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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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...
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

Overview

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Related Experiment Video

Updated: May 11, 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

NRAS mutant melanoma--undrugable?

Christian Posch1, Susana Ortiz-Urda

  • 1Department for Dermatology, University of California San Francisco, Mt Zion Cancer Research Center, California, USA. poschc@derm

Oncotarget
|May 11, 2013
PubMed
Summary

Mutations in neuroblastoma-RAS (NRAS) drive melanoma, but targeted therapies remain elusive. This study explores strategies to selectively inhibit mutant NRAS, addressing a critical challenge in melanoma treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Mutations in rat sarcoma (RAS) family genes, including neuroblastoma-RAS (NRAS), HRAS, and Kirsten-RAS (KRAS), are prevalent in approximately one-third of human cancers.
  • NRAS was among the initial oncogenes identified in cutaneous melanoma, with mutations occurring in up to 20% of these tumors.
  • Mutant NRAS triggers aberrant signaling through multiple downstream pathways, making it a significant therapeutic target in melanoma.

Purpose of the Study:

  • To address the challenge of designing small molecules that selectively inhibit mutant NRAS in melanoma.
  • To explore novel therapeutic strategies targeting NRAS-mutant melanoma.

Main Methods:

  • Investigating the molecular mechanisms of NRAS aberrant signaling in melanoma.

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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

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Last Updated: May 11, 2026

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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

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  • Developing and evaluating novel small molecule inhibitors for mutant NRAS.

    • Main Results:

    • Identification of key downstream signaling cascades affected by NRAS mutations.
    • Preliminary assessment of potential small molecule inhibitors against mutant NRAS.

    Conclusions:

    • Selective inhibition of mutant NRAS in melanoma presents a significant therapeutic opportunity.
    • Further research is needed to develop effective small molecule inhibitors for NRAS-mutant melanoma.