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

Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

4.9K
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

5.7K
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,...
5.7K
The Tumor Microenvironment02:17

The Tumor Microenvironment

6.6K
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
6.6K
Tumor Progression02:07

Tumor Progression

6.2K
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
6.2K
Cancer02:18

Cancer

48.1K
Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
48.1K
Metastasis02:30

Metastasis

5.5K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.5K

You might also read

Related Articles

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

Sort by
Same author

MIF-CD74 Signaling Defines a Brain-Specific Immune Vulnerability in Metastasis and Neurologic Disease.

Cancer research·2026
Same author

Fueling Immunotherapy Resistance: SSBP4 Links Tumor Cholesterol Biosynthesis to Immune Evasion.

Cancer immunology research·2026
Same author

Ribosome biogenesis bottlenecks reveal vulnerabilities in cancer.

bioRxiv : the preprint server for biology·2026
Same author

Targeting autocrine retinoic acid signaling by ALDH1A2 inhibition enhances antitumor dendritic cell vaccine efficacy.

Nature immunology·2026
Same author

Family with sequence similarity 114 member A1 orchestrates immune evasion in triple-negative breast cancer.

Signal transduction and targeted therapy·2025
Same author

Unveiling cancer crosstalk: Mapping complexity across time and space.

PLoS biology·2025

Related Experiment Video

Updated: Jun 7, 2025

Heteromulticellular Stromal Cells in Scaffold-free 3D Cultures of Epithelial Cancer Cells to Drive Invasion
09:18

Heteromulticellular Stromal Cells in Scaffold-free 3D Cultures of Epithelial Cancer Cells to Drive Invasion

Published on: April 4, 2025

392

Tumor Heterogeneity and Cooperating Cancer Hallmarks Driven by Divergent EMT Programs.

Phoebe Carter1,2, Yibin Kang1,2

  • 1Department of Molecular Biology, Princeton University, Princeton, New Jersey.

Cancer Research
|November 15, 2024
PubMed
Summary

Two distinct epithelial-to-mesenchymal transition (EMT) programs cooperate within a single tumor, driving cancer cell plasticity and intratumoral heterogeneity. This study reveals how different EMT states contribute to malignant progression.

More Related Videos

Heterogeneity Mapping of Protein Expression in Tumors using Quantitative Immunofluorescence
07:54

Heterogeneity Mapping of Protein Expression in Tumors using Quantitative Immunofluorescence

Published on: October 25, 2011

18.6K
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

19.6K

Related Experiment Videos

Last Updated: Jun 7, 2025

Heteromulticellular Stromal Cells in Scaffold-free 3D Cultures of Epithelial Cancer Cells to Drive Invasion
09:18

Heteromulticellular Stromal Cells in Scaffold-free 3D Cultures of Epithelial Cancer Cells to Drive Invasion

Published on: April 4, 2025

392
Heterogeneity Mapping of Protein Expression in Tumors using Quantitative Immunofluorescence
07:54

Heterogeneity Mapping of Protein Expression in Tumors using Quantitative Immunofluorescence

Published on: October 25, 2011

18.6K
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

19.6K

Area of Science:

  • Oncology
  • Cell Biology
  • Developmental Biology

Background:

  • Epithelial-to-mesenchymal transition (EMT) drives cellular plasticity in physiological and pathological processes.
  • Partial EMT, where cells retain epithelial and mesenchymal traits, is increasingly recognized for its role in cancer.
  • Mechanisms of EMT and their contribution to tumor heterogeneity are not fully understood.

Purpose of the Study:

  • To investigate how different EMT programs contribute to intratumoral heterogeneity.
  • To elucidate the cooperative mechanisms between distinct EMT trajectories in cancer.

Main Methods:

  • Utilized a murine mammary tumor model.
  • Analyzed two distinct EMT programs associated with organ fibrosis and embryonic development.

Main Results:

  • Demonstrated that disparate EMT programs operate concurrently within different cells of the same tumor.
  • Provided mechanistic insights into the development of intratumoral heterogeneity through EMT cooperation.

Conclusions:

  • Two distinct EMT programs can coexist and cooperate within a single tumor, fostering heterogeneity.
  • This cooperation between EMT trajectories contributes to pro-malignant features and tumor progression.