Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Targeted Cancer Therapies

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...

Tumor Immunotherapy

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.

Cytotoxic T Cells-mediated Immune Response

Cytotoxic T Cells-mediated Immune Response

Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
Immunological surveillance is the ability of immune cells to monitor and eliminate infected cells with intracellular pathogens, neoplastically transformed cells, and cells with non-self antigens. Cytotoxic T cells and NK...

Combination Therapies and Personalized Medicine

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...

You might also read

Related Articles

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

Sort by

Same author

S-phase targeted treatment triggers caspase-dependent lytic immunogenic cell death with pyroptotic features in cancers.

Cell death and differentiation·2026

Same author

Meeting Report From the 2025 Cure Ocular Melanoma (CURE OM) Global Science Meeting, Amsterdam, the Netherlands, October 2025.

Pigment cell & melanoma research·2026

Same author

Diacylglycerol Kinase Eta as a Novel Target in NRAS Mutant Melanoma.

Pigment cell & melanoma research·2026

Same author

MECP2-Dependent Cancers Can Be Targeted by Epigenetic Drugs: A New Role for Epigenetic Cancer Therapy.

Molecular cancer therapeutics·2026

Same author

MECP2-Dependent Cancers Can Be Targeted by Epigenetic Drugs: A New Role for Epigenetic Cancer Therapy.

Molecular cancer therapeutics·2025

Same author

Targeting TAZ-TEAD in minimal residual disease enhances the duration of targeted therapy in melanoma models.

Nature communications·2025

Search research articles

Related Experiment Video

Updated: Jan 6, 2026

Experimental Melanoma Immunotherapy Model Using Tumor Vaccination with a Hematopoietic Cytokine

Experimental Melanoma Immunotherapy Model Using Tumor Vaccination with a Hematopoietic Cytokine

Published on: February 24, 2023

Pyroptosis Modulates Multiple Immune Cell Populations in Targeted Therapy-Treated Melanoma.

Nicole A Wilski-Cronin¹, Dan A Erkes^1,2, Timothy J Purwin¹

¹Department of Pharmacology, Physiology, and Cancer Biology, Thomas Jefferson University, Philadelphia, Pennsylvania.

Cancer Immunology Research

|November 26, 2025

Summary

Gasdermin E (GSDME) drives anti-melanoma immunity by promoting T cell infiltration. GSDME-mediated pyroptosis is crucial for effective BRAF inhibitor plus MEK inhibitor therapy in melanoma.

More Related Videos

Author Spotlight: Flow Cytometric Determination of Pyroptosis in Avian Cells

Author Spotlight: Flow Cytometric Determination of Pyroptosis in Avian Cells

Published on: May 31, 2024

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Published on: May 3, 2024

Related Experiment Videos

Last Updated: Jan 6, 2026

Experimental Melanoma Immunotherapy Model Using Tumor Vaccination with a Hematopoietic Cytokine

Experimental Melanoma Immunotherapy Model Using Tumor Vaccination with a Hematopoietic Cytokine

Published on: February 24, 2023

Author Spotlight: Flow Cytometric Determination of Pyroptosis in Avian Cells

Author Spotlight: Flow Cytometric Determination of Pyroptosis in Avian Cells

Published on: May 31, 2024

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Published on: May 3, 2024

Area of Science:

Immunology
Oncology
Cell Biology

Background:

BRAF inhibitors plus MEK inhibitors (BRAFi + MEKi) enhance anti-melanoma immunity via pyroptosis, a cell death process mediated by gasdermin E (GSDME).
The precise mechanisms by which GSDME influences tumor immunity remain incompletely understood.

Purpose of the Study:

To investigate the role of GSDME in modulating the intratumoral immune microenvironment during BRAFi + MEKi treatment for melanoma.
To elucidate how GSDME affects immune cell infiltration and function, particularly regulatory T cells (Tregs).

Main Methods:

Single-cell RNA-sequencing (scRNA-seq) and flow cytometry were employed on melanoma models.
Gsdme knockout (KO) and engineered Gsdme mutant melanoma models were utilized.
BRAFi + MEKi treatment, alone and in combination with a TLR9 agonist, was administered.

Main Results:

Gsdme KO tumors exhibited reduced infiltration of T cells, NK cells, and Tregs compared to control tumors.
Tregs within Gsdme KO tumors showed diminished expression of the interleukin-2 receptor and suppressive markers.
Melanoma treatment with BRAFi + MEKi combined with a TLR9 agonist suppressed tumor regrowth and further decreased intratumoral Tregs in Gsdme-deficient models.

Conclusions:

GSDME plays a critical role in orchestrating the intratumoral immune response in melanoma treated with BRAFi + MEKi.
GSDME-mediated pyroptosis is essential for optimal T cell and NK cell infiltration and for reducing the suppressive function of Tregs.
Targeting GSDME or enhancing its function may represent a therapeutic strategy to improve responses to BRAFi + MEKi therapy in melanoma.