![]() ![]() At the beginning of the study, the researchers nudged the cells toward cancers by disabling the production of a key cancer-associated protein called p53 that regulates when and how often a cell divides. The cells were obtained from patients undergoing gastric bypass surgery to treat obesity. The researchers studied tiny, three-dimensional clumps of human stomach cells called gastric organoids. How does a cancer cell evolve, and is this evolutionary path repeatable? If we start with a given set of conditions, will we get the same result in every case?” “We wanted to know what happens at the very earliest stages. “Our studies of established tumors showed us that early genomic alterations seem to dictate what happens later, and that many of these changes seem to happen before tumor formation,” Curtis said. The research builds on previous work in Curtis’s laboratory indicating that some colon cancer cells are seemingly born to be bad - they acquire the ability to metastasize long before the disease is detectable. The lead authors of the study are former postdoctoral scholar Kasper Karlsson, PhD, and visiting graduate student Moritz Przybilla. “Can we identify a minimal constellation of genetic alterations that imply the cell will progress? And, if so, can we intervene? The striking reproducibility in the genetic changes we observed from multiple donors suggests it’s possible.”Ĭurtis is the senior author of the research, which was published on May 31 in Nature. “Ideally, we would find ways to intercept this progression before the cells become truly cancerous,” said Christina Curtis, PhD, professor of medicine, of genetics and of biomedical data science. Identifying the first steps associated with future cancer development could not only facilitate earlier-than-ever diagnosis - when a deadly outcome is but a twinkle in a rogue cell’s eye - but may also highlight novel interventions that could stop the disease in its tracks, the researchers say. The study is the first to exhaustively observe the natural evolution of the earliest stages of human cancers, starting with cells that have a single cancer-priming mutation and culminating with a panel of descendants harboring a galaxy of genetic abnormalities. Many of these changes affect pathways that control cell division, structure and internal messaging - leaving the cells poised to go bad long before any visible signs or symptoms occur. Cancer cells-to-be accumulate a series of specific genetic changes in a predictable and sequential way years before they are identifiable as pre-malignancies, researchers at Stanford Medicine have found. ![]()
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