Evidence map›Paper›PMID 27427984›Full record

ArticleThe Journal of clinical investigation2016

Schlafen 4-expressing myeloid-derived suppressor cells are induced during murine gastric metaplasia.

Lin Ding, Michael M Hayes, Amanda Photenhauer, Kathryn A Eaton, Qian Li, Ramon Ocadiz-Ruiz, Juanita L Merchant

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

60 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Myeloid-derived suppressor cells modulation in the context of tumor microenvironment for gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. iScience · 2024
    Article
  11. Review
  12. Article
  13. A Metabolic Axis of Immune Intractability.Cancer immunology research · 2024
    Article
  14. Review
  15. Review
  16. The Cxcr2Frontiers in immunology · 2023
    Article
  17. Article
  18. Schlafen4Frontiers in immunology · 2023
    Article
  19. Review
  20. DDS Profile: Juanita L. Merchant, MD, PhD.Digestive diseases and sciences · 2023
    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

7 authors at 2 institutions in 2 countries.

Lin Ding
Michael M Hayes
Amanda Photenhauer
Kathryn A Eaton
Qian Li
Ramon Ocadiz-Ruiz
Juanita L Merchant
University Gastroenterology · USInstitute of Laboratory Animal Science · CN

Funding

University of Michigan Center for Gastrointestinal ResearchP30DK034933 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI OMARY, BISHR · 1986 to 2021
$22.5M
Role of Hedgehog Signaling in Chronic Gastritis and MetaplasiaP01DK062041 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUMUCIO, DEBORAH L. · 2002 to 2017
$20.6M
NIDDK NIH HHS P01 DK062041NIDDK NIH HHS P30 DK034933
6 · The paper itself

Abstract

Chronic Helicobacter pylori infection triggers neoplastic transformation of the gastric mucosa in a small subset of patients, but the risk factors that induce progression to gastric metaplasia have not been identified. Prior to cancer development, the oxyntic gastric glands atrophy and are replaced by metaplastic cells in response to chronic gastritis. Previously, we identified schlafen 4 (Slfn4) as a GLI1 target gene and myeloid differentiation factor that correlates with spasmolytic polypeptide-expressing metaplasia (SPEM) in mice. Here, we tested the hypothesis that migration of SLFN4-expressing cells from the bone marrow to peripheral organs predicts preneoplastic changes in the gastric microenvironment. Lineage tracing in Helicobacter-infected Slfn4 reporter mice revealed that SLFN4+ cells migrated to the stomach, where they exhibited myeloid-derived suppressor cell (MDSC) markers and acquired the ability to inhibit T cell proliferation. SLFN4+ MDSCs were not observed in infected GLI1-deficient mice. Overexpression of sonic hedgehog ligand (SHH) in infected WT mice accelerated the appearance of SLFN4+ MDSCs in the gastric corpus. Similarly, in the stomachs of H. pylori-infected patients, the human SLFN4 ortholog SLFN12L colocalized to cells that expressed MDSC surface markers CD15+CD33+HLA-DRlo. Together, these results indicate that SLFN4 marks a GLI1-dependent population of MDSCs that predict a shift in the gastric mucosa to a metaplastic phenotype.

Indexed as

AnimalsBinding SitesBiomarkersBone Marrow CellsBone Marrow TransplantationCarrier ProteinsCell DifferentiationCell MovementGastric MucosaHedgehog ProteinsHelicobacter InfectionsHelicobacter pyloriHumansInterferon Type ILigandsMetaplasiaBiomarkersCarrier ProteinsHedgehog ProteinsInterferon Type ILigandsschlafen-4 protein, mouseShh protein, mouseSLFN12L protein, humanThioglycolates

Identifiers

PMID27427984
PMCPMC4966326
OpenAlexW2500572265

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.