Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Epigenetic Regulation01:46

Epigenetic Regulation

31.1K
Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
31.1K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Correction: GLYATL1 is associated with metabolic and epigenetic changes and with endocrine resistance in luminal breast cancer.

Clinical epigenetics·2026
Same author

The PRECISE European initiative for cancer-vulnerability mapping and prediction.

Nature genetics·2026
Same author

Assessing in house comprehensive genomic profiling by liquid biopsy for NSCLC patients.

Tumori·2026
Same author

Liquid biopsies for BRAF V600E assessment and monitoring in anaplastic thyroid carcinoma: a real-world study of a tertiary cancer center.

Endocrine·2026
Same author

EGFR deletion in myeloid cells reprograms the immunosuppressive landscape of colorectal cancer.

Cell death and differentiation·2026
Same author

Gene mutant dosage is associated with prognosis and metastatic tropism in 60,000 clinical cancer samples.

medRxiv : the preprint server for health sciences·2026

Related Experiment Video

Updated: Jun 29, 2025

An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation
08:48

An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation

Published on: June 30, 2015

8.3K

Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells.

Dalia Rosano1,2, Emre Sofyali1, Heena Dhiman1,2

  • 1Department of Surgery and Cancer, Imperial College London, London, United Kingdom.

Cancer Discovery
|March 25, 2024
PubMed
Summary

Endocrine therapies for estrogen receptor-positive breast cancer can induce dormant cancer cells through epigenetic reprogramming. These dormant cells can awaken unpredictably, leading to relapse, but targeting the epigenome shows promise in overcoming this resistance.

More Related Videos

Methyl-binding DNA capture Sequencing for Patient Tissues
08:40

Methyl-binding DNA capture Sequencing for Patient Tissues

Published on: October 31, 2016

8.6K
Time-lapse Imaging of Primary Preneoplastic Mammary Epithelial Cells Derived from Genetically Engineered Mouse Models of Breast Cancer
11:47

Time-lapse Imaging of Primary Preneoplastic Mammary Epithelial Cells Derived from Genetically Engineered Mouse Models of Breast Cancer

Published on: February 8, 2013

11.9K

Related Experiment Videos

Last Updated: Jun 29, 2025

An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation
08:48

An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation

Published on: June 30, 2015

8.3K
Methyl-binding DNA capture Sequencing for Patient Tissues
08:40

Methyl-binding DNA capture Sequencing for Patient Tissues

Published on: October 31, 2016

8.6K
Time-lapse Imaging of Primary Preneoplastic Mammary Epithelial Cells Derived from Genetically Engineered Mouse Models of Breast Cancer
11:47

Time-lapse Imaging of Primary Preneoplastic Mammary Epithelial Cells Derived from Genetically Engineered Mouse Models of Breast Cancer

Published on: February 8, 2013

11.9K

Area of Science:

  • Oncology
  • Cancer Biology
  • Epigenetics

Background:

  • Adjuvant endocrine therapies (ET) are used for estrogen receptor-positive breast cancer to prevent relapse by targeting micrometastases.
  • However, up to 50% of patients relapse decades later, suggesting unknown mechanisms like tumor dormancy.
  • The evolutionary strategies driving tumor awakening and resistance to ET remain poorly understood.

Purpose of the Study:

  • To investigate the genetic and transcriptional changes underlying tumor awakening in patients with late relapse.
  • To profile a rare cohort treated with long-term neoadjuvant ETs until progression.
  • To develop an in vitro evolutionary study to record adaptive strategies of individual cancer lineages.

Main Methods:

  • Analysis of late relapse patients and longitudinal profiling of patients on long-term neoadjuvant ETs.
  • In vitro evolutionary study of individual cancer lineages in parallel experiments.
  • Investigation of epigenetic reprogramming and nongenetic cell state transitions.

Main Results:

  • Endocrine therapies induce nongenetic cell state transitions into dormancy in a stochastic subset of cells via epigenetic reprogramming.
  • Single cancer lineages with divergent phenotypes awaken unpredictably, independent of recurrent genetic alterations.
  • Targeting the dormant epigenome demonstrates promising activity against adapting cancer cells.

Conclusions:

  • Epigenetic adaptation significantly contributes to the evolution of resistance to endocrine therapies in breast cancer.
  • Therapy-induced dormancy, driven by epigenetic rewiring, is a key mechanism for late relapse.
  • Targeting epigenetic changes offers a potential strategy to overcome ET resistance and prevent breast cancer recurrence.