Evidence map›Paper›PMID 27498859›Full record

ArticleCell reports2016

Sox2 Suppresses Gastric Tumorigenesis in Mice.

Abby Sarkar, Aaron J Huebner, Rita Sulahian, Anthony Anselmo, Xinsen Xu, Kyle Flattery, Niyati Desai, Carlos Sebastian, Mary Anna Yram, Katrin Arnold and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

52 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Wnt regulates cellular differentiation and retinoid metabolism genes in the mouse stomach.American journal of physiology. Gastrointestinal and liver physiology · 2026
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  5. Genomic analyses identify 15 risk loci and revealProceedings of the National Academy of Sciences of the United States of America · 2025
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  6. Review
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  9. Role of PDGFRANature communications · 2023
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Stem Cell Biomarkers and Tumorigenesis in Gastric Cancer.Journal of personalized medicine · 2022
    Review
  18. Article
  19. Review
  20. Review
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

17 authors at 5 institutions in 1 country.

Abby SarkarCancer Center and Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA; Howard Hughes Medical Institute and Department of Stem Cell and Regenerative Biology, 7 Divinity Avenue, Harvard University, Cambridge, MA 02138, USA.
Aaron J HuebnerCancer Center and Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA; Howard Hughes Medical Institute and Department of Stem Cell and Regenerative Biology, 7 Divinity Avenue, Harvard University, Cambridge, MA 02138, USA.
Rita SulahianHarvard Stem Cell Institute, Cambridge, MA 02138, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Anthony AnselmoDepartment of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA.
Xinsen XuDepartment of Medicine, Harvard Medical School, Boston, MA 02115, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Kyle FlatteryCancer Center and Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA; Howard Hughes Medical Institute and Department of Stem Cell and Regenerative Biology, 7 Divinity Avenue, Harvard University, Cambridge, MA 02138, USA.
Niyati DesaiDivision of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA.
Carlos SebastianCancer Center and Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Mary Anna YramCancer Center and Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA; Howard Hughes Medical Institute and Department of Stem Cell and Regenerative Biology, 7 Divinity Avenue, Harvard University, Cambridge, MA 02138, USA.
Katrin ArnoldCancer Center and Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA; Howard Hughes Medical Institute and Department of Stem Cell and Regenerative Biology, 7 Divinity Avenue, Harvard University, Cambridge, MA 02138, USA.
Miguel RiveraDivision of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA.
Raul MostoslavskyCancer Center and Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Roderick BronsonDepartment of Pathology, Harvard Medical School, Boston, MA 02115, USA.
Adam J BassDepartment of Medicine, Harvard Medical School, Boston, MA 02115, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Ruslan SadreyevDepartment of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA.
Ramesh A ShivdasaniHarvard Stem Cell Institute, Cambridge, MA 02138, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Konrad HochedlingerCancer Center and Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA 02114, USA; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA; Howard Hughes Medical Institute and Department of Stem Cell and Regenerative Biology, 7 Divinity Avenue, Harvard University, Cambridge, MA 02138, USA. Electronic address: khochedlinger@mgh.harvard.edu.
Massachusetts General Hospital · USHarvard University · USDana-Farber Cancer Institute · USHoward Hughes Medical Institute · USHarvard Stem Cell Institute · US

Funding

Transcriptional control of gut epithelial homeostasis and regenerationR01DK081113 · NIDDK · DANA-FARBER CANCER INST · PI SHIVDASANI, RAMESH A · 2009 to 2022
$5.6M
Novel Roles for Oncogenic SOX2 in Esophageal Squamous Cell CarcinomaR01CA187119 · NCI · DANA-FARBER CANCER INST · PI BASS, ADAM JOEL · 2015 to 2019
$1.9M
Role of Sox2 in stomach development, regeneration and cancerR01DK096034 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI HOCHEDLINGER, KONRAD · 2012 to 2015
$1.4M
NIDDK NIH HHS R01 DK081113NIDDK NIH HHS R01 DK096034
6 · The paper itself

Abstract

Sox2 expression marks gastric stem and progenitor cells, raising important questions regarding the genes regulated by Sox2 and the role of Sox2 itself during stomach homeostasis and disease. By using ChIP-seq analysis, we have found that the majority of Sox2 targets in gastric epithelial cells are tissue specific and related to functions such as endoderm development, Wnt signaling, and gastric cancer. Unexpectedly, we found that Sox2 itself is dispensable for gastric stem cell and epithelial self-renewal, yet Sox2(+) cells are highly susceptible to tumorigenesis in an Apc/Wnt-driven mouse model. Moreover, Sox2 loss enhances, rather than impairs, tumor formation in Apc-deficient gastric cells in vivo and in vitro by inducing Tcf/Lef-dependent transcription and upregulating intestinal metaplasia-associated genes, providing a mechanistic basis for the observed phenotype. Together, these data identify Sox2 as a context-dependent tumor suppressor protein that is dispensable for normal tissue regeneration but restrains stomach adenoma formation through modulation of Wnt-responsive and intestinal genes.

Indexed as

Gene Expression Regulation, NeoplasticAdenomaAdenomatous Polyposis Coli ProteinAnimalsBase SequenceCell Line, TumorCell ProliferationCell Transformation, NeoplasticEpithelial CellsHepatocyte Nuclear Factor 1-alphaLymphoid Enhancer-Binding Factor 1MiceMice, TransgenicSOXB1 Transcription FactorsStomach NeoplasmsWnt Signaling PathwayAdenomatous Polyposis Coli Proteinadenomatous polyposis coli protein, mouseHepatocyte Nuclear Factor 1-alphaHnf1a protein, mouseLef1 protein, mouseLymphoid Enhancer-Binding Factor 1Sox2 protein, mouseSOXB1 Transcription Factors

Identifiers

PMID27498859
PMCPMC13596863
OpenAlexW2485672262

What OpenQuestion holds

Textmetadata
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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.