Absence of BRAFV600E immunohistochemical expression in sporadic odontogenic keratocyst, syndromic odontogenic keratocyst and orthokeratinized odontogenic cyst.
BRAFV600E
immunohistochemistry
nevoid basal cell carcinoma syndrome
odontogenic keratocyst
orthokeratinized odontogenic cyst
rabbit monoclonal antibody clone rm8
Journal
Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
ISSN: 1600-0714
Titre abrégé: J Oral Pathol Med
Pays: Denmark
ID NLM: 8911934
Informations de publication
Date de publication:
Nov 2020
Nov 2020
Historique:
received:
23
02
2020
revised:
08
05
2020
accepted:
15
06
2020
pubmed:
27
6
2020
medline:
22
12
2020
entrez:
27
6
2020
Statut:
ppublish
Résumé
Odontogenic keratocyst (OKC) is a unique developmental odontogenic cyst that has the potential to behave aggressively and is associated with the nevoid basal cell carcinoma syndrome. Orthokeratinized odontogenic cyst (OOC) is a distinct, uncommon odontogenic cyst. It significantly differs from OKC not only in its epithelial lining but also in proliferating kinetics, clinical, immunohistochemical and biological behaviour. BRAF gene located on chromosome 7q34 encodes a cytoplasmic serine-threonine kinase. Various immunohistochemical studies have been conducted to express the BRAFV600E gene mutation in various odontogenic cyst and tumours with varying results. The present study was conducted to evaluate the possible role of BRAFV600E in the pathogenesis of sporadic OKC, syndromic OKC and OOC by immunohistochemistry. Formalin-fixed paraffin-embedded (FFPE) tissue blocks of 15 diagnosed cases each of sporadic OKC, syndromic OKC and OOC were retrieved from the archives of Department of Oral Pathology and subjected to immunohistochemical staining for the detection of BRAFV600E mutation using a novel rabbit monoclonal antibody clone RM8. Immunohistochemical analysis showed complete absence of BRAFV600E mutation in all cases of sporadic OKC, syndromic OKC and OOC. The negative immunohistochemical expression of BRAFV600E in sporadic OKC, syndromic OKC and OOC suggests that BRAFV600E plays no role in the pathogenesis of sporadic OKC, syndromic OKC and OOC.
Sections du résumé
BACKGROUND
BACKGROUND
Odontogenic keratocyst (OKC) is a unique developmental odontogenic cyst that has the potential to behave aggressively and is associated with the nevoid basal cell carcinoma syndrome. Orthokeratinized odontogenic cyst (OOC) is a distinct, uncommon odontogenic cyst. It significantly differs from OKC not only in its epithelial lining but also in proliferating kinetics, clinical, immunohistochemical and biological behaviour. BRAF gene located on chromosome 7q34 encodes a cytoplasmic serine-threonine kinase. Various immunohistochemical studies have been conducted to express the BRAFV600E gene mutation in various odontogenic cyst and tumours with varying results. The present study was conducted to evaluate the possible role of BRAFV600E in the pathogenesis of sporadic OKC, syndromic OKC and OOC by immunohistochemistry.
METHODS
METHODS
Formalin-fixed paraffin-embedded (FFPE) tissue blocks of 15 diagnosed cases each of sporadic OKC, syndromic OKC and OOC were retrieved from the archives of Department of Oral Pathology and subjected to immunohistochemical staining for the detection of BRAFV600E mutation using a novel rabbit monoclonal antibody clone RM8.
RESULTS
RESULTS
Immunohistochemical analysis showed complete absence of BRAFV600E mutation in all cases of sporadic OKC, syndromic OKC and OOC.
CONCLUSION
CONCLUSIONS
The negative immunohistochemical expression of BRAFV600E in sporadic OKC, syndromic OKC and OOC suggests that BRAFV600E plays no role in the pathogenesis of sporadic OKC, syndromic OKC and OOC.
Substances chimiques
Antibodies, Monoclonal
0
BRAF protein, human
EC 2.7.11.1
Proto-Oncogene Proteins B-raf
EC 2.7.11.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1061-1067Informations de copyright
© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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