Skip to content
DraconiticResearch
Search Sources API
203,234 studies31 sourcesUpdated 13 min ago
Peer-reviewedCC BYNAR cancer

Epigenetic adaptations and vulnerabilities in ovarian cancer drug-tolerant persister cells.

  • Mihai G Dumbrava1,2
  • Sierra J Hamernick1,3
  • Shariska P Harrington4
  • Alexandre Gaspar-Maia1
4 affiliations
  1. 1Division of Investigative Pathobiology, Department of Lab Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, United States.
  2. 2Mayo Medical Scientist Training Program, Mayo Clinic, Rochester, MN 55905, United States.
  3. 3Mayo Clinic Graduate School of Biomedical Sciences, Mayo Clinic, Rochester, MN 55905, United States.
  4. 4Department of Obstetrics and Gynecology, Mayo Clinic, Rochester, MN 55905, United States.
Read full textPDFDOICite

Abstract

High-grade serous ovarian carcinoma (HGSOC) recurs in most patients despite initial responses to chemotherapy and poly(ADP-ribose) polymerase inhibition. A leading explanation for the high rates of recurrence is the presence of minimal residual disease (MRD) comprised of drug-tolerant persister (DTP) cells that survive therapy through reversible epigenetic reprogramming. DTPs have various adaptations that enable them to tolerate therapy and eventually develop into resistant clones, including quiescence, metabolic and hypoxic stress responses, epithelial-mesenchymal plasticity, and immune evasion. Here, we discuss evidence from ovarian cancer of epigenetic mechanisms that coordinate DTP phenotypes, including DNA methylation, histone post-translational modifications, enhancer rewiring, and transcription factor gene-regulatory networks. Based on therapeutic vulnerabilities identified from increased resolution of DTPs, we highlight epigenetic therapies that are currently in clinical trials aimed at depleting MRD to delay or prevent relapse in HGSOC. Finally, we outline emerging technologies that have the potential to detect and monitor persister states in patients, including single-cell transcriptomic and epigenomic profiling, long-read sequencing, and spatial mapping of tumor biopsies.

Related

  1. Epigenetic rewiring of immunological memory in cancer: heterogeneity, mechanisms, and therapeutic vulnerabilities
    Wenna Liu, Xiaole Pan, Yujia Zhao +3
    Frontiers in ImmunologyPeer-reviewedCC BY 4.0Full textOncologyPMCCrossrefEurope PMC
  2. Circulating epigenetic and epitranscriptomic biomarkers identify EGFR status, predict TKI response and reveal therapeutic vulnerabilities in NSCLC
    Dorian Espi-Bastien, Judith Raimbourg, Gwenola Bougras-Cartron +13
    Scientific ReportsPeer-reviewedCC BYFull text1 citedOncologyDOAJ
  3. The developmental, genetic, and epigenetic basis of polyendocrine metabolic ovarian syndrome
    Abdallah Mahdi, Abeer Qannan, Nady El Hajj
    Frontiers in EndocrinologyPeer-reviewedCC BY 4.0Obstetrics, gynaecology & paediatricsCrossref
  4. Persister cells and their effects on cancer stabilization therapy
    M. Satouri, P. Altrock, J. Rezaei +1
    bioRxivPreprintCC BYFull textOncologybioRxiv
  5. Erasing the invisible: targeting persister cells to cure minimal residual disease
    Yu Wang, Zijian Shi, Fangquan Xu +8
    Holistic Integrative OncologyPeer-reviewedCC BYFull textOncologyDOAJ

Cite

BibTeXRIS
BibTeX
@article{dumbrava2026epigenetic,
  title = {{Epigenetic adaptations and vulnerabilities in ovarian cancer drug-tolerant persister cells.}},
  author = {Mihai G Dumbrava and Sierra J Hamernick and Shariska P Harrington and Alexandre Gaspar-Maia},
  journal = {NAR cancer},
  year = {2026},
  month = oct,
  doi = {10.1093/narcan/zcag030},
  url = {https://europepmc.org/article/MED/42923094},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Epigenetic adaptations and vulnerabilities in ovarian cancer drug-tolerant persister cells.
AU  - Mihai G Dumbrava
AU  - Sierra J Hamernick
AU  - Shariska P Harrington
AU  - Alexandre Gaspar-Maia
PY  - 2026
DA  - 2026/10/22
JO  - NAR cancer
DO  - 10.1093/narcan/zcag030
UR  - https://europepmc.org/article/MED/42923094
AB  - High-grade serous ovarian carcinoma (HGSOC) recurs in most patients despite initial responses to chemotherapy and poly(ADP-ribose) polymerase inhibition. A leading explanation for the high rates of recurrence is the presence of minimal residual disease (MRD) comprised of drug-tolerant persister (DTP) cells that survive therapy through reversible epigenetic reprogramming. DTPs have various adaptations that enable them to tolerate therapy and eventually develop into resistant clones, including quiescence, metabolic and hypoxic stress responses, epithelial-mesenchymal plasticity, and immune evasion. Here, we discuss evidence from ovarian cancer of epigenetic mechanisms that coordinate DTP phenotypes, including DNA methylation, histone post-translational modifications, enhancer rewiring, and transcription factor gene-regulatory networks. Based on therapeutic vulnerabilities identified from increased resolution of DTPs, we highlight epigenetic therapies that are currently in clinical trials aimed at depleting MRD to delay or prevent relapse in HGSOC. Finally, we outline emerging technologies that have the potential to detect and monitor persister states in patients, including single-cell transcriptomic and epigenomic profiling, long-read sequencing, and spatial mapping of tumor biopsies.
SN  - 2632-8674
ER  -