4.6 Article

Detection of deletions in 1q25, 1p36 and 1pTEL and chromosome 17 aneuploidy in oral epithelial dysplasia and oral squamous cell carcinoma by fluorescence in situ hybridization (FISH)

期刊

ORAL ONCOLOGY
卷 116, 期 -, 页码 -

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ELSEVIER
DOI: 10.1016/j.oraloncology.2021.105221

关键词

Mouth neoplasms; Squamous cell carcinoma; Chromosome deletion; Chromosome 17; Chromosome 1

资金

  1. National Council for Scientific and Technological Development - Brazil (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico - CNPq) (MTCI/CNPq) [14/2013]
  2. University of Fortaleza (Universidade de Fortaleza)

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The study identified a higher prevalence of chromosomal abnormalities in oral squamous cell carcinoma (OSCC) compared to oral epithelial dysplasia (OED), with higher frequencies of deletions in 1p36, 1q25, and 1pTEL in lesions with higher TNM staging. Deletion of 1p36, 1q25, and 1pTEL could be markers of worse prognosis in OSCC.
Objective: To identify chromosome deletions in 1q25, 1p36 and 1pTEL, and chromosome 17 ploidy status in oral epithelial dysplasia (OED) and oral squamous cell carcinoma (OSCC). Material and methods: Samples from 57 OED and 63 OSCC were selected. FISH was performed using centromeric probes 17 and n LSIR 1p36/LSI 1q25 Dual Color Probe. Results: In OED, deletions were found only in 1pTEL region (29.8%). In OSCC, there was a higher frequency of deletion in 1pTEL (79.4%), followed by 1p36 (73.0%), and 1q25 (20.6%). Advanced TNM clinical stages (III/IV) showed all the deletions studied; at early clinical stages (I/II) of OSCC, deletions were observed only in 1pTEL. The frequency of deletion in 1p36 was 17.0 times higher in OSCC at advanced clinical stages (PR: 17.00). The median number of cell nuclei with chromosome 17 aneuploidy was higher in OSCC than in OED (P < 0.001). Early clinical stages of OSCC showed lower median number nuclei with aneuploidy when compared to advanced tumors (P < 0.05). Tumors harboring deletions in 1p36, 1q25 and 1pTEL revealed higher median numbers of trisomic/polysomic nuclei when compared to lesions exhibiting no abnormalities in chromosome 1 (P < 0.05). Conclusion: A higher prevalence of chromosomal abnormalities was found in OSCC than in OED, while in OSCC, higher abnormalities were present in lesions with higher TNM staging. 1pTEL deletion and monosomy of chromosome 17 are possible markers for progression of OED to OSCC. 1p36 deletion and trisomy/polysomy of chromosome 17 could be markers of worse prognosis of OSCC.

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