Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

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Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid

Yeh, I; Lang, UE; Durieux, E; Tee, MK; Jorapur, A; Shain, AH; Haddad, V; Pissaloux, D; Chen, X; Cerroni, L; Judson, RL; LeBoit, PE; McCalmont, TH; Bastian, BC; de la Fouchardière, A.
Combined activation of MAP kinase pathway and β-catenin signaling cause deep penetrating nevi.
Nat Commun. 2017; 8(1):644-644 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG


Autor/innen der Med Uni Graz:
Cerroni Lorenzo

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Plum Analytics:
Number of Figures: 6
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Deep penetrating nevus (DPN) is characterized by enlarged, pigmented melanocytes that extend through the dermis. DPN can be difficult to distinguish from melanoma but rarely displays aggressive biological behavior. Here, we identify a combination of mutations of the β-catenin and mitogen-activated protein kinase pathways as characteristic of DPN. Mutations of the β-catenin pathway change the phenotype of a common nevus with BRAF mutation into that of DPN, with increased pigmentation, cell volume and nuclear cyclin D1 levels. Our results suggest that constitutive β-catenin pathway activation promotes tumorigenesis by overriding dependencies on the microenvironment that constrain proliferation of common nevi. In melanoma that arose from DPN we find additional oncogenic alterations. We identify DPN as an intermediate stage in the step-wise progression from nevus to melanoma. In summary, we delineate specific genetic alterations and their sequential order, information that can assist in the diagnostic classification and grading of these distinctive neoplasms.Deep penetrating nevi (DPN) are unusual melanocytic neoplasms with unknown genetic drivers. Here the authors show that majority of DPN harbor activating mutations in the β-catenin and the MAP-kinase pathways; this characteristic can help in the classification and grading of these distinctive neoplasms.
Find related publications in this database (using NLM MeSH Indexing)
DNA - genetics
DNA - metabolism
Gene Expression Regulation - physiology
Humans -
MAP Kinase Signaling System - physiology
Melanoma - genetics
Melanoma - metabolism
Mutation -
Nevus, Intradermal - genetics
Nevus, Intradermal - metabolism
beta Catenin - genetics
beta Catenin - metabolism

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