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

Tumor Immunotherapy01:27

Tumor Immunotherapy

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.
The Tumor Microenvironment02:17

The Tumor Microenvironment

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...
The Tumor Microenvironment02:17

The Tumor Microenvironment

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...
Cancer Vaccines01:30

Cancer Vaccines

Cancer treatment vaccines are a rapidly evolving field that offers a promising approach to immunotherapy. Unlike traditional vaccines that prevent diseases, cancer treatment vaccines are designed to treat existing cancers by stimulating the immune system to recognize and attack cancer cells.
Cancer vaccines come in two categories: preventive (prophylactic) and treatment (active). Preventive vaccines, such as the Human Papillomavirus (HPV) vaccine, protect against viruses that cause certain...
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,...
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,...

You might also read

Related Articles

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

Sort by
Same author

Circadian screening of neutrophils identifies therapeutic targets in multiple sclerosis.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Retraction Note: Time-of-day immunochemotherapy in non-small cell lung cancer: a randomized phase 3 trial.

Nature medicine·2026
Same author

Author Correction: Proteasome-guided haem signalling axis contributes to T cell exhaustion.

Nature·2026
Same author

The ABA-GmABI5-GmCDK8 regulatory axis compromises soybean resistance to Phytophthora sojae.

Plant physiology·2026
Same author

Proteasome-guided haem signalling axis contributes to T cell exhaustion.

Nature·2026
Same author

BMAL1 modulates glutamine supply to control haematopoietic stem and progenitor cell expansion.

Development (Cambridge, England)·2026

Related Experiment Video

Updated: Jun 12, 2026

Evaluation of Tumor-infiltrating Leukocyte Subsets in a Subcutaneous Tumor Model
07:49

Evaluation of Tumor-infiltrating Leukocyte Subsets in a Subcutaneous Tumor Model

Published on: April 13, 2015

Dec2 conceals tumors from the immune system.

Tianyue Sun1, Christoph Scheiermann2

  • 1Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.

Developmental Cell
|June 10, 2026
PubMed
Summary
This summary is machine-generated.

Researchers identified the circadian regulator Dec2 as a key factor enabling dormant pancreatic ductal adenocarcinoma (PDAC) cells to hide from the immune system. This discovery reveals a new mechanism of tumor immune evasion tied to the timing of biological processes.

More Related Videos

Tumor Transplantation for Assessing the Dynamics of Tumor-Infiltrating CD8+ T Cells in Mice
07:36

Tumor Transplantation for Assessing the Dynamics of Tumor-Infiltrating CD8+ T Cells in Mice

Published on: June 12, 2021

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

Related Experiment Videos

Last Updated: Jun 12, 2026

Evaluation of Tumor-infiltrating Leukocyte Subsets in a Subcutaneous Tumor Model
07:49

Evaluation of Tumor-infiltrating Leukocyte Subsets in a Subcutaneous Tumor Model

Published on: April 13, 2015

Tumor Transplantation for Assessing the Dynamics of Tumor-Infiltrating CD8+ T Cells in Mice
07:36

Tumor Transplantation for Assessing the Dynamics of Tumor-Infiltrating CD8+ T Cells in Mice

Published on: June 12, 2021

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

Area of Science:

  • Oncology
  • Immunology
  • Chronobiology

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with poor prognosis.
  • Tumor cells can enter a dormant state to evade therapy and immune surveillance.
  • Understanding mechanisms of immune evasion is critical for developing effective cancer treatments.

Purpose of the Study:

  • To establish a novel murine model for resectable pancreatic ductal adenocarcinoma (PDAC).
  • To identify molecular regulators involved in immune evasion by dormant PDAC cells.
  • To elucidate the role of circadian regulators in tumor immune evasion.

Main Methods:

  • Development of a resectable murine PDAC model.
  • Analysis of gene expression in dormant tumor cells.
  • Investigation of antigen presentation pathways.
  • Assessment of immune surveillance evasion.

Main Results:

  • The circadian regulator Dec2 was identified as a crucial driver in dormant PDAC cells.
  • Dec2 suppresses antigen presentation, thereby evading immune surveillance.
  • The study highlights the role of Dec2 in enabling tumor cells to hide from the immune system.

Conclusions:

  • Dec2 is a key mediator of immune evasion in dormant pancreatic cancer.
  • Targeting Dec2 or its downstream pathways may represent a novel therapeutic strategy.
  • These findings introduce a temporal aspect to tumor immune evasion.