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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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE28407 | GEO | 2011/11/18

SECONDARY ACCESSION(S): PRJNA139187

REPOSITORIES: GEO

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Project description:The aim of the study was to address the concept of field cancerization in oral cancer. The presence of genomic aberrations, indicative of chromosomal instability (CIN), in oral distant fields (ODFs) of visually normal and non-dysplastic mucosa at the mirror image from concomitant oral potentially malignant lesions (OPMLs) was investigated. This pilot study comprised 16 OPMLs (8 without dysplasia, nd-OPMLs; 8 with dysplasia, d-OPMLs) and 16 ODFs. DNA diploid (DNA Index, DI=1) and aneuploid (DIM-bM-^IM- 1) sublines were detected by high resolution DNA-flow cytometry (FCM) at (hr DNA-FCM) using DAPI stained nuclei suspensions. Nuclei with different DIs were FCM-sorted in order to enrich the epithelial component and to obtain genomic DNA for high resolution oligonucleotide array-Comparative Genomic Hybridization (a-CGH) analysis to provide a genome-wide measurement of DNA copy number aberrations (CNAs). The frequencies of DNA aneuploidy in ODFs and OPMLs were 6.2% and 43.8%, respectively (p=0.037). ODFs and nd-OPMLs were all near-diploid (DIM-bM-^IM- 1 and DIM-bM-^IM-$1.4), while d-OPMLs were also high-aneuploid (DI>1.4). CNA averages were 2.3 in ODFs (1.5 for nd-OPMLs and 3.1 for d-OPMLs), and 7.325 in OPMLs (3.0 in nd-OPMLs; 11.6 in d-OPMLs). CNAs were present in the DNA diploid sublines and often the same CNAs were observed in both ODFs and corresponding OPMLs DNA aneuploid sublines and CNAs in the present series of 16 ODFs are likely to represent early events of the natural history of oral carcinogenesis and to indicate an early onset of the field effect cancerization. Moreover, gains within 20q13.33-qter, 7p22.2-pter and 16p13.3-pter chromosomal regions in ODFs and in the relative OPMLs suggest that specific genes localized in these regions (RTEL1, MAD1L1 and TEL2) might contribute to the ODF/d-OPML transition. We analyzed: 8 samples of oral potentially malignant lesions with dysplasia, 8 samples of oral potentially malignant lesions without dysplasia and for each patient a corresponding oral distant field of visually normal mucosa.

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

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