Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2009-3-26
pubmed:abstractText
Mutational activation of the BRAF oncogene is the most common genetic alteration in cutaneous melanoma. Potentially, BRAF mutation analysis of sentinel lymph node (SLN) biopsies could enhance the detection of micrometastases and improve the accuracy of nodal staging for patients with melanoma. Nodal nevi are small aggregates of benign nevus cells that are commonly encountered in the SLNs of patients with melanoma. The status of the BRAF gene in nodal nevi is not known, but this unresolved issue is of critical importance to any future detection strategies that use genetic alterations as biomarkers of metastatic spread. Twenty-six nodal nevi from 26 patients were evaluated for the thymine (T)-->adenine (A) missense mutation at nucleotide 1796 of the BRAF gene using the LigAmp assay, which can detect 1 mutant allele among 10,000 wild-type alleles. For each case, a matching volume of adjacent lymphoid tissue was used as a negative control. BRAF mutations were detected in 13 of the 26 nodal nevi, but in just 1 of the 26 adjacent controls (50% vs. 4%, P<0.0005, Fisher exact). Novel strategies that rely on detection of putative melanoma-specific markers for the diagnosis of micrometastatic melanoma in SLNs need to take into account the molecular genetic profile of the benign nodal nevus. Indeed, these nodal nevi, like melanoma, frequently harbor activating mutations of the BRAF oncogene underscoring the potentially confounding impact of these inclusions on melanoma detection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1532-0979
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
568-71
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Benign nodal nevi frequently harbor the activating V600E BRAF mutation.
pubmed:affiliation
Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, MD, USA.
pubmed:publicationType
Journal Article