Evidence map›Paper›PMID 8440743›Full record

ArticleJournal of cancer research and clinical oncology1993

Molecular mechanism of stomach carcinogenesis.

E Tahara

Open access · greenAbstract readEditorial
In one paragraph

Article in Journal of cancer research and clinical oncology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
12.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 328 citations in OpenAlex.

  1. Pooled it
  2. Therapeutic strategy for scirrhous type gastric cancer.Japanese journal of clinical oncology · 2025
    Review
  3. Update on molecular pathogenesis ofWorld journal of gastrointestinal pathophysiology · 2025
    Review
  4. Article
  5. Anticancer Effects ofJournal of Cancer · 2021
    Article
  6. Role of HGF/c-Met in the treatment of colorectal cancer with liver metastasis.Journal of biochemical and molecular toxicology · 2019
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Gastric carcinogenesis.World journal of gastroenterology · 2012
    Article
  12. Endocrine carcinoma of the stomach: clinicopathological analysis of 27 surgically treated cases in a single institute.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2012
    Article
  13. Telomere shortening occurs early during gastrocarcinogenesis.Medical oncology (Northwood, London, England) · 2012
    Article
  14. Article
  15. Article
  16. Article
  17. p53 codon 72 polymorphism in patients with gastric and colorectal cancer in a Korean population.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2011
    Article
  18. Article
  19. Article
  20. Article

21 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

E Tahara
Hiroshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene changes in multiple oncogenes, multiple growth factors and multiple tumor-suppressor genes are observed in stomach cancer. Among them, those most commonly implicated in both well-differentiated adenocarcinoma and poorly differentiated adenocarcinoma are inactivation (mutations and allele loss) of the p53 gene, and activation (abnormal expression and amplification) of the c-met gene. Moreover, they occur at an early stage of stomach carcinogenesis. In addition, loss of heterozygosity (LOH) on chromosome 5q (APC locus) is frequently associated with well-differentiated adenocarcinoma. LOH on chromosome 18q (DCC locus) and LOH of the bcl-2 gene also are common events of well-differentiated adenocarcinoma. LOH on chromosomes 1q and 7q may be involved in the progression of well-differentiated adenocarcinoma. Conversely, the development of poorly differentiated adenocarcinoma, in addition to changes in p53 and c-met genes, requires reduction or dysfunction of cadherin. Overexpression of bcl-2 protein is observed in poorly differentiated adenocarcinoma or signet-ring cell carcinoma. Moreover, the K-sam gene is amplified preferentially in poorly differentiated adenocarcinoma of scirrhous carcinoma. K-sam amplification in scirrhous carcinoma often occurs independently of c-met gene amplification. LOH on chromosome 1p also is relatively common in poorly differentiated adenocarcinoma. Exceptionally, signet-ring cell carcinoma shares APC mutations. There are some differences in expression of the growth-factor/receptor system between well-differentiated adenocarcinoma and poorly differentiated adenocarcinoma. Moreover, interaction between cell-adhesion molecules in tumor cells expressing c-met and hepatocyte growth factor (HGF) from stromal cells is linked with morphogenesis of two histological types of stomach cancer. Intestinal metaplasia and adenoma of the stomach also contain p53 mutations and K-ras mutations or tpr-met rearrangement. Taken together, different genetic pathways of stomach carcinogenesis may exist for poorly differentiated and well-differentiated stomach cancers. Some of the latter may develop by a cumulative series of gene alterations similar to those of colorectal cancer.

Indexed as

HumansStomach Neoplasms

Identifiers

PMID8440743
PMCPMC12200070
OpenAlexW2020391792

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.