Related Experiment Video

Updated: Jun 5, 2026

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues
10:41

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues

Published on: April 5, 2018

Epigenetic heterogeneity and plasticity in therapy-induced tumor states through single-cell multi-omics

Hee Jung Kim1, Hwiyeong Lee2, Jin Hong2

  • 1Ajou Energy Science Research Center, Ajou University, Suwon, Korea.

Molecular Oncology
|June 4, 2026
PubMed

Insights

Epigenetic mechanisms drive cancer cell plasticity and therapeutic resistance by altering gene expression without changing DNA sequence. Understanding these epigenetic changes is key to developing new precision oncology strategies.

Area of Science:

  • Oncology
  • Epigenetics
  • Cancer Biology

Background:

  • Therapeutic resistance and disease recurrence are significant challenges in oncology.
  • Tumor heterogeneity and cancer cell plasticity are primary drivers of these challenges.
  • Epigenetic mechanisms are key regulators of adaptive transcriptional reprogramming under treatment pressure.

Purpose of the Study:

  • To review how diverse therapeutics induce epigenetic remodeling.
  • To explore the role of epigenetic changes in driving distinct cellular states.
  • To evaluate single-cell multi-omics platforms for profiling chromatin plasticity and identifying biomarkers.

Main Methods:

  • Review of current literature on epigenetic mechanisms in cancer therapy resistance.
  • Analysis of single-cell multi-omics approaches for dissecting epigenetic regulation.
  • Evaluation of therapeutic interventions including chemotherapy, targeted agents, immunotherapy, hormonal interventions, and epigenetic drugs.

Main Results:

  • Therapeutics induce widespread remodeling of DNA methylation, histone modifications, and chromatin accessibility.
  • These epigenetic changes drive transitions to drug-tolerant persister (DTP) phenotypes, senescence-like populations, epithelial-mesenchymal transition (EMT) states, and immune-evasive cell populations.
  • Single-cell multi-omics platforms enable profiling of chromatin-based plasticity and identification of clinically relevant biomarkers.

Conclusions:

  • Epigenetic plasticity is a critical mechanism underlying therapeutic resistance and cancer recurrence.
  • Single-cell multi-omics provides powerful tools to dissect these processes at high resolution.
  • Integrative analyses offer a framework for developing precision oncology strategies to overcome resistance.
Keywords:
cancer epigeneticscell state plasticitysingle‐cell multi‐omicstherapeutic resistancetumor heterogeneity

More Related Videos

Dissociation of Human and Mouse Tumor Tissue Samples for Single-cell RNA Sequencing05:58

Dissociation of Human and Mouse Tumor Tissue Samples for Single-cell RNA Sequencing

Published on: August 16, 2024

Generation of Heterogeneous Drug Gradients Across Cancer Populations on a Microfluidic Evolution Accelerator for Real-Time Observation10:24

Generation of Heterogeneous Drug Gradients Across Cancer Populations on a Microfluidic Evolution Accelerator for Real-Time Observation

Published on: September 19, 2019

Related Concept Videos

Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Chromatin Modification in iPS Cells01:32

Chromatin Modification in iPS Cells

Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
Compact chromatin makes reprogramming difficult. Enzymes, such as histone demethylases and acetyltransferases, are often added during reprogramming to loosen the chromatin, making the DNA more accessible to transcription factors. Molecules that inhibit histone...