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MAP kinase pathway gene copy alterations in NRAS/BRAF wild-type advanced melanoma

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MAP kinase pathway gene copy alterations in NRAS/BRAF wild-type advanced melanoma. / Orouji, Elias; Orouji, Azadeh; Gaiser, Timo; Larribère, Lionel; Gebhardt, Christoffer; Utikal, Jochen.

in: INT J CANCER, Jahrgang 138, Nr. 9, 01.05.2016, S. 2257-62.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Orouji, E, Orouji, A, Gaiser, T, Larribère, L, Gebhardt, C & Utikal, J 2016, 'MAP kinase pathway gene copy alterations in NRAS/BRAF wild-type advanced melanoma', INT J CANCER, Jg. 138, Nr. 9, S. 2257-62. https://doi.org/10.1002/ijc.29970

APA

Orouji, E., Orouji, A., Gaiser, T., Larribère, L., Gebhardt, C., & Utikal, J. (2016). MAP kinase pathway gene copy alterations in NRAS/BRAF wild-type advanced melanoma. INT J CANCER, 138(9), 2257-62. https://doi.org/10.1002/ijc.29970

Vancouver

Orouji E, Orouji A, Gaiser T, Larribère L, Gebhardt C, Utikal J. MAP kinase pathway gene copy alterations in NRAS/BRAF wild-type advanced melanoma. INT J CANCER. 2016 Mai 1;138(9):2257-62. https://doi.org/10.1002/ijc.29970

Bibtex

@article{cf1d0fbdef964dc7b1d60787dea3b379,
title = "MAP kinase pathway gene copy alterations in NRAS/BRAF wild-type advanced melanoma",
abstract = "Recent therapeutic advances have improved melanoma patient{\'s} clinical outcome. Novel therapeutics targeting BRAF, NRAS and cKit mutant melanomas are widely used in clinical practice. However therapeutic options in NRAS(wild-type) /BRAF(wild-type) /cKit(wild-type) melanoma patients are limited. Our study shows that gene copy numbers of members of the MAPK signaling pathway vary in different melanoma subgroups. NRAS(wild-type) /BRAF(wild-type) melanoma metastases are characterized by significant gains of MAP2K1 (MEK1) and MAPK3 (ERK1) gene loci. These additional gene copies could lead to an activation of the MAPK signaling pathway via a gene-dosage effect. Our results suggest that downstream analyses of the pMEK and pERK expression status in NRAS(wild-type) /BRAF(wild-type) melanoma patients identify patients that could benefit from targeted therapies with MEK and ERK inhibitors.",
keywords = "Aged, DNA Mutational Analysis, Female, GTP Phosphohydrolases, Gene Dosage, Humans, Immunohistochemistry, In Situ Hybridization, Fluorescence, MAP Kinase Signaling System, Male, Melanoma, Membrane Proteins, Middle Aged, Proto-Oncogene Proteins B-raf, Skin Neoplasms, Journal Article, Research Support, Non-U.S. Gov't",
author = "Elias Orouji and Azadeh Orouji and Timo Gaiser and Lionel Larrib{\`e}re and Christoffer Gebhardt and Jochen Utikal",
note = "{\textcopyright} 2015 UICC.",
year = "2016",
month = may,
day = "1",
doi = "10.1002/ijc.29970",
language = "English",
volume = "138",
pages = "2257--62",
journal = "INT J CANCER",
issn = "0020-7136",
publisher = "Wiley-Liss Inc.",
number = "9",

}

RIS

TY - JOUR

T1 - MAP kinase pathway gene copy alterations in NRAS/BRAF wild-type advanced melanoma

AU - Orouji, Elias

AU - Orouji, Azadeh

AU - Gaiser, Timo

AU - Larribère, Lionel

AU - Gebhardt, Christoffer

AU - Utikal, Jochen

N1 - © 2015 UICC.

PY - 2016/5/1

Y1 - 2016/5/1

N2 - Recent therapeutic advances have improved melanoma patientś clinical outcome. Novel therapeutics targeting BRAF, NRAS and cKit mutant melanomas are widely used in clinical practice. However therapeutic options in NRAS(wild-type) /BRAF(wild-type) /cKit(wild-type) melanoma patients are limited. Our study shows that gene copy numbers of members of the MAPK signaling pathway vary in different melanoma subgroups. NRAS(wild-type) /BRAF(wild-type) melanoma metastases are characterized by significant gains of MAP2K1 (MEK1) and MAPK3 (ERK1) gene loci. These additional gene copies could lead to an activation of the MAPK signaling pathway via a gene-dosage effect. Our results suggest that downstream analyses of the pMEK and pERK expression status in NRAS(wild-type) /BRAF(wild-type) melanoma patients identify patients that could benefit from targeted therapies with MEK and ERK inhibitors.

AB - Recent therapeutic advances have improved melanoma patientś clinical outcome. Novel therapeutics targeting BRAF, NRAS and cKit mutant melanomas are widely used in clinical practice. However therapeutic options in NRAS(wild-type) /BRAF(wild-type) /cKit(wild-type) melanoma patients are limited. Our study shows that gene copy numbers of members of the MAPK signaling pathway vary in different melanoma subgroups. NRAS(wild-type) /BRAF(wild-type) melanoma metastases are characterized by significant gains of MAP2K1 (MEK1) and MAPK3 (ERK1) gene loci. These additional gene copies could lead to an activation of the MAPK signaling pathway via a gene-dosage effect. Our results suggest that downstream analyses of the pMEK and pERK expression status in NRAS(wild-type) /BRAF(wild-type) melanoma patients identify patients that could benefit from targeted therapies with MEK and ERK inhibitors.

KW - Aged

KW - DNA Mutational Analysis

KW - Female

KW - GTP Phosphohydrolases

KW - Gene Dosage

KW - Humans

KW - Immunohistochemistry

KW - In Situ Hybridization, Fluorescence

KW - MAP Kinase Signaling System

KW - Male

KW - Melanoma

KW - Membrane Proteins

KW - Middle Aged

KW - Proto-Oncogene Proteins B-raf

KW - Skin Neoplasms

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1002/ijc.29970

DO - 10.1002/ijc.29970

M3 - SCORING: Journal article

C2 - 26684394

VL - 138

SP - 2257

EP - 2262

JO - INT J CANCER

JF - INT J CANCER

SN - 0020-7136

IS - 9

ER -