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Related Concept Videos

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
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...
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...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:

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Related Experiment Video

Updated: May 28, 2026

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
06:09

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Published on: June 7, 2019

Targeting the RAS pathway in melanoma.

Zhenyu Ji1, Keith T Flaherty, Hensin Tsao

  • 1Wellman Center for Photomedicine, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114, USA.

Trends in Molecular Medicine
|October 4, 2011
PubMed
Summary

Targeted therapies offer new hope for metastatic melanoma, a lethal skin cancer. Understanding BRAF inhibitors like vemurafenib is key to advancing treatment despite emerging resistance.

Area of Science:

  • Oncology
  • Dermatology
  • Molecular Biology

Background:

  • Metastatic melanoma is an aggressive skin cancer with poor prognosis.
  • Traditional chemotherapy is often ineffective against advanced melanoma.
  • Genetic insights have spurred the development of targeted therapies.

Purpose of the Study:

  • To review the current landscape of targeted therapy for melanoma.
  • To discuss the efficacy and limitations of BRAF inhibitors.
  • To highlight vemurafenib as a potent BRAF(V600E) inhibitor.

Main Methods:

  • Literature review of clinical trials and research on melanoma targeted therapy.
  • Analysis of genetic drivers of melanoma, focusing on the RAS/BRAF pathway.
  • Discussion of adverse effects and resistance mechanisms associated with targeted agents.

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A 3D Organotypic Melanoma Spheroid Skin Model
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A 3D Organotypic Melanoma Spheroid Skin Model

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Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma
08:18

Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma

Published on: September 8, 2021

Related Experiment Videos

Last Updated: May 28, 2026

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
06:09

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Published on: June 7, 2019

A 3D Organotypic Melanoma Spheroid Skin Model
08:49

A 3D Organotypic Melanoma Spheroid Skin Model

Published on: May 18, 2018

Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma
08:18

Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma

Published on: September 8, 2021

Main Results:

  • Targeted agents, particularly BRAF inhibitors, show significant promise.
  • Vemurafenib is a key example of a potent BRAF(V600E) inhibitor.
  • Adverse effects and resistance mechanisms are emerging challenges.

Conclusions:

  • Targeted therapy represents a major advance in melanoma treatment.
  • Defining the limits of current therapies is crucial for future progress.
  • Further research is needed to overcome resistance and improve patient outcomes.