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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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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...
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Tumor Immunotherapy01:27

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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.
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Skin Cancer01:30

Skin Cancer

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Skin cancer is a type of cancer that occurs when there is an abnormal growth of skin cells, usually triggered by damage to the DNA within the skin cells. It is primarily caused by exposure to ultraviolet (UV) radiation from the sun or artificial sources like tanning beds. Skin cancer is the most common type of cancer worldwide, and its incidence continues to rise.
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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.
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Mitogens and the Cell Cycle

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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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Related Experiment Video

Updated: Sep 28, 2025

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
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Targeted Therapy for Melanomas Without BRAF V600 Mutations.

Christian Menzer1, Jessica C Hassel2

  • 1Section of DermatoOncology, Department of Dermatology and National Center for Tumor Diseases (NCT), University Hospital Heidelberg, Im Neuenheimer Feld 460, 69120, Heidelberg, Germany.

Current Treatment Options in Oncology
|April 5, 2022
PubMed
Summary

Targeted therapy options are emerging for advanced melanoma patients with rare BRAF mutations beyond V600. Understanding these non-V600 BRAF mutations is crucial for developing effective second-line treatments when immunotherapy fails.

Keywords:
BRAFBRAF mutationBinimetinibC-kitCobimetinibImatinibMAPK pathwayMEKMelanomaNRASNon-V600Targeted therapyTrametinibV600

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Area of Science:

  • Oncology
  • Molecular Biology
  • Dermatology

Background:

  • Advanced melanoma treatment includes BRAF/MEK inhibitors for V600 mutations and checkpoint inhibitors for others.
  • Checkpoint inhibitors are first-line for non-V600 BRAF mutations, but approximately 50% of patients do not respond.
  • Effective second-line treatment options are needed for non-responders.

Purpose of the Study:

  • To review current clinical data on the characteristics of melanomas with non-V600 BRAF mutations.
  • To assess the efficacy of targeted therapies in patients with advanced melanoma lacking V600 BRAF mutations.
  • To classify BRAF mutations based on kinase activation and pathway dependence to guide targeted therapy selection.

Main Methods:

  • Review of current clinical data and genetic profiling studies.
  • Classification of BRAF mutations by kinase activation status and signaling pathway dependence.
  • Analysis of response rates and long-term outcomes for targeted therapies in advanced melanoma with non-V600 BRAF mutations.

Main Results:

  • Non-V600 BRAF mutations exhibit diverse kinase activation and varying dependence on alternative signaling pathways like RAS.
  • Response to BRAF plus MEK inhibition differs significantly among non-V600 BRAF mutants.
  • Targeted therapies for non-V600 mutants generally show inferior response and long-term outcomes compared to V600 mutants.

Conclusions:

  • Checkpoint inhibitors remain the standard first-line therapy for advanced melanoma patients with non-V600 BRAF mutations.
  • Further research into the characteristics of non-V600 BRAF mutations is needed to optimize targeted therapy strategies.
  • Understanding mutation-specific dependencies may lead to improved therapeutic options for refractory melanoma.