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

The Tumor Microenvironment02:17

The Tumor Microenvironment

7.6K
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...
7.6K
Tumor Immunotherapy01:27

Tumor Immunotherapy

1.7K
Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
1.7K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

7.7K
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
7.7K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

6.9K
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,...
6.9K
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

5.4K
Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
5.4K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

9.3K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
9.3K

You might also read

Related Articles

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

Sort by
Same author

Cis and trans regulatory mechanisms of extrachromosomal DNA segregation.

Nature cell biology·2026
Same author

Dose-dependent hormone actions at estrogen receptor enhancers specify distinct molecular and biological outcomes.

Science advances·2026
Same author

Accurate prediction of ecDNA in interphase cancer cells using deep neural networks.

Communications biology·2026
Same author

TWIST1 mediated transcriptional activation of SPON2 drives colorectal cancer peritoneal metastasis through stromal cell signaling network.

Oncogene·2026
Same author

Publisher Correction: PtdIns(3,5)P<sub>2</sub> is an endogenous ligand of STING in innate immune signalling.

Nature·2026
Same author

<i>Cis</i> and <i>Trans</i> Regulatory Mechanisms of ecDNA Segregation.

bioRxiv : the preprint server for biology·2026

Related Experiment Video

Updated: Jan 10, 2026

In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells
08:02

In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells

Published on: September 23, 2021

3.0K

ecDNA-driven oncogene super-expressors shape immunoevasive tumor microenvironment.

Kailiang Qiao1, Qing-Lin Yang1,2, Tuo Li2,3,4

  • 1Children's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.

Biorxiv : the Preprint Server for Biology
|November 26, 2025
PubMed
Summary

Extrachromosomal DNA (ecDNA) drives pancreatic cancer aggression and immune evasion by creating "super-expressor" cells. These cells remodel the tumor microenvironment, reducing T cell infiltration and promoting cancer growth.

More Related Videos

Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells
10:04

Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells

Published on: August 1, 2025

1.4K
Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells
09:04

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

1.4K

Related Experiment Videos

Last Updated: Jan 10, 2026

In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells
08:02

In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells

Published on: September 23, 2021

3.0K
Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells
10:04

Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells

Published on: August 1, 2025

1.4K
Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells
09:04

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

1.4K

Area of Science:

  • Oncology
  • Cancer Genetics
  • Immunology

Background:

  • Extrachromosomal DNA (ecDNA) contributes to cancer genetic heterogeneity.
  • Emerging evidence suggests a link between ecDNA and immune evasion, but the underlying mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the role of ecDNA in pancreatic ductal adenocarcinoma (PDAC) progression and immune evasion.
  • To elucidate the mechanism by which ecDNA influences the tumor microenvironment (TME) and anti-tumor immunity.

Main Methods:

  • Genetically engineered mouse models of PDAC.
  • Single-cell transcriptomic and histological analyses.
  • Analysis of TME components, including cancer-associated fibroblasts (CAFs) and T cells.

Main Results:

  • ecDNA-driven tumors, characterized by amplified Kras and Myc oncogenes, exhibit increased aggressiveness in immunocompetent mice.
  • ecDNA promotes rapid establishment of an immunoevasive TME with increased myofibroblastic CAFs (myCAFs) and reduced T cell infiltration.
  • A subset of cancer cells, termed "super-expressors," exhibit extremely high Kras expression, secrete amphiregulin, promote myCAF expansion, and suppress T cell infiltration.

Conclusions:

  • ecDNA plays a causal role in remodeling the TME, contributing to pancreatic cancer heterogeneity and immune evasion.
  • Super-expressor cells driven by ecDNA establish an immunoevasive niche in PDAC.
  • Targeting ecDNA or its downstream effectors may represent a novel therapeutic strategy for PDAC.