Evidence map›Paper›PMID 16482617›Full record

ReviewWorld journal of gastroenterology2006

Alterations of tumor suppressor and tumor-related genes in the development and progression of gastric cancer.

Gen Tamura

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 4 pooled it
6.8field-weighted citation impact, top 2% 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

93 citing papers in PubMed, 4 syntheses or guidelines pooled it, 221 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Review
  6. Article
  7. Mutational landscape of TP53 and CDH1 in gastric cancer.World journal of gastrointestinal surgery · 2024
    Article
  8. Article
  9. Article
  10. A RareGenes · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Precision medicine in gastric cancer.World journal of gastrointestinal oncology · 2019
    Review
  17. Loss ofCanadian journal of gastroenterology & hepatology · 2019
    Article
  18. Article
  19. Review
  20. Expression of gremlin1 in gastric cancer and its clinical significance.Medical oncology (Northwood, London, England) · 2018
    Article

33 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.

Gen TamuraDepartment of Pathology, Yamagata University School of Medicine, 2-2-2 Iida-nishi, Yamagata 990-9585, Japan. gtamura@med.id.yamagata-u.ac.jp
Yamagata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development and progression of gastric cancer involves a number of genetic and epigenetic alterations of tumor suppressor and tumor-related genes. The majority of differentiated carcinomas arise from intestinal metaplastic mucosa and exhibit structurally altered tumor suppressor genes, typified by p53, which is inactivated via the classic two-hit mechanism, i.e. loss of heterozygosity (LOH) and mutation of the remaining allele. LOH at certain chromosomal loci accumulates during tumor progression. Approximately 20% of differentiated carcinomas show evidence of mutator pathway tumorigenesis due to hMLH1 inactivation via hypermethylation of promoter CpG islands, and exhibit high-frequency microsatellite instability. In contrast, undifferentiated carcinomas rarely exhibit structurally altered tumor suppressor genes. For instance, while methylation of E-cadherin is often observed in undifferentiated carcinomas, mutation of this gene is generally associated with the progression from differentiated to undifferentiated carcinomas. Hypermethylation of tumor suppressor and tumor-related genes, including APC, CHFR, DAP-kinase, DCC, E-cadherin, GSTP1, hMLH1, p16, PTEN, RASSF1A, RUNX3, and TSLC1, can be detected in both differentiated and undifferentiated carcinomas at varying frequencies. However, the significance of the hypermethylation varies according to the analyzed genomic region, and hypermethylation of these genes can also be present in non-neoplastic gastric epithelia. Promoter demethylation of specific genes, such as MAGE and synuclein Y, can occur during the progressive stages of both histological types, and is associated with patient prognosis. Thus, while the molecular pathways of gastric carcinogenesis are dependent on histological background, specific genetic alterations can still be used for risk assessment, diagnosis, and prognosis.

Indexed as

Genes, Tumor SuppressorAdaptor Proteins, Signal TransducingCadherinsCarrier ProteinsDisease ProgressionEpigenesis, GeneticGenes, p53HumansLoss of HeterozygosityMicrosatellite RepeatsMutL Protein Homolog 1Nuclear ProteinsPrecancerous ConditionsPromoter Regions, GeneticStomach NeoplasmsAdaptor Proteins, Signal TransducingCadherinsCarrier ProteinsMLH1 protein, humanMutL Protein Homolog 1Nuclear Proteins

Identifiers

PMID16482617
PMCPMC4066026
OpenAlexW2125729230

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.