This is one step towards eradicating colon cancer.
Colorectal cancer ranks as the third most prevalent cancer globally and can be detected early through screenings. These screenings involve either a fecal immunochemical test, which identifies blood in the stool from polyps, or a colonoscopy that visualizes these growths.
There are two types of polyps: hyperplastic (typically harmless) and adenomatous (with a potential to become cancerous). The removal of these polyps, especially the precancerous serrated adenomas, poses a challenge due to their flat structure and challenging visibility within the colon, contributing to 15-30% of colorectal cancers known for their invasive nature and resistance to treatment.
Recent research from Weill Cornell Medicine, NY, featured in Nature Communications, sheds light on a metabolic mechanism linked to these adenomas. The study revealed that these polyps exhibit lower levels of a specific enzyme, protein kinase C (PKC), responsible for regulating genes in cell growth and metabolism, allowing these cells to evade the immune system and promote tumor growth.
The researchers, using a mouse model replicating these lesions, discovered heightened cholesterol synthesis in these tumor cells despite already high cholesterol levels. This dysregulation activated a transcription factor, SREBP2, driving cholesterol production, which, in turn, fueled cancerous growth.
The study expanded its findings to human cells, showcasing that only serrated adenomas exhibited low PKC levels and an accumulation of SREBP2. Dr. Misagh Karimi, a specialist in gastrointestinal cancers, highlighted the evolving understanding of cholesterol’s role in cancer, indicating its potential to trigger malignancy and impede the immune response to cancer cells.
To test these findings, researchers created organoids from cancer patients’ tumors and examined metabolite levels, exploring the effectiveness of atorvastatin (a commonly prescribed statin) in inhibiting the growth of cells with low PKC levels. Statins, known for reducing cholesterol in the blood, demonstrated promising results in inhibiting these cancerous cells.
Professors Jorge Moscat and Maria T. Diaz-Meco expressed plans to conduct clinical trials to evaluate statins’ role in lowering cancer risk for those with serrated adenomas. While designing such trials poses challenges due to the time it takes for polyps to reappear after removal, the potential of statins in chemo-prevention offers a simple yet potentially impactful strategy.
Dr. Karimi noted growing evidence supporting statins’ potential in reducing cancer risk across various types. However, he emphasized the need for further evidence before widespread prescription, advocating healthy lifestyle choices and understanding individual genetic risk as crucial measures against colorectal cancer.
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