Evidence map›Paper›PMID 29795405›Full record

ArticleOncogene2018

Myeloid-restricted ablation of Shp2 restrains melanoma growth by amplifying the reciprocal promotion of CXCL9 and IFN-γ production in tumor microenvironment.

P Xiao, Y Guo, H Zhang, X Zhang, H Cheng, Q Cao, Y Ke

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

31 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Prognostic gene expression signature for high-grade serous ovarian cancer.Annals of oncology : official journal of the European Society for Medical Oncology · 2020
    Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. NanoSHP099-Targeted SHP2 Inhibition Boosts Ly6CAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  11. Tyrosine phosphataseFrontiers in immunology · 2024
    Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
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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.

P XiaoDepartment of Pathology and Pathophysiology, and Department of Gastroenterology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 310058, Hangzhou, China.
Y GuoDepartment of Pathology and Pathophysiology, Program in Molecular Cell Biology, Zhejiang University School of Medicine, 310058, Hangzhou, China.
H ZhangDepartment of Pathology and Pathophysiology, Program in Molecular Cell Biology, Zhejiang University School of Medicine, 310058, Hangzhou, China.
X ZhangDepartment of Pathology and Pathophysiology, Program in Molecular Cell Biology, Zhejiang University School of Medicine, 310058, Hangzhou, China.
H ChengDepartment of Pathology and Pathophysiology, Program in Molecular Cell Biology, Zhejiang University School of Medicine, 310058, Hangzhou, China.
Q CaoDepartment of Pathology and Pathophysiology, and Department of Gastroenterology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 310058, Hangzhou, China. 0000232@zju.edu.cn.
Y KeDepartment of Pathology and Pathophysiology, Program in Molecular Cell Biology, Zhejiang University School of Medicine, 310058, Hangzhou, China. yke@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Src homology 2 domain-containing protein tyrosine phosphatase 2 (Shp2) is generally considered to be an oncogene owing to its ability in enhancing the malignancy of multiple types of tumor cells; however, its role in modulating tumor immunity remains largely elusive. Here, we reported that myeloid-restricted ablation of Shp2 suppressed melanoma growth. Mechanistically, loss of Shp2 potentiates macrophage production of CXCL9 in response to IFN-γ and tumor cell-derived cytokines, thereby facilitating the tumor infiltration of IFN-γ-producing T cells that could in turn support CXCL9 production within tumor microenvironment. Collectively, our findings highlight a causative role of myeloid Shp2 in dampening T cell-mediated antitumor immunity by restraining the macrophage/CXCL9-T cell/IFN-γ feedback loop. Thus, targeting macrophage Shp2 may help to create a Th1-dominant tumor immune microenvironment.

Indexed as

AnimalsCell Line, TumorCell ProliferationChemokine CXCL9Interferon-gammaMacrophagesMelanomaMiceMyeloid CellsProtein Tyrosine Phosphatase, Non-Receptor Type 11Signal TransductionT-LymphocytesTumor MicroenvironmentChemokine CXCL9Cxcl9 protein, mouseInterferon-gammaProtein Tyrosine Phosphatase, Non-Receptor Type 11Ptpn11 protein, mouse

Identifiers

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.