Growth factors and oncogenes in human gastrointestinal carcinomas View Full Text


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Article Info

DATE

1990-03

AUTHORS

Eiichi Tahara

ABSTRACT

Multi-autocrine loops of the epidermal growth factor (EGF), transforming growth factorα (TGFα), platelet-derived growth factor (PDGF) and TGFβ system are expressed in human gastrointestinal carcinomas. In esophageal and gastric carcinomas, they evidently play an important role in tumor progression. Gastrin, one of the major gut hormones, may also act as an autocrine growth factor for gastric and colonic carcinomas. TheHST1 andINT-2 genes, belonging to the fibroblast growth factor gene family, are coamplified in approximately 50% of primary tumors and in all the metastatic tumors of esophageal carcinoma. TGFα and EGF are the ligands of the tumor cells that overexpress EGF receptor in esophageal carcinomas. The synchronous expression of EGF and its receptor, as well as TGFα andras p21, is evidently correlated with the depth of tumor invasion, metastasis and prognosis of gastric carcinomas. Amplification of c-erbB-2 and EGF receptor genes has been observed in many metastatic sites of gastric carcinomas regardless of histological type. In addition to TGFα and EGF, TGFβ and PDGF A chain produced by tumor cells may stimulate collagen synthesis not only by fibroblasts but also by tumor cells themselves, resulting in extensive progression and diffuse fibrosis of scirrhous gastric carcinomas. Moreover, TGFα or EGF and estrogen may also play a cooperative role in the development of scirrhous gastric carcinoma. In colorectal carcinoma, it has been shown that the accumulation of several alterations inras genes and p53 genes is most important for the conversion of adenoma to carcinoma. Critical genetic changes, including activation of oncogenes, mutation and deletion of tumor suppressor genes and disturbances in transcriptional regulatory sequences, may bring about aberrant expression of growth factors and their receptors in gastrointestinal carcinomas. The understanding of the significance of EGF-related growth factors in tumor progression provides a framework for a biological approach to the therapy of human gastrointestinal carcinomas. 8-Cl-cAMP, which inhibits expression of oncogenes and TGFα, may be useful not only for cancer therapy but also for the study of cell differentiation. More... »

PAGES

121-131

References to SciGraph publications

  • 1989-01. Amplification of epidermal growth factor receptor (EGFR) gene and oncogenes in human gastric carcinomas in CELL PATHOLOGY
  • 1984-02. Close similarity of epidermal growth factor receptor and v-erb-B oncogene protein sequences in NATURE
  • 1989-05. Clonal allele loss in gastrointestinal cancers in BRITISH JOURNAL OF CANCER
  • 1985-02. Autocrine growth factors and cancer in NATURE
  • 1988-04. The cytoplasmic protein GAP is implicated as the target for regulation by the ras gene product in NATURE
  • 1987-05. Prevalence of ras gene mutations in human colorectal cancers in NATURE
  • 1988-04. A structure and some function in NATURE
  • 1988. Endocrine Tumors of the Gastrointestinal Tract: Classification, Function and Biological Behavior in DIGESTIVE DISEASE PATHOLOGY
  • 1986. Structural Relationships Between Growth Factor Precursors and Cell Surface Receptors in ONCOGENES AND GROWTH CONTROL
  • 1988-11. Morphological changes in a human scirrhous gastric carcinoma cell line (KATO-III) when cultured in collagen-coated dishes in CELL PATHOLOGY
  • 1985-05. Clustering of breakpoints on chromosome 11 in human B-cell neoplasms with the t(11 ; 14) chromosome translocation in NATURE
  • 1988-08. Gastrin receptors in human gastric scirrhous carcinoma in JOURNAL OF GASTROENTEROLOGY
  • 1983-07-01. Platelet-derived growth factor is structurally related to the putative transforming protein p28sis of simian sarcoma virus in NATURE
  • 1988-07. Estrogen receptors in gastric adenocarcinoma: A retrospective immunohistochemical analysis in VIRCHOWS ARCHIV A PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY
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    URI

    http://scigraph.springernature.com/pub.10.1007/bf01612665

    DOI

    http://dx.doi.org/10.1007/bf01612665

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1009854790

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/2157713


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