Evidence map›Paper›PMID 35725813›Full record

ArticleBritish journal of cancer2022

M-CSF as a therapeutic target in BRAF

C Barceló, P Sisó, I de la Rosa, C Megino-Luque, R Navaridas, O Maiques, I Urdanibia, N Eritja, X Soria, M Potrony and 5 more

Open access · greenAbstract read
In one paragraph

Article in British journal of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Exploring association of melanoma-specific Bcl-xL with tumor immune microenvironment.Journal of experimental & clinical cancer research : CR · 2023
    Article
  8. Article
  9. Review
  10. Phytochemicals as Immunomodulatory Agents in Melanoma.International journal of molecular sciences · 2023
    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

15 authors at 3 institutions in 2 countries.

C Barceló *Oncologic Pathology Group, University of Lleida, IRBLleida, Lleida, Spain.
P Sisó *Oncologic Pathology Group, University of Lleida, IRBLleida, Lleida, Spain.
I de la RosaOncologic Pathology Group, University of Lleida, IRBLleida, Lleida, Spain.
C Megino-LuqueOncologic Pathology Group, University of Lleida, IRBLleida, Lleida, Spain.
R NavaridasOncologic Pathology Group, University of Lleida, IRBLleida, Lleida, Spain.ORCID http://orcid.org/0000-0003-1622-5311
O MaiquesCentre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID http://orcid.org/0000-0002-2172-4388
I UrdanibiaOncologic Pathology Group, University of Lleida, IRBLleida, Lleida, Spain.
N EritjaOncologic Pathology Group, University of Lleida, IRBLleida, Lleida, Spain.
X SoriaDepartment of Dermatology, Hospital Universitari Arnau de Vilanova, University of Lleida, IRBLleida, Lleida, Spain.
M PotronyBiomedical Research Networking Center on Rare Diseases (CIBERER), ISCIII, Barcelona, Spain.
N Calbet-LlopartBiomedical Research Networking Center on Rare Diseases (CIBERER), ISCIII, Barcelona, Spain.
S PuigBiomedical Research Networking Center on Rare Diseases (CIBERER), ISCIII, Barcelona, Spain.ORCID http://orcid.org/0000-0003-1337-9745
X Matías-GuiuCentre of Biomedical Research on Cancer (CIBERONC), Instituto de Salud Carlos III (ISCIII), Madrid, Spain.
R M MartíCentre of Biomedical Research on Cancer (CIBERONC), Instituto de Salud Carlos III (ISCIII), Madrid, Spain. marti@medicina.udl.cat.ORCID http://orcid.org/0000-0001-6866-6114
A MaciàOncologic Pathology Group, University of Lleida, IRBLleida, Lleida, Spain. amacia@irblleida.cat.ORCID http://orcid.org/0000-0001-6038-178X
Universitat de Lleida · ESInstituto de Salud Carlos III · ESQueen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDisseminated BRAF

methodsConditioned media from melanoma cells were analysed by citoarray. Viability and migration/invasion assays were performed with paired melanoma cells and tumour growth in xenografted SCID mice. We evaluated the impact of M-CSF plasma levels with clinical prognosis from 35 metastatic BRAF

resultsBRAFi-resistant melanoma cells secretome is rich in pro-tumour cytokines. M-CSF secretion is essential to induce a Vemurafenib-resistant phenotype in melanoma cells. Further, we demonstrated that M-CSF mAb in combination with Vemurafenib and autophagy blockers synergistically induce apoptosis, impair migration and reduce tumour growth in BRAFi-resistant melanoma cells. Interestingly, lower M-CSF plasma levels are associated with better prognosis in metastatic melanoma patients.

conclusionsSecreted M-CSF induces a BRAFi-resistant phenotype and means worse prognosis in BRAF

Indexed as

MelanomaProto-Oncogene Proteins B-rafAnimalsCell Line, TumorDrug Resistance, NeoplasmIndolesMacrophage Colony-Stimulating FactorMiceMice, SCIDMutationProtein Kinase InhibitorsSulfonamidesVemurafenibIndolesMacrophage Colony-Stimulating FactorProtein Kinase InhibitorsProto-Oncogene Proteins B-rafSulfonamidesVemurafenib

Identifiers

PMID35725813
PMCPMC9470708
OpenAlexW4283162058

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.