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29

Diverse routes to oral cancer differing in genome instability and risk for cervical node metastasis


ABSTRACT: Clinically evident oral lesions, oral epithelial dysplasia, precede development of oral squamous cell carcinomas (SCC) and are considered to transform to cancer by acquisition of genetic or epigenetic alterations. Here, we show that, +3q24-qter, -8pter-p23.1, +8q12-q24.2 and +20 are early events identifying two pathways to oral cancers that differ in clinical behavior. One or more of these copy number aberrations is present in the major subgroup (3q8pq20 subtype, 75-80% of lesions) that develops with chromosomal instability and risk for metastasis, while they are absent from the smaller and chromosomally stable non-3q8pq20 subgroup (20-25% of lesions) associated with low risk for metastasis. Thus, +3q, -8p, +8q and +20 is a biomarker for oral SCC metastasis. On the other hand, while increased numbers of genomic alterations can be harbingers of progression to cancer, dysplastic lesions lacking copy number changes cannot be considered benign as they are potential precursors to non-3q8pq20 oral SCC. Overall design: 63 oral SCCs and adjacent regions of normal tissue, 44 oral dysplasias

INSTRUMENT(S): UCSF HumArray 3.1

ORGANISM(S): Homo sapiens  

SUBMITTER: Taku Tokuyasu  

PROVIDER: GSE28407 | GEO | 2011-11-18

SECONDARY ACCESSION(S): PRJNA139187

REPOSITORIES: GEO

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