Colonic Polyps

March is Colorectal Cancer Awareness Month and incidence rates of early onset colorectal cancer are on the rise CENTER VALLEY, Pa., March 5, 2024 /PRNewswire/ -- As the American Cancer Society reports an increase in death rates from colorectal cancer for patients under the age of 50,1 Olympus Corporation of the Americas and the Colorectal Cancer Alliance (CCA) offer a reminder about the importance of preventive screenings and knowing your family health history. Continue Reading During Colorectal Cancer Awareness Month, Olympus Corp. of the Americas and the Colorectal Cancer Alliance are offering a reminder about the importance of preventive screenings and knowing your family health history. During Colorectal Cancer Awareness Month in March, Olympus and CCA are asking people to take an active role in their healthcare by learning about the recommended screening age and screening options, engaging their primary care providers (PCPs) in those discussions and being aware of family health history. More than 20 years ago, colorectal cancer (CRC) was known to be the fourth-leading cause of cancer death in men and women under the age of 50, according to the American Cancer Society. Now, CRC is the leading cause of cancer death for men under the age of 50 and the second leading cause for women under 50. Since 2015, incidence rates of CRC in adults younger than 55 have increased by 1% to 2% annually.1 Marking the importance of knowing one's family health history is the fact that nearly one in three people diagnosed with CRC before age 50 have a family history or genetic predisposition. A history of CRC in first-degree relatives such as a parent or sibling increases the risk of developing cancer.2 Colonoscopy Guidelines and the Importance of the PCP The U.S. Preventive Services Task Force (USPSTF) in 2021 lowered its recommended screening age for those at average risk of CRC from 50 to 45.3 Gastroenterologists support the lowered screening age,4 and Olympus supports the USPSTF guidelines for CRC screening beginning at age 45, evidence-based recommendations with relevance in the presence of increased early-onset CRC incidence. Screening modalities include colonoscopy, which allows physicians to remove polyps that could develop into cancer.5 There are other screening options, including a fecal immunochemical test (FIT), which checks for hidden blood in the stool from the lower intestines. Such a test must be done every year, and a colonoscopy will be necessary if the test returns abnormal results.6 The best screening option, however, is the one someone is willing and able to get done, and Olympus encourages people to have those discussions with their PCP. A recent study looked at the key role PCPs play in offering screenings particularly among underserved populations. The study reviewed patients at safety-net hospital systems diagnosed with CRC between the ages of 50 and 75 and found that those with a primary care doctor had significantly reduced odds of late-stage CRC. 7 Early detection is key as the 5-year relative survival rate is about 90% when caught at a localized stage and about 73% when detected at a regional stage.8 Silver Lining: Technology Improvements Support Higher Adenoma Detection Rates The American Cancer Society reports that CRC deaths have been dropping in older adults for decades likely, in part, due to screenings such as colonoscopy that find polyps before they can develop into cancer or finding cancer earlier when it's more treatable.9 Olympus technologies like Texture and Color Enhancement Imaging (TXI™) technology, which leads to improved visibility of potential lesions, are helping physicians to potentially reduce miss rates for early mucosal changes.10 A study evaluating the use of TXI technology on polyp detection during screening colonoscopies found that TXI technology significantly increased ADR and increased the number of adenomas found by physicians measuring 5mm or larger, as compared to those found during a procedure using high-definition white-light endoscopy. ADR was also higher with TXI technology (as compared to white light) in patients who were being screened as a result of a positive non-invasive test or due to a history of polyps or bowel cancer.11 TXI technology is not intended to replace histopathological sampling as a means of diagnosis but is an adjunctive tool for endoscopic examination that can be used to supplement Olympus white light imaging. But technologies that help improve preventive screenings are most effective when a patient takes the time and care to prepare for their colonoscopy. "Technologies like TXI are valuable tools in the fight to prevent colon cancer. One of the most effective tools in the fight, however, is the commitment to taking control of your health," said Dr. John de Csepel, Chief Medical Officer, Olympus Corp. "Talk to your doctor about your health history and risks and the screening options that are best for you. Should you decide that a colonoscopy is the right choice, make sure to focus on your prep, so your gastroenterologist can get the best results possible. Colorectal cancer is preventable, and the power to prevent it rests in your hands." About Olympus At Olympus, we are committed to Our Purpose of making people's lives healthier, safer and more fulfilling. As a global medical technology company, we partner with healthcare professionals to provide best-in-class solutions and services for early detection, diagnosis and minimally invasive treatment, aiming to improve patient outcomes by elevating the standard of care in targeted disease states. For more than 100 years, Olympus has pursued a goal of contributing to society by producing products designed with the purpose of delivering optimal outcomes for its customers around the world. Olympus Corporation of the Americas, a wholly owned subsidiary of Olympus Corporation, is headquartered in Center Valley, Pennsylvania, USA, and employs more than 4,500 employees throughout locations in North and South America. For more information, visit olympusamerica.com. 1 "Cancer statistics, 2024," CA: A Cancer Journal for Clinicians." Pub. Jan. 17, 2024 2 American Cancer Society, "Colorectal Cancer Risk Factors." Rev. July 2023 3 U.S. Preventive Services Task Force, "Final Recommendation Statement, Colorectal Cancer: Screening." May 18, 2021. 4 American Gastroenterological Assoc., "GI Societies support starting CRC screening in mid-to-late 40s." May, 18 2021 5 Centers for Disease Control and Prevention, "Basic Information About Colorectal Cancer." Rev. February 2023 6 American Cancer Society, "Colorectal Cancer Screening Tests." Rev. June 2020 7 Dimaano, K.; Croman, M.; Montero, S., et al, "Engaging primary care physicians is critical in the screening and diagnosis of colorectal cancer at safety-net hospital systems." Surgery Open Science, pub. January 2024 8 American Cancer Society, "Survival Rates for Colorectal Cancer." Rev. Jan. 17, 2024 9 American Cancer Society, "Key Statistics for Colorectal Cancer." Rev. Jan. 17, 2024 10 Data on file with Olympus (DC00489968) 11 Young, E.; Rajagopalan, A.; Tee, D., et al, "Texture and Color Enhancement Imaging Improves Colonic Adenoma Detection: A Multicenter Randomized Controlled Trial." Gastroenterology AGA Journal, pub. October 2023 SOURCE Olympus Corporation of the Americas

Hard-to-detect colorectal pre-cancerous lesions known as serrated polyps, and the aggressive tumors that develop from them, depend heavily on the ramped-up production of cholesterol, according to a preclinical study. The finding points to the possibility of using cholesterol-lowering drugs to prevent or treat such tumors. Hard-to-detect colorectal pre-cancerous lesions known as serrated polyps, and the aggressive tumors that develop from them, depend heavily on the ramped-up production of cholesterol, according to a preclinical study from researchers at Weill Cornell Medicine. The finding points to the possibility of using cholesterol-lowering drugs to prevent or treat such tumors. In the study, published Oct. 13 in Nature Communications, the researchers analyzed mice that develop serrated polyps and tumors, detailing the chain of molecular events in these tissues that leads to increased cholesterol production. They confirmed their findings in analyses of human serrated polyps and tumors, and showed in mouse models that replicate the human cancer that blocking cholesterol production prevented the progression of these types of intestinal tumors. "Serrated-type polyps and tumors currently are not treated differently from other colorectal neoplasias, but as our work shows, they have this specific metabolic vulnerability that can be targeted," said study co-senior author Dr. Jorge Moscat, a Homer T. Hirst III Professor of Oncology in Pathology, Vice-Chair for Cell and Cancer Pathobiology in the Department of Pathology and Laboratory Medicine and a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine. The other co-senior author is Dr. Maria Diaz-Meco, also a Homer T. Hirst III Professor of Oncology in Pathology and a member of the Meyer Cancer Center at Weill Cornell Medicine. The study's first author is Dr. Yu Muta, a postdoctoral associate in the Moscat/Diaz-Meco laboratories. Cholesterol is generally considered a pro-growth molecule, being a building block for cell membranes and having other growth-supporting functions. Prior studies have linked high blood cholesterol levels to various cancers, including colorectal cancers. However, it hasn't been clear that lowering cholesterol, for example with common statin drugs, can prevent colorectal cancers. "Trials of statins to prevent colorectal cancer have had conflicting results," Dr. Diaz-Meco said. "Our findings suggest that this is because targeting cholesterol has a preventive but selective effect only against polyps and tumors of this serrated type." Serrated polyps are so-called because of their sawtooth appearance under a microscope. They are flatter than ordinary colorectal polyps and can often be missed during colonoscopies. Yet the tumors into which they develop, which account for roughly 15 to 30 percent of colorectal cancers, contain many "metaplastic" cells that are particularly invasive and resistant to treatments. Several years ago, the Moscat/Diaz-Meco team linked serrated polyps and tumors to low levels of two enzymes known as aPKCs. They showed that mice engineered to lack these aPKC enzymes in their gut linings reliably form serrated polyps and then aggressive tumors. In the new study, the scientists found that in serrated-type tumors in these mice, and even in intestinal tissue poised to develop these types of cancerous lesions, cholesterol synthesis was strikingly upregulated, suggesting that cholesterol may be an early driver of tumor development. The researchers revealed how the absence of aPKC enzymes, especially in metaplastic tumor cells, unleashes the activation of a transcription factor called SREBP2, which switches on cholesterol production. Tests on colorectal polyp and tumor samples from human patients dovetailed with the mouse findings. They found, for example, that only serrated-type tumors had low aPKC levels concomitant with the accumulation of SREBP2, a driver and a marker of upregulated cholesterol biosynthesis in the serrated cancer cells. Lastly, the researchers tested a combination of two cholesterol synthesis-blocking drugs, including the widely used atorvastatin. The treatment, delivered when the low-aPKC mice were still quite young, significantly lowered the rate at which both serrated polyps and tumors later formed -- and the serrated-type tumors that did form were less aggressive than those normally arising in the untreated mice. The results indicate that targeting cholesterol could be a viable strategy for treating and preventing serrated-type colorectal tumors. The Moscat and Diaz-Meco labs are now hoping to set up an initial clinical trial of a cholesterol-lowering intervention in patients from whom serrated colorectal polyps have been removed. "Currently when these polyps are detected early with colonoscopy, they are removed and patients have to hope that they don't come back," Dr. Moscat said. "In the future, we hope to have a more active method to prevent this very aggressive form of cancer before it is fully developed and more difficult to treat."

AUBURN, Ala., Dec. 1, 2023 /PRNewswire/ -- For most academic scientists conducting biomedical research, the possibility of advancing a new medicine to the clinic is, at best, an aspiration. Despite the odds, Gary Piazza and his research team in Auburn University's Harrison College of Pharmacy discovered a highly potent and selective anticancer drug and are collaborating with investigators at the University of Alabama-Birmingham (UAB) O'Neal Comprehensive Cancer Center to advance a new drug candidate to clinical trials for patients with the most fatal of cancers. Continue Reading Gary Piazza, left, is a highly respected cancer investigator with over 35 years of research experience. At Auburn University's Harrison College of Pharmacy, he is director of the Cancer Research Center, a professor and department head. Piazza joined the Harrison College of Pharmacy (HCOP) in 2021 as the W.W. Walker Professor and head of the Department of Drug Discovery and Development. A highly respected cancer investigator, Piazza is a UAB graduate with over 35 years of research experience, including 10 years as a professor at the University of South Alabama Mitchell Cancer Institute (MCI) in Mobile and 10 years as a principal scientist with Southern Research in Birmingham. Along with his administrative responsibilities, Piazza continues his groundbreaking research as director of the newly created Cancer Research Center at HCOP. His collaborators also made the move from MCI to Auburn including medicinal chemist Xi Chen, cancer biologist Adam Keeton, pharmacologist Yulia Maxuitenko and lab manager Kristy Berry. "Having a multidisciplinary team with diverse scientific expertise has allowed us to solve many technical problems as we seek to advance our experimental drugs to the clinic," said Piazza. Piazza also brought with him multiple actively funded research projects, including three R01 projects from the National Institutes of Health National Cancer Institute and a project from the Breast Cancer Research Foundation of Alabama, along with several million dollars in funding. Selective targeting From his early research in a class of drugs known as non-steroidal anti-inflammatory drugs (NSAID), Piazza was the first to publish evidence a drug called sulindac could kill cancer cells by a specific mechanism known as apoptosis, or programmed cell death. This research supported the clinical development of a sulindac derivative called exisulind to treat precancerous colon adenomas (polyps) in patients with familial adenomatous polyposis who are at high risk of developing colorectal cancer. "NSAIDs are not considered to have strong anticancer activity and are not FDA approved for long-term use to either prevent or treat cancer because of potentially fatal gastrointestinal and other toxicities," said Piazza. "Yet, this unusual anticancer activity of NSAIDs commonly used to treat everything from headaches to arthritis inspired me to better understand the underlying mechanism of action." His research looks to use his novel series of compounds to inhibit a protein called RAS, a protein in which mutations in RAS genes have been known for decades to be responsible for many human cancers and those that are the most fatal, especially pancreatic, colorectal and lung. A unique approach Piazza is optimistic that their lead compound, ADT-1004, is an attractive drug candidate inching closer and closer to clinical trials. Although more research is needed, Piazza is encouraged by the promising anticancer activity that ADT-1004 has shown in mouse models of pancreatic cancer and our detailed understanding of how the drug can selectively kill cancer cells. "In many ways, cancer cells are just like normal cells, especially those cells in tissues where there is rapid cell division, for example, in the gut," said Piazza. "The difficulty in cancer drug development has always been the ability to find target-directed small molecules that can selectively kill cancer cells without harming normal cells." Potential at Auburn Piazza is excited about what can be accomplished on The Plains to be a beacon of hope in the battle to fight cancer. "Most of my career prior to joining Auburn was in the pharmaceutical industry where I learned the value of collaboration and in cancer centers, I saw sick patients every day coming in for chemotherapy, which made me more determined not to be satisfied with only conducting basic research," said Piazza. "At Auburn, I recognized the diverse expertise within the college, which I believed could help solve some of the major hurdles we encountered to advance our experimental anticancer drugs to the clinic." To read more on the Piazza lab's work, visit . SOURCE Auburn University