[Biological malignancy in human gastric carcinoma--molecular aspects]

Gan To Kagaku Ryoho. 1991 May;18(6):927-33.
[Article in Japanese]

Abstract

Overexpression of many growth factors/receptors and decreased expression of TGF beta type I play an important role in progression of human gastric carcinomas. Abnormal regulation of transcription of these genes should be involved in cancer progression. Advanced gastric carcinomas showing metastasis sometimes reveal amplification of oncogenes. Development and progression of scirrhous gastric carcinoma are brought about by the accumulation of growth factors such as TGF beta, IGF, PDGF and FGF and by the amplification of SAM gene. Loss of heterozygosity (LOH) on chromosomes 1q, 5q and 17p frequently takes place in well differentiated type gastric carcinomas, while no LOH on chromosomes 1q and 5q occurs in poorly differentiated type. LOH on chromosomes 5q and 17p is detected even in early gastric carcinomas, although LOH on 1q and 7p is found only in advanced gastric carcinomas. Thus, the accumulation of multi-autocrine growth factors and multiple genetic alterations evidently participates in biological malignancy of gastric carcinomas.

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / metabolism
  • Adenocarcinoma / pathology
  • Chromosomes, Human, Pair 17
  • ErbB Receptors / genetics*
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / metabolism
  • Stomach Neoplasms / pathology
  • Transforming Growth Factor alpha / genetics
  • Transforming Growth Factor beta / genetics*

Substances

  • Transforming Growth Factor alpha
  • Transforming Growth Factor beta
  • ErbB Receptors