Evidence map›Paper›PMID 20047123›Full record

ReviewGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2009

Current understanding of SPEM and its standing in the preneoplastic process.

Victoria G Weis, James R Goldenring

Open access · bronzeAbstract readReview
In one paragraph

Review in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
7.4field-weighted citation impact, top 3% 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

75 citing papers in PubMed, 134 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Autoimmune Gastritis andInternational journal of molecular sciences · 2025
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Gastric epithelial histology and precancerous conditions.World journal of gastrointestinal oncology · 2022
    Review
  19. Article
  20. Article

15 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

2 authors at 1 institution in 1 country.

Victoria G WeisDepartments of Surgery and Cell and Developmental Biology, Epithelial Biology Center, Vanderbilt University School of Medicine, 10435G MRB IV, 2213 Garland Avenue, Nashville, TN 37232, USA.
James R Goldenring
Vanderbilt University · US

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Mechanisms of Gastric Mucous Cell MetaplasiaR01DK071590 · NIDDK · VANDERBILT UNIVERSITY · PI GOLDENRING, JAMES RICHARD · 2008 to 2012
$2.2M
Oxyntic Atrophy and Novel Gastric Lineages.I01BX000930 · VA · VETERANS HEALTH ADMINISTRATION · PI GOLDENRING, JAMES RICHARD · 2011 to 2025
–
BLRD VA I01 BX000930NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK071590
6 · The paper itself

Abstract

Gastric cancer is the second leading cause of cancer-related death worldwide, but the details of gastric carcinogenesis remain unclear. In humans, two preneoplastic metaplasias are associated with the precancerous stomach: intestinal metaplasia and spasmolytic polypeptide-expressing metaplasia (SPEM). While mouse models of Helicobacter sp. infection have not shown intestinal metaplasia, a number of mouse models lead to the evolution of SPEM. In this review, we summarize increasing data that indicates that SPEM arises in the setting of parietal cell loss, either following acute druginduced oxyntic atrophy or in chronic oxyntic atrophy associated with H. felis infection. Importantly, recent investigations support the origin of SPEM through transdifferentiation from mature chief cells following parietal cell loss. Novel biomarkers of SPEM, such as HE4, hold promise as specific markers of the metaplastic process distinct from normal gastric lineages. Staining with HE4 in humans and other studies in gerbils suggest that SPEM arises initially in the human stomach following parietal cell loss and then further evolves into intestinal metaplasia, likely in association with chronic inflammation. Further studies are needed to broaden our knowledge of metaplasia and early cancer-specific biomarkers that could give insights into both lineage derivation and preneoplasia detection.

Indexed as

AnimalsCell Transformation, NeoplasticDisease Models, AnimalGastric MucosaGerbillinaeHumansIntercellular Signaling Peptides and ProteinsMetaplasiaMiceParietal Cells, GastricPeptidesPrecancerous ConditionsStomach NeoplasmsIntercellular Signaling Peptides and ProteinsPeptidesspasmolytic polypeptide

Identifiers

PMID20047123
PMCPMC4502916
OpenAlexW2076430260

What OpenQuestion holds

Textmetadata
LicenceTDM
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.