Evidence map›Paper›PMID 36774337›Full record

ReviewOncogenesis2023

The mechanical phenotypic plasticity of melanoma cell: an emerging driver of therapy cross-resistance.

Serena Diazzi, Sophie Tartare-Deckert, Marcel Deckert

Open access · goldAbstract readReview
In one paragraph

Review in Oncogenesis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
11.5field-weighted citation impact, top 1% 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

35 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
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  6. Modulating tumor mechanics and vascular barriers to enhance chemotherapy efficacy in pancreatic tumors and melanoma.Journal of controlled release : official journal of the Controlled Release Society · 2026
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  16. Review
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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

3 authors at 1 institution in 1 country.

Serena DiazziUniversité Côte d'Azur, INSERM, C3M, Microenvironment, Signaling and Cancer, 06200, Nice, France.
Sophie Tartare-DeckertUniversité Côte d'Azur, INSERM, C3M, Microenvironment, Signaling and Cancer, 06200, Nice, France. tartare@unice.fr.ORCID http://orcid.org/0000-0001-8680-5720
Marcel DeckertUniversité Côte d'Azur, INSERM, C3M, Microenvironment, Signaling and Cancer, 06200, Nice, France. deckert@unice.fr.ORCID http://orcid.org/0000-0003-2094-559X
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advanced cutaneous melanoma is the deadliest form of skin cancer and one of the most aggressive human cancers. Targeted therapies (TT) against BRAF mutated melanoma and immune checkpoints blockade therapies (ICB) have been a breakthrough in the treatment of metastatic melanoma. However, therapy-driven resistance remains a major hurdle in the clinical management of the metastatic disease. Besides shaping the tumor microenvironment, current treatments impact transition states to promote melanoma cell phenotypic plasticity and intratumor heterogeneity, which compromise treatment efficacy and clinical outcomes. In this context, mesenchymal-like dedifferentiated melanoma cells exhibit a remarkable ability to autonomously assemble their own extracellular matrix (ECM) and to biomechanically adapt in response to therapeutic insults, thereby fueling tumor relapse. Here, we review recent studies that highlight mechanical phenotypic plasticity of melanoma cells as a hallmark of adaptive and non-genetic resistance to treatment and emerging driver in cross-resistance to TT and ICB. We also discuss how targeting BRAF-mutant dedifferentiated cells and ECM-based mechanotransduction pathways may overcome melanoma cross-resistance.

Identifiers

PMID36774337
PMCPMC9922263
OpenAlexW4320040253

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.