Molecular nevogenesis

Andrew L. Ross, Margaret I. Sanchez, James M Grichnik

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

Despite recent advances, the biology underlying nevogenesis remains unclear. Activating mutations in NRAS, HRAS, BRAF, and GNAQ have been identified in benign nevi. Their presence roughly correlates with congenital, Spitz, acquired, and blue nevi, respectively. These mutations are likely to play a critical role in driving nevogenesis. While each mutation is able to activate the MAP kinase pathway, they also interact with a host of different proteins in other pathways. The different melanocytic developmental pathways activated by each mutation cause the cells to migrate, proliferate, and differentiate to different extents within the skin. This causes each mutation to give rise to a characteristic growth pattern. The exact location and differentiation state of the cell of origin for benign moles remains to be discovered. Further research is necessary to fully understand nevus development given that most of the same developmental pathways are also present in melanoma.

Original languageEnglish
Article number463184
JournalDermatology Research and Practice
Volume2011
DOIs
StatePublished - Jan 1 2011

Fingerprint

Mutation
Nevus
Epithelioid and Spindle Cell Nevus
Blue Nevus
Cell Differentiation
Melanoma
Phosphotransferases
Skin
Growth
Research
Proteins

ASJC Scopus subject areas

  • Dermatology

Cite this

Ross, A. L., Sanchez, M. I., & Grichnik, J. M. (2011). Molecular nevogenesis. Dermatology Research and Practice, 2011, [463184]. https://doi.org/10.1155/2011/463184

Molecular nevogenesis. / Ross, Andrew L.; Sanchez, Margaret I.; Grichnik, James M.

In: Dermatology Research and Practice, Vol. 2011, 463184, 01.01.2011.

Research output: Contribution to journalArticle

Ross, AL, Sanchez, MI & Grichnik, JM 2011, 'Molecular nevogenesis', Dermatology Research and Practice, vol. 2011, 463184. https://doi.org/10.1155/2011/463184
Ross AL, Sanchez MI, Grichnik JM. Molecular nevogenesis. Dermatology Research and Practice. 2011 Jan 1;2011. 463184. https://doi.org/10.1155/2011/463184
Ross, Andrew L. ; Sanchez, Margaret I. ; Grichnik, James M. / Molecular nevogenesis. In: Dermatology Research and Practice. 2011 ; Vol. 2011.
@article{0a855e7e9c1b471cae8359414f8e0c6b,
title = "Molecular nevogenesis",
abstract = "Despite recent advances, the biology underlying nevogenesis remains unclear. Activating mutations in NRAS, HRAS, BRAF, and GNAQ have been identified in benign nevi. Their presence roughly correlates with congenital, Spitz, acquired, and blue nevi, respectively. These mutations are likely to play a critical role in driving nevogenesis. While each mutation is able to activate the MAP kinase pathway, they also interact with a host of different proteins in other pathways. The different melanocytic developmental pathways activated by each mutation cause the cells to migrate, proliferate, and differentiate to different extents within the skin. This causes each mutation to give rise to a characteristic growth pattern. The exact location and differentiation state of the cell of origin for benign moles remains to be discovered. Further research is necessary to fully understand nevus development given that most of the same developmental pathways are also present in melanoma.",
author = "Ross, {Andrew L.} and Sanchez, {Margaret I.} and Grichnik, {James M}",
year = "2011",
month = "1",
day = "1",
doi = "10.1155/2011/463184",
language = "English",
volume = "2011",
journal = "Dermatology Research and Practice",
issn = "1687-6105",
publisher = "Hindawi Publishing Corporation",

}

TY - JOUR

T1 - Molecular nevogenesis

AU - Ross, Andrew L.

AU - Sanchez, Margaret I.

AU - Grichnik, James M

PY - 2011/1/1

Y1 - 2011/1/1

N2 - Despite recent advances, the biology underlying nevogenesis remains unclear. Activating mutations in NRAS, HRAS, BRAF, and GNAQ have been identified in benign nevi. Their presence roughly correlates with congenital, Spitz, acquired, and blue nevi, respectively. These mutations are likely to play a critical role in driving nevogenesis. While each mutation is able to activate the MAP kinase pathway, they also interact with a host of different proteins in other pathways. The different melanocytic developmental pathways activated by each mutation cause the cells to migrate, proliferate, and differentiate to different extents within the skin. This causes each mutation to give rise to a characteristic growth pattern. The exact location and differentiation state of the cell of origin for benign moles remains to be discovered. Further research is necessary to fully understand nevus development given that most of the same developmental pathways are also present in melanoma.

AB - Despite recent advances, the biology underlying nevogenesis remains unclear. Activating mutations in NRAS, HRAS, BRAF, and GNAQ have been identified in benign nevi. Their presence roughly correlates with congenital, Spitz, acquired, and blue nevi, respectively. These mutations are likely to play a critical role in driving nevogenesis. While each mutation is able to activate the MAP kinase pathway, they also interact with a host of different proteins in other pathways. The different melanocytic developmental pathways activated by each mutation cause the cells to migrate, proliferate, and differentiate to different extents within the skin. This causes each mutation to give rise to a characteristic growth pattern. The exact location and differentiation state of the cell of origin for benign moles remains to be discovered. Further research is necessary to fully understand nevus development given that most of the same developmental pathways are also present in melanoma.

UR - http://www.scopus.com/inward/record.url?scp=84861481682&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84861481682&partnerID=8YFLogxK

U2 - 10.1155/2011/463184

DO - 10.1155/2011/463184

M3 - Article

AN - SCOPUS:84861481682

VL - 2011

JO - Dermatology Research and Practice

JF - Dermatology Research and Practice

SN - 1687-6105

M1 - 463184

ER -