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Updated: Jun 6, 2026

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
Targeted therapy in BRAF‑mutant melanoma: Advances and challenges (Review)
Lu Zhang1, Dongliang Shen1, Jianguo Feng2
1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing 400044, P.R. China.
BRAF and MEK inhibitors effectively treat melanoma by targeting the MAPK pathway. However, acquired drug resistance remains a significant challenge, necessitating further research into resistance mechanisms for improved melanoma therapies.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Melanoma is often driven by BRAF mutations, leading to MAPK pathway hyperactivation.
- BRAF and MEK inhibitors are approved melanoma therapies targeting this pathway.
- Acquired drug resistance limits the long-term efficacy of these treatments.
Purpose of the Study:
- To summarize the discovery and development of BRAF and MEK inhibitors for melanoma.
- To review the clinical efficacy of these inhibitors in melanoma treatment.
- To elucidate the mechanisms of acquired resistance to BRAF and MEK inhibitors.
Main Methods:
- Literature review of BRAF and MEK inhibitors in melanoma.
- Analysis of clinical trial data for efficacy and resistance patterns.
- Summary of research on molecular mechanisms of acquired resistance.
Main Results:
- BRAF and MEK inhibitors show significant efficacy in reducing melanoma tumor burden.
- Nearly all patients eventually develop resistance to these targeted therapies.
- Understanding resistance mechanisms is key to overcoming treatment failure.
Conclusions:
- BRAF and MEK inhibitors represent a major advance in melanoma treatment.
- Acquired resistance is a critical hurdle requiring further investigation.
- Developing strategies to overcome resistance is essential for durable melanoma control.
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