientists, including those at the Johns Hopkins Kimmel Cancer Center, found an alteration in a gene called SOX2 associated with early embryonic development.
“Small cell lung cancers are very aggressive. Most are found late, when the cancer has spread and typical survival is less than a year after diagnosis,” says Charles Rudin, M.D., Ph.D., professor of oncology at the Johns Hopkins Kimmel Cancer Center. “Our genomic studies may help identify genetic pathways responsible for the disease and give us new ideas on developing drugs to treat it.”
The scientists found an increase in the copy number of the SOX2 gene in about 27 percent of small cell lung cancer samples. The resulting overproduction of proteins made by the SOX2 gene may play a role in igniting or sustaining abnormal cell growth in the lung. SOX2 offers a new target for scientists working to develop new drugs to combat this intractable cancer, say the investigators.
Erlotinib improves progression-free survival as first-line therapy in advanced lung cancer
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For patients with advanced lung cancer whose tumors carry EGFR activating mutations, first-line treatment with erlotinib nearly tripled progression-free survival compared to a standard chemotherapy combination, show results from the first prospective Phase-III study to report findings in this setting.
The new results from the OPTIMAL trial were reported at the 35th Congress of the European Society for Medical Oncology (ESMO) in Milan, Italy.
“Erlotinib is very effective and well tolerated in advanced NSCLC patients who harbor EGFR activating mutations. It is 2 to 3 times more effective than doublet chemotherapy,” said study leader Professor Caicun Zhou of Shanghai Pulmonary Hospital, Tongji University, China.
Lung Cancer Culprit Could Offer Target for Therapy
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A tiny molecule that spurs the progression of non-small-cell lung cancer could become a player in fighting the disease, say researchers at UT Southwestern Medical Center, who published a study on how the molecule behaves in mice in the Sept. 14 issue of Cancer Cell.
Scientists have known that the molecule microRNA-21, or miR-21, is present in overabundant quantities in human tumors, including non-small-cell lung cancer (NSCLC). Until now, however, it was unclear whether miR-21 contributed to the development of lung cancer, or whether it was simply an indicator of the presence of the disease.
To find out, lead study author Dr. Mark Hatley, an instructor of pediatric hematology/oncology, and UT Southwestern colleagues used mice that had been altered specifically to harbor non-small-cell lung cancer. In some of these mice, they genetically engineered the animals to produce too much miR-21. In another group, they deleted the miR-21 gene altogether, which eliminated the molecule in the rodents.
Testing lung tumors tailors drug treatments
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Researchers said they helped advanced lung cancer patients fare better by matching their tumors to targeted drugs, in what they said is the first significant trial to show it is possible to choose the best drug for an individual patient.
They tested four so-called targeted therapies in patients with specific biomarkers - mutations that the drugs were designed to counteract.
After eight weeks, 46 percent of the patients on the trial had their tumors grow more slowly or shrink, compared with about 30 percent of usual lung cancer patients.
In Battle Against Lung Cancer, Investigators Eye Oncolytic Virus Therapy
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A virus that destroys cancer cells but leaves normal cells unharmed may offer hope to those affected by squamous cell carcinoma of the lungs (SCC lung cancer), according to investigators from the Cancer Therapy & Research Center (CTRC) at the University of Texas Health Science Center at San Antonio. The CTRC has started patient enrollment in a US Phase 2 clinical trial using intravenous administration of REOLYSIN® in combination with carboplatin and paclitaxel in patients with SCC lung cancer.
REOLYSIN is an experimental treatment derived from a common virus called the reovirus. REOLYSIN directly kills many types of cancer cells and works synergistically with many approved chemotherapies and radiation.
When the reovirus enters a cancer cell, it produces thousands of copies of itself, causing the cell to burst. But the reovirus can replicate only in cancer cells with mutations along a signaling pathway in the cell called the Ras pathway, while leaving normal cells unharmed. Approximately two-thirds of all human cancers express this particular mutation and are therefore a potential target for REOLYSIN treatment.
Men who eat soy may have lower lung cancer risk
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Men who don’t smoke and eat a lot of soy may have a lower risk of lung cancer, according to a new study.
Soy contains isoflavones, which act similarly to the hormone estrogen, and may have anti-cancer qualities in hormone-related cancers of the breast and prostate, the researchers note in the American Journal of Clinical Nutrition. Cells in the lung have properties that suggest they may also respond to isoflavones.
Dr. Taichi Shimazu, of the National Cancer Center in Tokyo, and colleagues studied more than 36,000 Japanese men and more than 40,000 Japanese women, 45 to 74 years old and free of cancer at the start of the study.
Lung Cancer Conference Leaders Honor Paul A. Bunn Jr., M.D.
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The American Association for Cancer Research and the International Association for the Study of Lung Cancer (IASLC) honored Paul A. Bunn Jr., M.D., for his leadership in lung cancer research at the first Molecular Origins of Lung Cancer conference this week. The conference, held from Jan. 11-14, 2010, drew more than 300 people from around the world. Bunn is professor of medicine and the James Dudley chair in cancer research at the University of Colorado, Denver.
“Dr. Bunn has been an inspiration to physicians and scientists working in the field of lung cancer. He deserves this award for everything that he has contributed to this important field past, present and future,” said conference co-chairperson Roy Herbst, M.D., Ph.D., chief of the section of thoracic medical oncology at The University of Texas M. D. Anderson Cancer Center.
Conference co-chairperson David Carbone, M.D., Ph.D., Harold L. Moses chair in cancer research and director of the Specialized Program of Research Excellence in Lung Cancer at Vanderbilt-Ingram Cancer Center, concurred.
A new mouse could help understand how some lung cancer cells evade drug treatment
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Lung cancer is the leading cause of cancer mortality worldwide and lung adenocarcinoma is the most common type. Many cases of lung adenocarcinoma are attributed to a mutation in a gene for the epidermal growth factor receptor (EGFR). Lung cancer with changes in EGFR is initially treatable with a family of chemotherapeutic agents called tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib. However, patients often develop resistance to these drugs through the acquisition of additional changes or secondary mutations that allow cancer cells to evade treatment.
Some secondary mutations to the EGFR gene that allow lung cancer cells to survive in the presence of current chemotherapy are known. These secondary changes are now the focus of targeted efforts to create drugs to specifically interfere with the mutated form of the protein. Unfortunately, in 40% of the cases in which patients become resistant to therapy, the molecular events that confer this resistance are not known. Without knowing the changes that sustain the survival of these cells it remains impossible to specifically and effectively target them with anti-cancer drugs.
Scientists now describe a mouse model of lung cancer that develops resistance to TKI drugs in at least some of the same ways that humans do. Lung cancer occurs in these mice due to a mutation in EGFR that is the same as the mutation that underlies many human lung adenocarcinomas. Some of the defined secondary changes to EGFR, which are known to confer drug resistance in humans, also occur in these mice. But most of these drug resistant mice bear tumors that do not contain known mutations. This important similarity to the human situation suggests that this mouse model might help identify the currently unknown mutations that make lung cancer cells resistant to therapy.
Tiny RNA has big impact on lung cancer tumors
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Researchers from Yale University and Mirna Therapeutics, Inc., reversed the growth of lung tumors in mice using a naturally occurring tumor suppressor microRNA. The study reveals that a tiny bit of RNA may one day play a big role in cancer treatment, and provides hope for future patients battling one of the most prevalent and difficult to treat cancers.
“This is the first time anybody has shown a positive effect of microRNAs in shrinking lung cancer,” said Frank Slack, Ph.D., co-senior author of the paper, researcher at the Yale Cancer Center and professor of molecular, cellular & developmental biology.
The tumors in mice with non-small cell lung cancer shrank after the Yale team delivered an intranasal dose containing a type of micro-RNA called let-7, the authors reported in the Dec. 7 issue of the journal Oncogene. MicroRNAs are small bits of genetic material most often associated with transmission of information encoded in DNA. However in the past decade microRNAs have been shown to play crucial roles in gene regulation and/or gene silencing
Molecule Plays Early Role In Nonsmoking Lung Cancer
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The cause of lung cancer in never-smokers is poorly understood, but a study led by investigators at the Ohio State University Comprehensive Cancer Center and at the National Cancer Institute has identified a molecule believed to play an early and important role in its development.
The findings, published online recently in the Proceedings of the National Academy of Sciences, may lead to improved therapy for lung cancer in both never-smokers and smokers, including those with tumors resistant to targeted drugs such as gefitinib.
The study examined lung tumors from people who had never smoked and found high levels of a molecule called miR-21. The levels were even higher in tumors that had mutations in a gene called EGFR, a common feature of lung cancer in never-smokers.
Common Cold Virus Efficiently Delivers Corrected Gene to Cystic Fibrosis Cells
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Scientists have worked for 20 years to perfect gene therapy for the treatment of cystic fibrosis, which causes the body to produce dehydrated, thicker-than-normal mucus that clogs the lungs and leads to life threatening infections.
Now University of North Carolina at Chapel Hill School of Medicine scientists have found what may be the most efficient way to deliver a corrected gene to lung cells collected from cystic fibrosis patients. They also showed that it may take this high level of efficiency for cystic fibrosis (CF) patients to see any benefit from gene therapy.
Using parainfluenza virus, one of the viruses that causes common colds, the UNC scientists found that delivery of a corrected version of the CFTR gene to 25 percent of cells grown in a tissue culture model that resembles the lining of the human airways was sufficient to restore normal function back to the tissue.
Cancer “culprits” in tobacco smoke revealed
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Scientists have detected two substances in tobacco smoke that directly cause lung cancer, and they said on Sunday the finding may help one day predict which smokers will develop the disease.
They said people with high concentrations in their urine of a nicotine byproduct called NNAL had double the risk of developing lung cancer compared to smokers with lower NNAL concentrations in their urine.
And smokers who had high urine levels of both NNAL and another nicotine by-product called cotinine had more than eight times the risk of lung cancer compared to smokers with the lowest concentrations of these two compounds.
