BRAFV600E: implications for carcinogenesis and molecular therapy.

Hdl Handle:
http://hdl.handle.net/10147/207794
Title:
BRAFV600E: implications for carcinogenesis and molecular therapy.
Authors:
Cantwell-Dorris, Emma R; O'Leary, John J; Sheils, Orla M
Affiliation:
Department of Histopathology, Trinity College, Sir Patrick Dun Research, Laboratory, Pathology Building, St. James' Hospital, Dublin 8, Ireland., cantweer@tcd.ie
Citation:
Mol Cancer Ther. 2011 Mar;10(3):385-94.
Journal:
Molecular cancer therapeutics
Issue Date:
1-Feb-2012
URI:
http://hdl.handle.net/10147/207794
DOI:
10.1158/1535-7163.MCT-10-0799
PubMed ID:
21388974
Abstract:
The mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway is frequently mutated in human cancer. This pathway consists of a small GTP protein of the RAS family that is activated in response to extracellular signaling to recruit a member of the RAF kinase family to the cell membrane. Active RAF signals through MAP/ERK kinase to activate ERK and its downstream effectors to regulate a wide range of biological activities including cell differentiation, proliferation, senescence, and survival. Mutations in the v-raf murine sarcoma viral oncogenes homolog B1 (BRAF) isoform of the RAF kinase or KRAS isoform of the RAS protein are found as activating mutations in approximately 30% of all human cancers. The BRAF pathway has become a target of interest for molecular therapy, with promising results emerging from clinical trials. Here, the role of the most common BRAF mutation BRAF(V600E) in human carcinogenesis is investigated through a review of the literature, with specific focus on its role in melanoma, colorectal, and thyroid cancers and its potential as a therapeutic target.
Language:
eng
MeSH:
Animals; Cell Transformation, Neoplastic/*genetics; Extracellular Signal-Regulated MAP Kinases/genetics/metabolism; Humans; Mice; Mitogen-Activated Protein Kinases/*genetics/metabolism; *Molecular Targeted Therapy; *Mutation; Proto-Oncogene Proteins B-raf/*genetics
ISSN:
1538-8514 (Electronic); 1535-7163 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorCantwell-Dorris, Emma Ren_GB
dc.contributor.authorO'Leary, John Jen_GB
dc.contributor.authorSheils, Orla Men_GB
dc.date.accessioned2012-02-01T10:44:54Z-
dc.date.available2012-02-01T10:44:54Z-
dc.date.issued2012-02-01T10:44:54Z-
dc.identifier.citationMol Cancer Ther. 2011 Mar;10(3):385-94.en_GB
dc.identifier.issn1538-8514 (Electronic)en_GB
dc.identifier.issn1535-7163 (Linking)en_GB
dc.identifier.pmid21388974en_GB
dc.identifier.doi10.1158/1535-7163.MCT-10-0799en_GB
dc.identifier.urihttp://hdl.handle.net/10147/207794-
dc.description.abstractThe mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway is frequently mutated in human cancer. This pathway consists of a small GTP protein of the RAS family that is activated in response to extracellular signaling to recruit a member of the RAF kinase family to the cell membrane. Active RAF signals through MAP/ERK kinase to activate ERK and its downstream effectors to regulate a wide range of biological activities including cell differentiation, proliferation, senescence, and survival. Mutations in the v-raf murine sarcoma viral oncogenes homolog B1 (BRAF) isoform of the RAF kinase or KRAS isoform of the RAS protein are found as activating mutations in approximately 30% of all human cancers. The BRAF pathway has become a target of interest for molecular therapy, with promising results emerging from clinical trials. Here, the role of the most common BRAF mutation BRAF(V600E) in human carcinogenesis is investigated through a review of the literature, with specific focus on its role in melanoma, colorectal, and thyroid cancers and its potential as a therapeutic target.en_GB
dc.language.isoengen_GB
dc.subject.meshAnimalsen_GB
dc.subject.meshCell Transformation, Neoplastic/*geneticsen_GB
dc.subject.meshExtracellular Signal-Regulated MAP Kinases/genetics/metabolismen_GB
dc.subject.meshHumansen_GB
dc.subject.meshMiceen_GB
dc.subject.meshMitogen-Activated Protein Kinases/*genetics/metabolismen_GB
dc.subject.mesh*Molecular Targeted Therapyen_GB
dc.subject.mesh*Mutationen_GB
dc.subject.meshProto-Oncogene Proteins B-raf/*geneticsen_GB
dc.titleBRAFV600E: implications for carcinogenesis and molecular therapy.en_GB
dc.contributor.departmentDepartment of Histopathology, Trinity College, Sir Patrick Dun Research, Laboratory, Pathology Building, St. James' Hospital, Dublin 8, Ireland., cantweer@tcd.ieen_GB
dc.identifier.journalMolecular cancer therapeuticsen_GB
dc.description.provinceLeinster-

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