ArticleEpigenomes2018
Targeting EZH2 in Multiple Myeloma-Multifaceted Anti-Tumor Activity.
Article in Epigenomes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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.
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.
Who cites it
22 citing papers in PubMed, 26 citations in OpenAlex.
- EZH2 inhibition overcomes immunomodulatory drug resistance in multiple myeloma via a cereblon-dependent pathway.Haematologica · 2026Article
- Genome-wide copy number profiling enhances risk stratification in multiple myeloma by shallow whole-genome sequencing.Blood advances · 2026Article
- Epigenetic reprogramming in multiple myeloma-Challenges and opportunities.International journal of cancer · 2026Review
- EZH1/EZH2 inhibition enhances adoptive T cell immunotherapy against multiple cancer models.Cancer cell · 2025Article
- The SAGA acetyltransferase module is required for the maintenance of MAF and MYC oncogenic gene expression programs in multiple myeloma.Genes & development · 2024Article
- The SAGA acetyltransferase module is required for the maintenance of MAF and MYC oncogenic gene expression programs in multiple myeloma.bioRxiv : the preprint server for biology · 2024Article
- Epigenetic regulation of CD38/CD48 by KDM6A mediates NK cell response in multiple myeloma.Nature communications · 2024Article
- CRISPR/Cas9‑mediated EZH2 knockout suppresses the proliferation and migration of triple‑negative breast cancer cells.Oncology letters · 2023Article
- Review
- Review
- Multiple Myeloma: Bioinformatic Analysis for Identification of Key Genes and Pathways.Bioinformatics and biology insights · 2022Article
- Inhibition of cytoplasmic EZH2 induces antitumor activity through stabilization of the DLC1 tumor suppressor protein.Nature communications · 2021Article
- Insights into high-risk multiple myeloma from an analysis of the role of PHF19 in cancer.Journal of experimental & clinical cancer research : CR · 2021Review
- The long non-coding RNA CRNDE regulates growth of multiple myeloma cells via an effect on IL6 signalling.Leukemia · 2021Article
- The role and mechanisms of polycomb repressive complex 2 on the regulation of osteogenic and neurogenic differentiation of stem cells.Cell proliferation · 2021Review
- CTCF-silenced miR-137 contributes to EMT and radioresistance in esophageal squamous cell carcinoma.Cancer cell international · 2021Article
- Treatment Strategies Considering Micro-Environment and Clonal Evolution in Multiple Myeloma.Cancers · 2021Review
- Role of Polycomb Complexes in Normal and Malignant Plasma Cells.International journal of molecular sciences · 2020Review
- Acquired resistance to DZNep-mediated apoptosis is associated with copy number gains of AHCY in a B-cell lymphoma model.BMC cancer · 2020Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The enhancer of zeste homolog 2 (EZH2) is the enzymatic subunit of the polycomb repressive complex 2 (PRC2) that exerts important functions during normal development as well as disease. PRC2 through EZH2 tri-methylates histone H3 lysine tail residue 27 (H3K27me3), a modification associated with repression of gene expression programs related to stem cell self-renewal, cell cycle, cell differentiation, and cellular transformation. EZH2 is deregulated and subjected to gain of function or loss of function mutations, and hence functions as an oncogene or tumor suppressor gene in a context-dependent manner. The development of highly selective inhibitors against the histone methyltransferase activity of EZH2 has also contributed to insight into the role of EZH2 and PRC2 in tumorigenesis, and their potential as therapeutic targets in cancer. EZH2 can function as an oncogene in multiple myeloma (MM) by repressing tumor suppressor genes that control apoptosis, cell cycle control and adhesion properties. Taken together these findings have raised the possibility that EZH2 inhibitors could be a useful therapeutic modality in MM alone or in combination with other targeted agents in MM. Therefore, we review the current knowledge on the regulation of EZH2 and its biological impact in MM, the anti-myeloma activity of EZH2 inhibitors and their potential as a targeted therapy in MM.
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Identifiers
What OpenQuestion holds
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.