Evidence map›Paper›PMID 31323160›Full record

ArticlePigment cell & melanoma research2020

Osteoblasts contribute to a protective niche that supports melanoma cell proliferation and survival.

Jennifer Ferguson, Daniel J Wilcock, Sophie McEntegart, Andrew P Badrock, Mitch Levesque, Reinhard Dummer, Claudia Wellbrock, Michael P Smith

Open access · hybridAbstract read
In one paragraph

Article in Pigment cell & melanoma research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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  6. Association of Genetic Polymorphisms inJournal of oncology · 2020
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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

8 authors at 2 institutions in 2 countries.

Jennifer FergusonManchester Cancer Research Centre, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.
Daniel J WilcockManchester Cancer Research Centre, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.
Sophie McEntegartManchester Cancer Research Centre, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.
Andrew P BadrockManchester Cancer Research Centre, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.
Mitch LevesqueDepartment of Dermatology, Universitäts Spital Zürich, University of Zürich, Zurich, Switzerland.
Reinhard DummerDepartment of Dermatology, Universitäts Spital Zürich, University of Zürich, Zurich, Switzerland.
Claudia WellbrockManchester Cancer Research Centre, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.ORCID 0000-0002-3825-6381
Michael P SmithManchester Cancer Research Centre, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.ORCID 0000-0002-5980-7840
Manchester Academic Health Science Centre · GBUniversity of Zurich · CH

Funding

Cancer Research UK 16416Cancer Research UK C11591/A16416
6 · The paper itself

Abstract

Melanoma is the deadliest form of skin cancer; a primary driver of this high level of morbidity is the propensity of melanoma cells to metastasize. When malignant tumours develop distant metastatic lesions the new local tissue niche is known to impact on the biology of the cancer cells. However, little is known about how different metastatic tissue sites impact on frontline targeted therapies. Intriguingly, melanoma bone lesions have significantly lower response to BRAF or MEK inhibitor therapies. Here, we have investigated how the cellular niche of the bone can support melanoma cells by stimulating growth and survival via paracrine signalling between osteoblasts and cancer cells. Melanoma cells can enhance the differentiation of osteoblasts leading to increased production of secreted ligands, including RANKL. Differentiated osteoblasts in turn can support melanoma cell proliferation and survival via the secretion of RANKL that elevates the levels of the transcription factor MITF, even in the presence of BRAF inhibitor. By blocking RANKL signalling, either via neutralizing antibodies, genetic alterations or the RANKL receptor inhibitor SPD304, the survival advantage provided by osteoblasts could be overcome.

Indexed as

Cell DifferentiationCell Line, TumorCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticHumansMelanomaMicrophthalmia-Associated Transcription FactorOsteoblastsProto-Oncogene Proteins B-rafRANK LigandSignal TransductionMicrophthalmia-Associated Transcription FactorProto-Oncogene Proteins B-rafRANK LigandBRAFmelanomaMITFOsteoblastsRANKLresistance

Identifiers

PMID31323160
PMCPMC6972519
OpenAlexW2961630471

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.