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<\/a>In the laboratory of Daniel W. Rosenberg<\/a> in UConn Health\u2019s Center for Molecular Medicine<\/a>, concurrent studies \u2013 epidemiological, genomic, and molecular \u2013 are ongoing and are expected to yield a series of published papers this year and next. One of them will be published in the June edition of\u00a0Molecular Cancer Research<\/em><\/a>, a major scientific journal of the American Association for Cancer Research. It describes how the Rosenberg lab uncovered evidence of the origins of colorectal cancer that historically have been poorly understood.<\/p>\n Cancer evolves from what is known as neoplasia\u00a0\u2013 or new, abnormal growth of tissue. Not all neoplasias become malignant tumors, but they are considered an early warning sign of possible cancer.<\/p>\n \u201cUnderstanding early neoplasia has become such a major focus at the National Cancer Institute \u2013 how do we characterize these early changes so we can prevent cancer,\u201d says Rosenberg, HealthNet Inc. Endowed Chair in Cancer Biology and professor of medicine, \u201cand I believe we\u2019re at the forefront of answering this question.\u201d<\/p>\n MD\/Ph.D. candidate Allen Mo, first author on the Molecular Cancer Research<\/em> paper, says colon cancer is thought to be an epithelial disease, meaning that it starts with a mutation in the tissue that lines the surface of the colon (the epithelium), and grows and then invades the underlying support tissue. “People historically believed these are separate compartments, that there is no interaction between the epithelium and the support tissue until the cells become cancerous and break through the membrane,\u201d Mo says. \u201cWe\u2019ve been able to demonstrate that, even at the very early stage, prior to the polyp stage, the supportive tissue is actually influencing how these epithelial initiate cells are evolving.\u201d<\/p>\n That\u2019s important because it provides another potential early intervention point \u2013 if scientists can figure out a reliable way to make alterations to the signaling pathways between the two tissue types, perhaps they could influence how the mutate cells progress.<\/p>\n The Devers Data<\/strong><\/p>\n The work includes collaborators from both within and outside the institution, but central to all of it is Dr. Thomas Devers<\/a>, a UConn Health gastroenterologist whose volume of consecutive colonoscopies over the past five and a half years has yielded data from 5,000 patients. The resulting demographic database has been powering the engine driving the research that has helped substantiate epidemiological findings, such as how smoking completely cancels the protective properties of aspirin, how consumption of diets rich in Omega-3 fatty acids appears to reduce risk of early neoplasia in the colon, and how walnuts may have protective properties, as described in a study\u00a0recently published in Cancer Prevention Research<\/em><\/a>.<\/p>\n \u201cDr. Devers routinely screens patients at a resolution that only a handful of clinicians are doing,\u201d Rosenberg says.<\/p>\n Devers uses a high-definition endoscope with contrast dye-spray that enables him to detect tiny \u2013 less than 5 mm \u2013 lesions that are scattered throughout the colon.<\/p>\n \u201cMany of the subjects have already returned for follow-up [surveillance] colonoscopy, so we actually have genomic data from three and five years ago that we can use to predict the possibility they may develop advanced adenomas or even cancer,\u201d Rosenberg says. \u201cWe\u2019re actually at the point now where we can follow the impact of these early changes over time.\u201d<\/p>\n The work involves the intensive application of bioinformatics, the collection and analysis of complex biochemical and biological information.<\/p>\n