Beta-catenin and the Morphogenesis of Colorectal Cancer

Virchows Arch. 2002 Jul;441(1):1-11. doi: 10.1007/s00428-002-0642-9. Epub 2002 Apr 27.

Abstract

Tumor growth and progression are morphogenetic processes that are characterized by ongoing changes in tumor structure and differentiation. These processes show similarities to morphogenesis in embryonic development, as supported by the fact that the main pathways regulating morphogenesis in early embryogenesis and organogenesis are directly or indirectly altered in most neoplasms. In colorectal adenocarcinomas, different morphogenetic areas can be clearly defined. The focus of this review is on combining morphology-based aspects and recent molecular and genetic data on the progression of colorectal carcinomas. The decisive genetic alteration in most colorectal cancers is the loss of function mutation in the adenomatous polyposis coli tumor suppressor gene, leading to an accumulation of the oncoprotein beta-catenin, the main effector of the embryonic Wnt/wingless pathway. The possibility is discussed that, on the basis of this genetic alteration, the tumor microenvironment is an additional driving force of tumor progression.

Publication types

  • Review

MeSH terms

  • Colorectal Neoplasms* / etiology
  • Colorectal Neoplasms* / genetics
  • Colorectal Neoplasms* / metabolism
  • Cytoskeletal Proteins / genetics*
  • Cytoskeletal Proteins / metabolism
  • Humans
  • Mutation
  • Trans-Activators / genetics*
  • Trans-Activators / metabolism
  • beta Catenin

Substances

  • CTNNB1 protein, human
  • Cytoskeletal Proteins
  • Trans-Activators
  • beta Catenin