Molecular biological observations in gastric cancer

Semin Oncol. 1996 Jun;23(3):307-15.


Alterations in the structure and function of oncogenes and tumor suppressor genes, as well as genetic instability at several other genetic foci may be responsible for stomach carcinogenesis. The particular combination of multiple gene changes found in gastric cancer differs depending on the two histological types, strongly indicating that different genetic pathways exist for well differentiated or intestinal type and poorly differentiated or diffuse type gastric cancers. In general, genetic instability, telomerase activity, CD44 abnormal transcripts, and p53 mutation, all of which are common events of two types of gastric cancer, may be involved mainly in the early stage of stomach carcinogenesis, whereas activation of oncogenes and overexpression of the epidermal growth factor-related growth factor system may chiefly confer progression on gastric cancer. A new strategy of molecular diagnosis of gastrointestinal cancer, which has been implemented as a routine service in the Hiroshima University Clinical Laboratory, may provide new opportunities for early cancer diagnosis and more accurate evaluation of prognosis or grade of malignancy.

Publication types

  • Review

MeSH terms

  • Disease Progression
  • Epidermal Growth Factor / genetics
  • Gene Expression Regulation, Neoplastic
  • Genes, Tumor Suppressor / genetics
  • Genes, p53 / genetics
  • Humans
  • Hyaluronan Receptors / genetics
  • Molecular Biology
  • Mutation / genetics
  • Oncogenes / genetics
  • Prognosis
  • Stomach Neoplasms / diagnosis
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / pathology
  • Telomerase / genetics
  • Transcription, Genetic / genetics


  • Hyaluronan Receptors
  • Epidermal Growth Factor
  • Telomerase