Presence of Human Polyomavirus 6 in Mutation-Specific BRAF Inhibitor–Induced Epithelial Proliferations | Zendy

David Schrama | Zendy; Leopold Groesser | Zendy; Selma Ugurel | Zendy; Christian Hafner | Zendy; Diana V. Pastrana | Zendy; Christopher B. Buck | Zendy; Lorenzo Cerroni | Zendy; Anna Theiler | Zendy; Jürgen C. Becker | Zendy

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Presence of Human Polyomavirus 6 in Mutation-Specific BRAF Inhibitor–Induced Epithelial Proliferations

Author(s) -

David Schrama,

Leopold Groesser,

Selma Ugurel,

Christian Hafner,

Diana V. Pastrana,

Christopher B. Buck,

Lorenzo Cerroni,

Anna Theiler,

Jürgen C. Becker

Publication year - 2014

Publication title -

jama dermatology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.128

H-Index - 166

eISSN - 2168-6084

pISSN - 2168-6068

DOI - 10.1001/jamadermatol.2014.1116

Subject(s) - vemurafenib , hras , cancer research , medicine , melanoma , merkel cell polyomavirus , neuroblastoma ras viral oncogene homolog , kras , mutation , merkel cell carcinoma , pathology , gene , biology , cancer , carcinoma , biochemistry , colorectal cancer , metastatic melanoma

A frequent adverse effect of mutation-specific BRAF inhibitor therapy is the induction of epithelial proliferations including cutaneous squamous cell carcinomas. To date, the only factor identified contributing to their development is the activation of the mitogen-activated signal transduction cascade by mutations in the RAS genes. However, these mutations explain only 60% of the tumors; hence, it is important to identify what is causing the remaining tumors.

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