Chromosomal imbalances in oral squamous cell carcinoma: Examination of 31 cell lines and review of the literature

Abstract

Classical and molecular cytogenetic analysis, including fluorescence in situ hybridization (FISH) and chromosomal comparative genomic hybridization (CGH), were used to examine genetic changes involved in the development and/or progression of oral squamous cell carcinoma (OSCC). Of 31 OSCC cell lines studied, more than one-third expressed clonal structural abnormalities involving chromosomes 3, 7, 8, 9, and 11. Eleven OSCC cell lines were evaluated using CGH to identify novel genome-wide gains, losses, or amplifications. By CGH, more than half of the cell lines showed loss of 3p, gain of 3q, 8q, and 20q. Further, molecular cytogenetic analyses by FISH of primary tumors showed that the karyotypes of cell lines derived from those tumors correlated with specific gains and losses in the tumors from which they were derived. The most frequent nonrandom aberration identified by both karyotype and CGH analyses was amplification of chromosomal band 11q13 in the form of a homogeneously staining region. Our data suggest that loss of 9p and 11q13 amplification may be of prognostic benefit in the management of OSCC, which is consistent with the literature. The results of this study validate the relationship between these OSCC cell lines and the tumors from which they were derived. The results also emphasize the usefulness of these cell lines as in vitro experimental models and provide important genetic information on these OSCC cell lines that were recently reported in this journal.

Copy number changes of CRISP3 in oral squamous cell carcinoma

“…Cytogenetic analyses in conjunction with molecular genetics analyses by a number of research groups have shown an accumulation of genetic abnormalities during the development and/or progression of OSCC (23). In this study, we identified 11 downregulated genes, CRISP3, SCGB3A1, AGR2, PIP, C20orf114, TFF1, STATH, AZGP1, MUC7, DMBT1 and LOC389429, and 2 up-regulation genes, LNM, lymph node metastasis confirmed by histopathological examination within the 12-month follow-up period.…”

Deciphering the Role of the Barr Body in Malignancy: An insight into head and neck cancer

“…39 However, a sex link was dubious; the loss of the short arm of the Xi was a common observation in females and Y loss was observed in about 50% of males. 39 In HNSCC cases, Xi reactivation can potentially be considered a marker of heterochromatin instability associated with poor prognosis as, much like cervical cancer, the disease may be associated with epigenetic modifications as well as oncoviruses that could alter the X-linked genes. 11,36,37 Thus, the destabilised genomic repertoire in HNSCC appears to be further undermined by epigenetic events.…”

“…11,36,37 Thus, the destabilised genomic repertoire in HNSCC appears to be further undermined by epigenetic events. 39,40 However, before considering an association between the Barr body and HNSCC, a causal relation between X-linked TSGs and HNSCC development must be established. A summary of the X-linked genes involved in HNSCC development and their various loci, functions and mechanisms can be found in Table 1.…”

Expressão de transcritos de genes localizados no cromossomo 11q em carcinoma epidermóide de boca e sua relação com critérios de agressividade

“…De forma abrangente, análises citogenéticas e genéticas moleculares em carcinoma epidermóide de boca revelaram perdas cromossômicas em 3p, 4p, 8p, 11q, e 18q, e ganhos em 3q, 5p, 7p/q, 8q, 9q, 11q, 14q, 19q, e 20q (GOLLIN, 2001;JIN et al, 1995;JIN et al, 2006a;LESE et al, 1995;MARTIN et al, 2008;SPEICHER et al, 1995;WREESMANN;). Uma vez que alterações cromossômicas numéricas e estruturais são responsáveis pelo acúmulo de aberrações genéticas que conduzem ao desenvolvimento e progressão tumoral (SAUNDERS et al, 2000), Weber et al (1998) MARTIN et al, 2008).…”

“…No câncer da região de cabeça e pescoço, as mais frequentes envolvem ganhos em 3q, 8q, 9q, 20q, 7p, 11q13, e 5p e perdas em 3p, 9p, 21q, 5q, 13q, 18q, e 8p (GOLLIN, 2001). A região cromossômica 11q13 foi descrita como alterada em diferentes neoplasias, inclusive em carcinomas epidermóides de boca MARTIN et al, 2008 -7). A escolha desses genes para validação por qRT-PCR (reação em cadeia da polimerase quantitativa precedida de transcrição reversa) em um grupo amostral maior se fez necessária no intuito de legitimar a utilidade desses genes como marcadores moleculares no carcinoma epidermóide de boca.…”