Evidence map›Paper›PMID 35432344›Full record

ReviewFrontiers in immunology2022

Cancer Cell Phenotype Plasticity as a Driver of Immune Escape in Melanoma.

Valentin Benboubker, Félix Boivin, Stéphane Dalle, Julie Caramel

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03225365 (Immune Modulation Study in Patients With Metastatic Melanoma Treated With a First Line Therapy of Nivolumab +/- Ipilimumab), which is not on this map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.0field-weighted citation impact, top 8% 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.

NCT03225365 nacompletednot on this map

Immune Modulation Study in Patients With Metastatic Melanoma Treated With a First Line Therapy of Nivolumab +/- Ipilimumab (IMMUNONIVO/MelpredictPD1).

TypeinterventionalSponsorHospices Civils de LyonRan2019 to 2021Enrolled5ConditionsMetastatic MelanomaArmsBlood and biopsy sampling
3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 40 citations in OpenAlex.

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  10. bioRxiv : the preprint server for biology · 2025
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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

4 authors at 3 institutions in 1 country.

Valentin BenboubkerCancer Research Center of Lyon, Université de Lyon, Université Claude Bernard Lyon 1, INSERM, CNRS, Centre Léon Bérard, "Cancer cell Plasticity in Melanoma" team, Lyon, France.
Félix BoivinCancer Research Center of Lyon, Université de Lyon, Université Claude Bernard Lyon 1, INSERM, CNRS, Centre Léon Bérard, "Cancer cell Plasticity in Melanoma" team, Lyon, France.
Stéphane DalleCancer Research Center of Lyon, Université de Lyon, Université Claude Bernard Lyon 1, INSERM, CNRS, Centre Léon Bérard, "Cancer cell Plasticity in Melanoma" team, Lyon, France.
Julie CaramelCancer Research Center of Lyon, Université de Lyon, Université Claude Bernard Lyon 1, INSERM, CNRS, Centre Léon Bérard, "Cancer cell Plasticity in Melanoma" team, Lyon, France.
Centre de Recherche en Cancérologie de Lyon · FRCentre Léon Bérard · FRHospices Civils de Lyon · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunotherapies blocking negative immune checkpoints are now approved for the treatment of a growing number of cancers. However, even in metastatic melanoma, where sustained responses are observed, a significant number of patients still do not respond or display resistance. Increasing evidence indicates that non-genetic cancer cell-intrinsic alterations play a key role in resistance to therapies and immune evasion. Cancer cell plasticity, mainly associated with the epithelial-to-mesenchymal transition in carcinoma, relies on transcriptional, epigenetic or translational reprogramming. In melanoma, an EMT-like dedifferentiation process is characterized by the acquisition of invasive or neural crest stem cell-like features. Herein, we discuss recent findings on the specific roles of phenotypic reprogramming of melanoma cells in driving immune evasion and resistance to immunotherapies. The mechanisms by which dedifferentiated melanoma cells escape T cell lysis, mediate T cell exclusion or remodel the immune microenvironment will be detailed. The expanded knowledge on tumor cell plasticity in melanoma should contribute to the development of novel therapeutic combination strategies to further improve outcomes in this deadly metastatic cancer.

Indexed as

MelanomaEpithelial-Mesenchymal TransitionHumansImmunotherapyNeural CrestPhenotypeTumor Microenvironmentcancer cell plasticityEMT-likeimmune escapeimmunotherapy resistancemelanoma

Identifiers

PMID35432344
PMCPMC9012258
OpenAlexW4221010007

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.