C S Farah1,2, F Kordbacheh2, K John2, N Bennett2, S A Fox1. 1. Australian Centre for Oral Oncology Research & Education, UWA Dental School, University of Western Australia, Nedlands, WA, Australia. 2. University of Queensland Centre for Clinical Research, The University of Queensland, Herston, QLD, Australia.
Abstract
OBJECTIVE: To define molecular differences between autofluorescence and white light defined excision margins in oral potentially malignant disorders (OPMD) using transcriptome expression profiles. MATERIALS AND METHODS: Excisional biopsy specimens were taken from 11 patients at three different sites for each lesion: centre, white light margin and autofluorescence margin. The lesions were diagnosed histopathologically as oral epithelial dysplasia, oral lichenoid dysplasia, oral lichen planus or other. Transcriptome analysis was performed by RNA sequencing, hierarchical clustering, differential expression and biological pathway analysis. RESULTS: For hierarchical clustering, the samples broadly clustered according to histology rather than the margins with lichenoid samples clustering together. Differential expression analysis showed that independent of histology, there was greater molecular dysregulation between the lesion centre and autofluorescence margin compared to the lesion centre and white light margin. Furthermore, the autofluorescence and white light margins were molecularly distinct, indicating the white light margins harboured abnormality. CONCLUSION: Our results indicate that the molecular profile of OPMD changes with divergence away from the centre of the lesion, and that autofluorescence determined margins are superior to the white light margin in achieving a clear molecular margin when excising an OPMD.
OBJECTIVE: To define molecular differences between autofluorescence and white light defined excision margins in oral potentially malignant disorders (OPMD) using transcriptome expression profiles. MATERIALS AND METHODS: Excisional biopsy specimens were taken from 11 patients at three different sites for each lesion: centre, white light margin and autofluorescence margin. The lesions were diagnosed histopathologically as oral epithelial dysplasia, oral lichenoid dysplasia, oral lichen planus or other. Transcriptome analysis was performed by RNA sequencing, hierarchical clustering, differential expression and biological pathway analysis. RESULTS: For hierarchical clustering, the samples broadly clustered according to histology rather than the margins with lichenoid samples clustering together. Differential expression analysis showed that independent of histology, there was greater molecular dysregulation between the lesion centre and autofluorescence margin compared to the lesion centre and white light margin. Furthermore, the autofluorescence and white light margins were molecularly distinct, indicating the white light margins harboured abnormality. CONCLUSION: Our results indicate that the molecular profile of OPMD changes with divergence away from the centre of the lesion, and that autofluorescence determined margins are superior to the white light margin in achieving a clear molecular margin when excising an OPMD.
Authors: Stephen A Boppart; J Quincy Brown; Camile S Farah; Esther Kho; Laura Marcu; Christobel M Saunders; Henricus J C M Sterenborg Journal: J Biomed Opt Date: 2017-12 Impact factor: 3.170
Authors: Marco Cicciù; Gabriele Cervino; Luca Fiorillo; Cesare D'Amico; Giacomo Oteri; Giuseppe Troiano; Khrystyna Zhurakivska; Lorenzo Lo Muzio; Alan Scott Herford; Salvatore Crimi; Alberto Bianchi; Dario Di Stasio; Rosario Rullo; Gregorio Laino; Luigi Laino Journal: Dent J (Basel) Date: 2019-09-04