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Area of Science:

  • Gastroenterology
  • Oncology
  • Molecular Biology

Background:

  • Long-standing mucosal inflammation is a suspected driver of colitis-associated colorectal cancer (CA-CRC).
  • Not all ulcerative colitis (UC) patients develop CA-CRC, suggesting other factors influence cancer progression.
  • Early molecular events in carcinogenesis may occur in non-neoplastic mucosa distant from tumors.

Purpose of the Study:

  • To investigate if UC patients who progress to neoplasia (progressors) have a distinct molecular inflammatory profile compared to non-progressors.
  • To identify molecular differences in the non-neoplastic colonic mucosa of UC progressors versus non-progressors.

Main Methods:

  • Transcriptomic profiling of 143 mucosal biopsies from UC progressors and non-progressors using microarrays.
  • Gene set ontology analyses to identify enriched biological processes.
  • Immunohistochemistry to assess lymphocyte infiltration in adjacent mucosal biopsies.

Main Results:

  • UC progressors exhibit a distinct gene expression profile with 529 deregulated genes compared to non-progressors, even after adjusting for disease duration.
  • Inflamed mucosa in progressors was negatively enriched for adaptive immune responses and complement activity.
  • Progressors showed fewer infiltrating B cells and less lymphoid aggregates, supporting reduced immune cell infiltration and activity.

Conclusions:

  • The inflamed colonic mucosa in UC patients who progress to dysplasia or cancer has a different gene expression profile than in non-progressors.
  • This distinct profile suggests reduced immune cell attraction and infiltration in progressors.
  • Progressors may have an impaired ability to mount adaptive immune responses against malignant transformation.