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    Why Would An 18-Year-Old Who Never Smoked Get Lung Cancer? The Answer
    By News Staff | May 29th 2014 09:42 AM | Print | E-mail | Track Comments
    In the pop culture world of mainstream media, magic bullets are common. Every week there is a new miracle vegetable and then the following work there will be scare journalism about some chemical.

    In the world of magic bullets, smoking causes lung cancer. Yet science knows that a risk factor is not genetic determinism. If lung cancer among non-smokers were itemized separately from smokers, it would be in the top 10 killers all on its own, and shockingly few smokers get lung cancer compared to the hundred million who are smoking just in America.

    Cancer happens. But when an 18-year-old who never smoked gets lung cancer, scientists are going to tackle that mystery. Investigators from the Montefiore Einstein Center for Cancer Care will present discovery of a new gene alteration that can aid in detection and treatment of certain lung cancers and insights into lung cancer patient populations, at the 50th Annual Meeting of the American Society of Clinical Oncology (ASCO) June 3rd in Chicago.

    Lead author Haiying Cheng, M.D., medical oncologist and assistant professor at the Albert Einstein College of Medicine, identified amplification of RICTOR, a key component of the mTOR protein complex that regulates cell proliferation and cytoskeleton organization, as a new genomic alteration in an 18-year-old lung cancer patient who never smoked.

    That initial finding was further explored in a next generation sequencing database of lung cancer patients and RICTOR amplification was found in 8.2 percent (92/1,128) of cases. In 11 percent (10/92) of those cases, RICTOR amplification was the only potentially actionable target. Based on these data, RICTOR amplification may identify a new subgroup of lung cancer patients responsive to molecularly targeted therapy. 

    “The discovery of the amplification of RICTOR is important as nearly half of lung cancers do not have a known oncogenic driver,” said co-author Roman Perez-Soler, M.D., chairman of the Department of Medical Oncology at Montefiore and professor at Einstein. “RICTOR signaling also has been suggested to play a critical role in regulating cancer cell migration, invasion and metastasis in breast, ovarian and colorectal cancers. Consequently, we see great potential for new diagnosis and treatment opportunities and look forward to continuing our research in this area.”

    Source:  Montefiore Einstein Center for Cancer Care