Evidence map›Paper›PMID 27573785›Full record

ReviewAdvances in experimental medicine and biology2016

Recapitulating Human Gastric Cancer Pathogenesis: Experimental Models of Gastric Cancer.

Lin Ding, Mohamad El Zaatari, Juanita L Merchant

Open access · greenAbstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact, top 77% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026
    Review
  3. Pathogenicity ofWorld journal of clinical oncology · 2025
    Review
  4. Review
  5. Article
  6. The immune microenvironment in gastric adenocarcinoma.Nature reviews. Gastroenterology & hepatology · 2022
    Review
  7. EarlyCancers · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
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

3 authors at 2 institutions in 1 country.

Lin DingDepartments of Internal Medicine and Molecular and Integrative Physiology, University of Michigan, 109 Zina Pitcher PL, BSRB 2051, Ann Arbor, MI, 48109-2200, USA.
Mohamad El ZaatariDepartments of Internal Medicine and Molecular and Integrative Physiology, University of Michigan, 1150 West Medical Center Drive, 6518 MSRB 1, Ann Arbor, MI, 48109-5682, USA.
Juanita L MerchantDepartments of Internal Medicine and Molecular and Integrative Physiology, University of Michigan, 109 Zina Pitcher PL, BSRB 2051, Ann Arbor, MI, 48109-2200, USA. Merchanj@med.umich.edu.
University of Michigan–Ann Arbor · USRegional West Medical Center · US

Funding

Role of Hedgehog Signaling in Chronic Gastritis and MetaplasiaP01DK062041 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MERCHANT, JUANITA L. · 2002 to 2017
$20.6M
NIDDK NIH HHS P01 DK062041
6 · The paper itself

Abstract

This review focuses on the various experimental models to study gastric cancer pathogenesis, with the role of genetically engineered mouse models (GEMMs) used as the major examples. We review differences in human stomach anatomy compared to the stomachs of the experimental models, including the mouse and invertebrate models such as Drosophila and C. elegans. The contribution of major signaling pathways, e.g., Notch, Hedgehog, AKT/PI3K is discussed in the context of their potential contribution to foregut tumorigenesis. We critically examine the rationale behind specific GEMMs, chemical carcinogens, dietary promoters, Helicobacter infection, and direct mutagenesis of relevant oncogenes and tumor suppressor that have been developed to study gastric cancer pathogenesis. Despite species differences, more efficient and effective models to test specific genes and pathways disrupted in human gastric carcinogenesis have yet to emerge. As we better understand these species differences, "humanized" versions of mouse models will more closely approximate human gastric cancer pathogenesis. Towards that end, epigenetic marks on chromatin, the gut microbiota, and ways of manipulating the immune system will likely move center stage, permitting greater overlap between rodent and human cancer phenotypes thus providing a unified progression model.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsDisease Models, AnimalHelicobacter InfectionsHumansMiceMutationSignal TransductionStomach NeoplasmsTumor Suppressor ProteinsTumor Suppressor ProteinsGastrinGEMMsgp130HedgehogINS-GASMNUNotchSPEM

Identifiers

PMID27573785
PMCPMC5499694
OpenAlexW2516475554

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.