Molecular Alterations Associated with Colitis-Associated Colon Carcinogenesis

Steven Itzkowitz, Lea Ann Chen

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review


Patients with longstanding ulcerative colitis and Crohn's colitis are at increased risk of colorectal neoplasia Chronic inflammation is considered to be the driving force that predisposes to developing colorectal neoplasia in IBD. The same molecular pathways that contribute to sporadic colon carcinogenesis also occur with colitis-associatedcolorectal cancer, albeit with different frequency and timing. Some molecular markers, such as aneuploidy, correlate with colon cancer risk, but so far no marker has beenintegrated into clinical practice for predicting cancer risk. Newer markers and approaches hold promise for helping to identify IBD patients at high risk of developing colorectalcancer.

Original languageEnglish
Title of host publicationInflammatory Bowel Disease
Subtitle of host publicationTranslating basic science into clinical practice
Number of pages10
ISBN (Print)9781405157254
StatePublished - 18 May 2010


  • Anti-inflammatory agents - 5-aminosalicylic acid, steroids, purine immunomodulators
  • Molecular alterations - colitis-associated colon carcinogenesis
  • Oxidative stress - associated with inflammation
  • TLR4 - cell surface receptor recognizing bacterial products
  • Tumor suppressor genes - cellular genes controlling cell proliferation, death and differentiation
  • Types of genomic instability - chromosomal instability, microsatellite instability
  • p53 protein - preventing clonal expansion of mutant cells


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