Related Experiment Video

Updated: Jul 11, 2025

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
07:29

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies

Published on: June 20, 2015

19.7K

Persister cell plasticity in tumour drug resistance

Paul C McDonald1, Shoukat Dedhar2

  • 1Department of Integrative Oncology, BC Cancer Research Institute, Vancouver, BC V5Z 1L3, Canada.

Seminars in Cell & Developmental Biology
|November 17, 2023
PubMed

Insights

Therapeutic resistance in cancer is often driven by non-genetic, plastic changes in drug-tolerant persister (DTP) cells. Understanding DTP cell plasticity and vulnerability to ferroptosis is key to overcoming treatment failure.

Area of Science:

  • Oncology
  • Cancer Biology
  • Cellular Plasticity

Background:

  • Therapeutic resistance is a major cause of cancer mortality.
  • Non-genetic mechanisms, particularly cellular plasticity, drive acquired resistance.
  • Drug-tolerant persister (DTP) cells emerge due to this plasticity, contributing to tumor heterogeneity and treatment failure.

Purpose of the Study:

  • To review the key features of DTP cells.
  • To highlight phenotypic and metabolic plasticity as drivers of DTP cell tolerance and persistence.
  • To explore the connection between DTP cell plasticity and ferroptosis vulnerability.

Main Methods:

  • Literature review focusing on DTP cells.
  • Analysis of phenotypic and metabolic plasticity in cancer resistance.
  • Examination of the relationship between DTP cells, anastasis, and ferroptosis.

Main Results:

  • DTP cells exhibit significant phenotypic and metabolic plasticity.
  • This plasticity contributes to reversible therapeutic resistance.
  • DTP cells may be vulnerable to ferroptosis, a cell death pathway.

Conclusions:

  • Cellular plasticity is a critical factor in the emergence of DTP cells and therapeutic resistance.
  • Targeting DTP cell plasticity and exploiting ferroptosis presents a potential strategy to overcome treatment resistance.
  • Further research into DTP cells, anastasis, and ferroptosis is warranted for improved cancer therapies.
Keywords:
AnastasisDrug tolerant persister cellEpithelial-to-mesenchymal transitionFerroptosisPlasticityTherapy resistance

More Related Videos

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel06:44

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel

Published on: September 8, 2017

13.4K
Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

7.2K

Related Concept Videos

Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.3K
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
4.9K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.8K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
7.7K
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...
4.9K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.5K