G. Emilion
University of Cambridge
8 Papers
331 Citations
G. Emilion is an academic researcher from University of Cambridge. The author has contributed to research in topics: Epidermoid carcinoma & Mouth neoplasm. The author has an hindex of 8, co-authored 8 publications.
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Papers
•Journal Article
A case-control study confirms that microsatellite assay can identify patients at risk of developing oral squamous cell carcinoma within a field of cancerization.
Maxine Partridge,Stelios Pateromichelakis,E. Phillips,G. Emilion,Roger P. A’Hern,John Langdon +5 more
TL;DR: It is suggested that the process of field cancerization is more widespread than previously recognized and recommended complete excision of all suspicious areas that show AI at two or more key loci, regardless of the degree of dysplasia.
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Field Cancerisation of the Oral Cavity: Comparison of the Spectrum of Molecular Alterations in Cases Presenting with Both Dysplastic and Malignant Lesions
TL;DR: The finding of identical 'genetic fingerprints' in dysplastic lesions and invasive carcinoma from the same patient provides strong evidence that these dysplasias are precursor lesions and that multiple lesions have probably arisen due to transfer of the progeny of an altered cell.
81
LOH at 3p correlates with a poor survival in oral squamous cell carcinoma
TL;DR: This study is the first to demonstrate the prognostic significance of LOH at 3p for oral cancer and may help to identify patients who should receive more aggressive treatment.
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Location of candidate tumour suppressor gene loci at chromosomes 3p, 8p and 9p for oral squamous cell carcinomas.
TL;DR: A more limited analysis of polymorphic sequences at 8p and 9p supports the existence of at least 2 areas that harbour tumour suppressor genes at 7p and evidence that additional targets for deletion reside centromeric and telomeric to the p16 gene at 9p21.
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New insights into p53 protein stabilisation in oral squamous cell carcinoma.
TL;DR: While it is possible that some tumours harbour p53 mutations outside the open reading frames examined, or are missed due to sequencing a mixture of normal and tumour tissue, a subgroup of tumours may express high levels of wild-type p53 as a reflection of the high FAL score and ongoing genomic stress.
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