[Genetic aspects of colorectal carcinogenesis]

Wiad Lek. 2004;57(1-2):74-9.
[Article in Polish]

Abstract

Colorectal cancer (CRC) is one of the most common forms of cancer and the second leading cause of death in Poland. Most cases of CRC are sporadic but a small percentage occurs in heritable syndromes such as dominant autosomal adenomatous and hamartomatous polyposis syndromes and hereditary nonpolyposis colorectal cancers. In a majority of cases CRCs are thought to develop in a step wise progression from normal epithelium through polyp form to carcinoma. Many genetic changes are observed in this process like inactivation of the tumor suppressor genes as well as the activation of specific oncogenes. Molecular biological studies have shown mutations of p53, Apc, k-ras and/or changes in proteins like APC and DNA microsatellite instability or loss of heterozygosity. For several years now great progress in this field and new concepts of screening strategies and therapeutic options have been made (gene therapy).

Publication types

  • English Abstract
  • Review

MeSH terms

  • Adenomatous Polyposis Coli / genetics
  • Colorectal Neoplasms / diagnosis
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms, Hereditary Nonpolyposis / genetics
  • DNA, Neoplasm
  • Humans
  • Loss of Heterozygosity
  • Microsatellite Repeats
  • Mutation
  • Peutz-Jeghers Syndrome / genetics*

Substances

  • DNA, Neoplasm