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...
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 specific...

You might also read

Related Articles

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

Sort by
Same author

The quintessential high-risk profile: advanced management strategies for placenta accreta spectrum in patients with advanced maternal age and IVF conception.

BMC pregnancy and childbirth·2026
Same author

Missed diagnosis of pelvic organ prolapse complicated with cervical cancer: a retrospective case series of five patients and review of literature.

Gynecology and pelvic medicine·2026
Same author

RYBP regulates selective genomic binding of TrxG and PcG components in embryonic stem cell fate control.

The EMBO journal·2026
Same author

Precision oncology in gynecologic cancers: molecular taxonomy, biomarker-guided therapeutics, and the challenge of therapeutic resistance.

Frontiers in oncology·2026
Same author

TUT1-catalyzed U6 snRNA 3'-end maturation is essential for RNA splicing and stem cell survival.

EMBO reports·2026
Same author

Enhanced P-TEFb activity compromises dentate gyrus neurogenesis in mice.

The EMBO journal·2026

Related Experiment Video

Updated: Jun 27, 2026

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

Beyond PD-1/PD-L1: Reprogramming the Gynecologic Tumor Microenvironment by Targeting TIGIT and Myeloid Suppression.

Shanza Waseem1,2,3,4, Jun Zhan1,2,3,4, Xue Xiao1,2,3,4

  • 1Department of Gynecology and Obstetrics, West China Second University Hospital, Sichuan University, Chengdu 610041, China.

International Journal of Molecular Sciences
|June 26, 2026
PubMed
Summary
This summary is machine-generated.

Dual blockade of PD-1 and TIGIT offers a promising strategy to overcome resistance to cancer immunotherapy in gynecologic malignancies. This approach targets the immunosuppressive tumor microenvironment, enhancing T-cell function for improved treatment outcomes.

Keywords:
TIGITgynecologic oncologyimmune checkpoint inhibitorsmyeloid-derived suppressor cellsregulatory T cellstranslational immunotherapytumor immunoeditingtumor microenvironment

Related Experiment Videos

Last Updated: Jun 27, 2026

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
  • Gynecologic Oncology

Background:

  • Immune checkpoint inhibitors targeting PD-1/PD-L1 have limited efficacy in gynecologic cancers, particularly ovarian carcinoma.
  • Therapeutic resistance is driven by an immunosuppressive tumor microenvironment (TME) involving regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), and inhibitory cytokines.
  • TIGIT acts as a key checkpoint regulator, influencing T-cell exhaustion and NK-cell dysfunction.

Purpose of the Study:

  • To review the current understanding of the gynecologic TME.
  • To delineate the synergistic mechanisms of dual PD-1 and TIGIT blockade.
  • To propose a framework for accelerating biomarker-driven therapeutic development.

Main Methods:

  • Literature review synthesizing current knowledge on TME and TIGIT/PD-1 synergy.
  • Critical evaluation of ongoing clinical trials for dual checkpoint blockade.
  • Proposal of an integrative framework using advanced technologies.

Main Results:

  • The immunosuppressive TME in gynecologic malignancies is a complex network that limits immunotherapy efficacy.
  • Dual blockade of PD-1 and TIGIT is a mechanistically sound strategy to overcome this resistance.
  • Synergy between PD-1 and TIGIT blockade addresses multiple immunosuppressive pathways.

Conclusions:

  • Overcoming TME-mediated resistance in gynecologic cancers requires targeting multiple checkpoints, including PD-1 and TIGIT.
  • Integrated approaches combining spatial transcriptomics and single-cell profiling are crucial for biomarker discovery.
  • Accelerating the development of effective immunotherapies for gynecologic malignancies is achievable through rational combination strategies.