Novel Targeted Therapies for Metastatic Melanoma
Related Experiment Video
Updated: Mar 8, 2026

A 3D Organotypic Melanoma Spheroid Skin Model
Published on: May 18, 2018
Wade T Iams1, Jeffrey A Sosman, Sunandana Chandra
1From the Division of Hematology/Oncology, Northwestern Feinberg School of Medicine, Chicago, IL.
Abstract:
Oncogene-targeted therapy is a major component of precision oncology, and although patients with metastatic melanoma have experienced improved outcomes with this strategy, there are a number of potential therapeutic targets currently under study that may further increase the drug armamentarium for this patient population. In this review, we discuss the landscape of targeted therapies for patients with advanced melanoma, focusing on oncogene mutation-specific targets. In patients with typical BRAF V600-mutant melanoma, combination BRAF and MEK inhibition has surpassed outcomes compared with monotherapy with BRAF or MEK inhibition alone, and current strategies seek to address inevitable resistance mechanisms. For patients with NRAS-mutant melanoma, MEK inhibitor monotherapy and combined MEK and CDK4/6 inhibition are burgeoning strategies; for patients with KIT-mutant melanoma, tyrosine kinase inhibition is being leveraged, and for NF-1-mutant melanoma, mTOR and MEK inhibition is being actively evaluated. In patients with atypical, non-V600 BRAF-mutant melanoma, MEK inhibitor monotherapy is the potential novel targeted approach on the horizon. For advanced uveal melanoma, novel targets such as IMCgp100 and glembatumumab have shown activity in early studies. We review additional strategies that remain in the preclinical and early clinical pipeline, so there is much hope for the future of targeted agents for distinct molecular cohorts of patients with advanced melanoma.
Insights
Targeted therapies are advancing precision oncology for metastatic melanoma. New strategies target specific oncogene mutations like BRAF, NRAS, and KIT, offering hope for improved patient outcomes and overcoming resistance.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Precision oncology utilizes oncogene-targeted therapy, significantly improving outcomes for metastatic melanoma patients.
- Ongoing research identifies novel therapeutic targets to expand treatment options for advanced melanoma.
Purpose of the Study:
- To review the current landscape of targeted therapies for advanced melanoma, emphasizing oncogene mutation-specific targets.
- To discuss emerging strategies and future directions in melanoma treatment.
Main Methods:
- Review of current literature on targeted therapies for advanced melanoma.
- Focus on oncogene mutation-specific targets including BRAF, NRAS, KIT, NF-1, and atypical BRAF mutations.
- Discussion of combination therapies and emerging agents.
Main Results:
- Combination BRAF and MEK inhibition shows superior outcomes in BRAF V600-mutant melanoma.
- Emerging strategies for NRAS-mutant melanoma include MEK inhibitor monotherapy and MEK/CDK4/6 inhibition.
- Tyrosine kinase inhibitors for KIT-mutant melanoma and mTOR/MEK inhibition for NF-1-mutant melanoma are under evaluation.
Conclusions:
- Targeted therapies are crucial for distinct molecular subtypes of advanced melanoma.
- MEK inhibitor monotherapy is a promising approach for atypical BRAF-mutant melanoma.
- Novel agents like IMCgp100 and glembatumumab show early activity in uveal melanoma, with continued preclinical and clinical development offering future hope.
Related Concept Videos
Targeted Cancer Therapies
There are several types of targeted therapies against...
Tumor Immunotherapy
Combination Therapies and Personalized Medicine
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...
Mitogens and the Cell Cycle
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...

