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Cancer Prevention02:59

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Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
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Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
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Colonic Epithelial-Derived Selenoprotein P Is the Source for Antioxidant-Mediated Protection in Colitis-Associated

Sarah P Short1, Jennifer M Pilat2, Caitlyn W Barrett2

  • 1Department of Medicine, Division of Gastroenterology, Vanderbilt University Medical Center, Nashville, Tennessee; Program in Cancer Biology, Vanderbilt University, Nashville, Tennessee; Center for Mucosal Inflammation and Cancer, Vanderbilt University Medical Center, Nashville, Tennessee.

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Colonic epithelial selenoprotein P (SELENOP) is crucial for preventing colon cancer in inflammatory bowel disease (IBD). Reduced SELENOP in the gut lining increases cancer risk, unlike systemic levels, highlighting its role as a biomarker.

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Area of Science:

  • Gastroenterology
  • Oncology
  • Molecular Biology

Background:

  • Inflammatory bowel disease (IBD) patients have selenium deficiencies and increased colon cancer risk.
  • Reduced selenoprotein P (SELENOP), an antioxidant protein, exacerbates experimental colitis-associated cancer (CAC).

Purpose of the Study:

  • To investigate the tissue-specific roles of SELENOP in intestinal inflammation and cancer.
  • To determine the clinical relevance of SELENOP in ulcerative colitis (UC).

Main Methods:

  • Used genetically modified mice (liver, myeloid, or epithelial SELENOP deletion) in a CAC model.
  • Assessed SELENOP in human UC organoids and patient samples.

Main Results:

  • Epithelial-specific SELENOP deletion, but not liver or myeloid deletion, increased CAC.
  • Epithelial SELENOP loss elevated oxidative stress, genomic instability, and tumor initiation.
  • SELENOP was downregulated in UC biopsies, correlating with disease severity and calprotectin levels.

Conclusions:

  • Colonic epithelial SELENOP, not plasma levels, is critical for preventing CAC.
  • Colonic SELENOP is a key indicator of selenium status in IBD patients.
  • SELENOP may serve as a biomarker for UC severity and CAC predisposition.