Toward a Molecular-Genetic Classification of Spitzoid Neoplasms

Michael Tetzlaff; Alexandre Reuben; Steven D. Billings; Victor Prieto; Jonathan L Curry

doi:10.1016/j.cll.2017.05.003

Toward a Molecular-Genetic Classification of Spitzoid Neoplasms

Michael Tetzlaff, Alexandre Reuben, Steven D. Billings, Victor Prieto, Jonathan L Curry

Research output: Contribution to journal › Review article › peer-review

26 Scopus citations

Abstract

The histopathologic spectrum of Spitzoid neoplasms includes Spitz nevi, atypical Spitz tumors, and Spitzoid melanomas. Advances in molecular genetics have evolved to the point that Spitzoid lesions can now be reasonably classified according to their distinctive molecular-genetic alterations: Spitzoid lesions with (1) 11p amplification and/or HRAS mutations; (2) isolated loss of 6q23 by fluorescence in situ hybridization (FISH); (3) homozygous deletion of 9p21 by FISH; (4) BAP1 loss and BRAFV600 E mutation; (5) translocations involving any of a number of different oncogenic kinase drivers, including ROS1, ALK, NTRK1, NTRK3, MET, BRAF, and RET; and (6) TERT promoter mutations.

Original language	English (US)
Pages (from-to)	431-448
Number of pages	18
Journal	Clinics in Laboratory Medicine
Volume	37
Issue number	3
DOIs	https://doi.org/10.1016/j.cll.2017.05.003
State	Published - Sep 1 2017

Keywords

Atypical Spitz tumor
BAP1
Comparative genomic hybridization
Fluorescence in situ hybridization
HRAS
Spitz nevus
Spitzoid melanoma
Telomerase promoter

ASJC Scopus subject areas

Clinical Biochemistry
Biochemistry, medical

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10.1016/j.cll.2017.05.003

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title = "Toward a Molecular-Genetic Classification of Spitzoid Neoplasms",

abstract = "The histopathologic spectrum of Spitzoid neoplasms includes Spitz nevi, atypical Spitz tumors, and Spitzoid melanomas. Advances in molecular genetics have evolved to the point that Spitzoid lesions can now be reasonably classified according to their distinctive molecular-genetic alterations: Spitzoid lesions with (1) 11p amplification and/or HRAS mutations; (2) isolated loss of 6q23 by fluorescence in situ hybridization (FISH); (3) homozygous deletion of 9p21 by FISH; (4) BAP1 loss and BRAFV600 E mutation; (5) translocations involving any of a number of different oncogenic kinase drivers, including ROS1, ALK, NTRK1, NTRK3, MET, BRAF, and RET; and (6) TERT promoter mutations.",

keywords = "Atypical Spitz tumor, BAP1, Comparative genomic hybridization, Fluorescence in situ hybridization, HRAS, Spitz nevus, Spitzoid melanoma, Telomerase promoter",

author = "Michael Tetzlaff and Alexandre Reuben and Billings, {Steven D.} and Victor Prieto and Curry, {Jonathan L}",

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T1 - Toward a Molecular-Genetic Classification of Spitzoid Neoplasms

AU - Tetzlaff, Michael

AU - Reuben, Alexandre

AU - Billings, Steven D.

AU - Prieto, Victor

AU - Curry, Jonathan L

PY - 2017/9/1

Y1 - 2017/9/1

N2 - The histopathologic spectrum of Spitzoid neoplasms includes Spitz nevi, atypical Spitz tumors, and Spitzoid melanomas. Advances in molecular genetics have evolved to the point that Spitzoid lesions can now be reasonably classified according to their distinctive molecular-genetic alterations: Spitzoid lesions with (1) 11p amplification and/or HRAS mutations; (2) isolated loss of 6q23 by fluorescence in situ hybridization (FISH); (3) homozygous deletion of 9p21 by FISH; (4) BAP1 loss and BRAFV600 E mutation; (5) translocations involving any of a number of different oncogenic kinase drivers, including ROS1, ALK, NTRK1, NTRK3, MET, BRAF, and RET; and (6) TERT promoter mutations.

AB - The histopathologic spectrum of Spitzoid neoplasms includes Spitz nevi, atypical Spitz tumors, and Spitzoid melanomas. Advances in molecular genetics have evolved to the point that Spitzoid lesions can now be reasonably classified according to their distinctive molecular-genetic alterations: Spitzoid lesions with (1) 11p amplification and/or HRAS mutations; (2) isolated loss of 6q23 by fluorescence in situ hybridization (FISH); (3) homozygous deletion of 9p21 by FISH; (4) BAP1 loss and BRAFV600 E mutation; (5) translocations involving any of a number of different oncogenic kinase drivers, including ROS1, ALK, NTRK1, NTRK3, MET, BRAF, and RET; and (6) TERT promoter mutations.

KW - Atypical Spitz tumor

KW - BAP1

KW - Comparative genomic hybridization

KW - Fluorescence in situ hybridization

KW - HRAS

KW - Spitz nevus

KW - Spitzoid melanoma

KW - Telomerase promoter

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DO - 10.1016/j.cll.2017.05.003

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SN - 0272-2712

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JO - Clinics in Laboratory Medicine

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ER -

Toward a Molecular-Genetic Classification of Spitzoid Neoplasms

Abstract

Keywords

ASJC Scopus subject areas

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