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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...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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.
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Cancers Originate from Somatic Mutations in a Single Cell

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Skin Cancer

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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Updated: Jul 20, 2026

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

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Published on: June 7, 2019

High BRAF mutation frequency does not characterize all melanocytic tumor types.

Gerald Saldanha1, David Purnell, Alan Fletcher

  • 1Department of Cancer Studies and Molecular Medicine, University of Leicester, Leicester, United Kingdom. gss4@le.ac.uk

International Journal of Cancer
|July 15, 2004
PubMed
Summary

BRAF and NRAS mutations are common in many melanocytic tumors but not essential for all types. Some skin cancers and benign nevi develop through alternative pathways, highlighting diverse mechanisms in melanocytic neoplasia.

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Area of Science:

  • Oncology
  • Dermatology
  • Molecular Biology

Background:

  • Cutaneous melanoma (CM) is a lethal skin cancer.
  • BRAF and NRAS mutations are frequently observed in CM and some benign melanocytic tumors.
  • The necessity of these mutations for all melanocytic neoplasia remains unclear.

Purpose of the Study:

  • To investigate the frequency of BRAF and NRAS mutations across various melanocytic tumor types.
  • To assess the activity of the MAPK pathway in tumors with low BRAF/NRAS mutation rates.
  • To determine if BRAF/NRAS mutations are essential for melanocytic tumor development.

Main Methods:

  • Screening of 79 melanocytic tumors for BRAF and NRAS mutations.
  • Immunohistochemistry analysis of MAPK pathway activation (phosphorylated ERK1/2) in a subset of tumors.
  • Statistical analysis to compare mutation frequencies across different tumor types.

Main Results:

  • Significant differences in BRAF exon 15 mutation frequency were observed: high in common acquired nevi (87.5%) and CMs (75%), but absent in Spitz nevi and low in blue nevi (12%).
  • NRAS mutations were infrequent across all tumor types studied.
  • Spitz nevi exhibited strong MAPK pathway activation despite low BRAF/NRAS mutation rates, while blue nevi showed weak activation.

Conclusions:

  • BRAF and NRAS mutations are not universally required for the development of all melanocytic tumors.
  • Spitz nevi and potentially other tumor types may arise through alternative molecular mechanisms.
  • Understanding these alternative pathways is crucial for comprehensive diagnosis and treatment of melanocytic neoplasia.