Evidence map›Paper›PMID 25294815›Full record

ArticleOncotarget2014

Melanoma-initiating cells exploit M2 macrophage TGFβ and arginase pathway for survival and proliferation.

Muly Tham, Kar Wai Tan, Jo Keeble, Xiaojie Wang, Sandra Hubert, Luke Barron, Nguan Soon Tan, Masashi Kato, Armelle Prevost-Blondel, Veronique Angeli and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  5. Review
  6. Article
  7. Article
  8. Article
  9. Arginine Metabolism and Its Potential in Treatment of Colorectal Cancer.Frontiers in cell and developmental biology · 2021
    Review
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  11. 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

11 authors at 7 institutions in 4 countries.

Muly ThamSingapore Immunology Network, BMSI, A-STAR, Singapore.
Kar Wai TanSingapore Immunology Network, BMSI, A-STAR, Singapore. Department of Clinical Research, Singapore General Hospital, Singapore.
Jo KeebleSingapore Immunology Network, BMSI, A-STAR, Singapore.
Xiaojie WangSingapore Immunology Network, BMSI, A-STAR, Singapore.
Sandra HubertSingapore Immunology Network, BMSI, A-STAR, Singapore.
Luke BarronLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Nguan Soon TanSchool of Biological Sciences, Nanyang Technological University, Singapore.
Masashi KatoDepartment of Occupational and Environmental Health, Nagoya University Graduate School of Medicine, Japan.
Armelle Prevost-BlondelInstitut Cochin, Université Paris Descartes, CNRS UMR, Paris, France.
Veronique AngeliDepartment of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Jean-Pierre AbastadoSingapore Immunology Network, BMSI, A-STAR, Singapore. Institut de Recherche Internationales Servier, 50 rue Carnot, Suresnes cedex, France.
Agency for Science, Technology and Research · SGSingapore Immunology Network · SGNagoya University · JPNanyang Technological University · SGNational Institutes of Health · USNational University of Singapore · SGUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

M2 macrophages promote tumor growth and metastasis, but their interactions with specific tumor cell populations are poorly characterized. Using a mouse model of spontaneous melanoma, we showed that CD34- but not CD34+ tumor-initiating cells (TICs) depend on M2 macrophages for survival and proliferation. Tumor-associated macrophages (TAMs) and macrophage-conditioned media protected CD34- TICs from chemotherapy in vitro. In vivo, while inhibition of CD115 suppressed the macrophage-dependent CD34- TIC population, chemotherapy accelerated its development. The ability of TICs to respond to TAMs was acquired during melanoma progression and immediately preceded a surge in metastatic outgrowth. TAM-derived transforming growth factor-β (TGFβ) and polyamines produced via the Arginase pathway were critical for stimulation of TICs and synergized to promote their growth.

Indexed as

AnimalsArginaseCell ProliferationCell SurvivalDisease Models, AnimalFemaleMacrophagesMaleMelanomaMiceMice, Mutant StrainsNeoplastic Stem CellsSignal TransductionTransforming Growth Factor betaArginaseTransforming Growth Factor beta

Identifiers

PMID25294815
PMCPMC4322977
OpenAlexW1935766386

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.