ReviewBioscience reports2026
Epigenetic mechanisms and clinical translation in ovarian cancer: from molecular pathways to precision therapy.
Review in Bioscience 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.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Ovarian cancer remains one of the deadliest gynecological malignancies, mainly due to its late diagnosis, biological heterogeneity, and frequent development of chemoresistance. Recent evidence indicates that epigenetic dysregulation including aberrant DNA methylation, histone modifications, chromatin remodeling, and non-coding RNA networks plays an important role in the initiation, progression, and therapeutic response of ovarian cancer. Unlike genetic alterations, epigenetic modifications are reversible, making them attractive targets for drug development and precision oncology. In this review, we provide a detailed overview of the epigenetic mechanisms that control ovarian cancer biology, with specific focus on their role in drug resistance and disease recurrence. We discuss the role of epigenetic plasticity in enabling transition of tumor cells into drug tolerant, stem like phenotypes, leading to minimal residual disease and eventual relapse without permanent genetic changes. Attention is given to the influence of DNA methyltransferases, histone deacetylases, enhancer of zeste homolog 2, and chromatin remodeling complexes in the maintenance of adaptive resistance programs. We also discuss the evolving paradigm of epigenetic regulation, immune modulation and viral mimicry and provide the rationale for combining epigenetic therapies with immunotherapy and poly(ADP-ribose) polymerase inhibition. The article also reviews the results of recent clinical trials and evaluate the most recent advances in biomarker development, such as circulating DNA methylation signatures, microRNAs, and artificial intelligence-based liquid biopsy platforms. Finally, we discussed the potential implications of applying epigenetic profiling in the clinic for improved patient stratification and the potential for real-time monitoring of chemoresistance. These progresses make epigenetic regulation a promising strategy to overcome chemoresistance and improve personalized medicine of ovarian cancer.
Indexed as
Identifiers
What Socratic 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 Socratic graph.