Evidence map›Paper›PMID 42257802›Full record

ReviewCurrent oncology reports2026

The Role of EZH2 ın Malıgnant Pleural Mesothelıoma and Beyond: Current Practıce and Future Perspectıves.

Mehmet Kucukoner, Tarik Demir, Abduljalil Mohammed Alsubaie, Ulas Alabalik, Aisha K Ibrahim, Mariaelena Pierobon, Lance Liotta

Abstract readReview
In one paragraph

Review in Current oncology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Mehmet KucukonerDepartment of Medical Oncology, Dicle University Faculty of Medicine, Diyarbakır, Turkey.ORCID 0000-0001-7336-871X
Tarik DemirThe Ohio State University Wexner Medical Center, Columbus, OH, USA.ORCID 0000-0001-6334-4079
Abduljalil Mohammed AlsubaieCenter for Applied Proteomics and Molecular Medicine, George Mason University, VA, USA.
Ulas AlabalikDepartment of Pathology, Dicle University Faculty of Medicine, Diyarbakir, Turkey.ORCID 0000-0003-4551-8439
Aisha K IbrahimCenter for Applied Proteomics and Molecular Medicine, George Mason University, VA, USA.
Mariaelena PierobonCenter for Applied Proteomics and Molecular Medicine, George Mason University, VA, USA.ORCID 0000-0003-2084-1029
Lance LiottaCenter for Applied Proteomics and Molecular Medicine, George Mason University, VA, USA. liotta.lance@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewMalignant pleural mesothelioma (MPM) remains a rare but highly aggressive malignancy with limited treatment options and poor prognosis. For nearly twenty years, platinum-pemetrexed chemotherapy has persisted as the unchanged standard treatment; although recent progress in immunotherapy has modestly disrupted this therapeutic plateau, survival outcomes remain disappointingly limited. This review aims to provide a comprehensive overview of the epigenetic landscape of MPM, focusing particularly on the oncogenic and therapeutic implications of enhancer of zeste homolog 2 (EZH2), and to discuss its potential as a target for novel therapeutic strategies and combination regimens. RECENT

findingsEpigenetic dysregulation has emerged as a central driver of mesothelioma pathogenesis. EZH2, the catalytic component of the polycomb repressive complex 2 (PRC2), mediates histone H3K27 trimethylation, silencing tumor suppressor genes and promoting malignant transformation. In addition to its canonical role, EZH2 has non-canonical oncogenic effects that modulate transcription, apoptosis, DNA repair, and immune evasion. High EZH2 expression correlates with BAP1 loss, which enhances chromatin remodeling defects and disease aggressiveness. Preclinical and early clinical data demonstrate that EZH2 inhibitors-including tazemetostat, valemetostat, GSK126, EPZ011989, tulmimetostat, and novel PROTAC-based degraders such as MS1943-can suppress tumor progression, modulate the tumor immune microenvironment, and restore therapeutic sensitivity. Furthermore, combination approaches integrating EZH2 inhibition with chemotherapy or immune checkpoint blockade show synergistic potential in overcoming resistance. EZH2 represents a pivotal epigenetic regulator and a promising therapeutic target in MPM. Further understanding the dual canonical and non-canonical roles of EZH2 in tumor biology will be key to optimizing targeted and combinatorial treatment strategies. Future research should focus on translating EZH2 inhibition into clinical benefit, identifying predictive biomarkers of response, and exploring rational combinations with chemotherapy, targeted drugs, or immunotherapy to improve survival outcomes in mesothelioma patients.

Indexed as

Enhancer of Zeste Homolog 2 ProteinMesotheliomaMesothelioma, MalignantPleural NeoplasmsEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanBAP1EpigeneticsEZH2ImmunotherapyMesotheliomaPRC2

Identifiers

PMID42257802
PMCPMC13246576

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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.