OBJECTIVEThe purpose of this study was to investigate whether the fundamental genetic character of oral carcinoma-associated fibroblasts changes through contrasting and analyzing the oral carcinoma-associated fibroblasts and the normal fibroblasts of oral mucosa.

METHODSThe two kinds of cells were treated with colchicine and microsometic fluid, and then were expanded with cold acetic acid and formalized with methyl alcohol. The cells were observed under the oil microscope after Giemsa staining. The chromosome karyotype of the two kinds of cells was analyzed by Visus 2. 1.

RESULTSThere were not obvious differences in the way of chromosome karyotype between the oral carcinoma-associated fibroblasts and the normal fibroblasts of oral mucosa.

CONCLUSIONThe basic genetic characteristics of the normal cells are conserved in the oral carcinoma-associated fibroblasts, which means the cells have no malignant changes.

Chromosomes ; Fibroblasts ; Humans ; Karyotype ; Karyotyping ; Mouth Mucosa ; Mouth Neoplasms ; genetics

OBJECTIVETo investigate the relationship between centrosome abnormalities and aneuploidy in oral squamous cell carcinoma (OSCC) and elucidate the possible underlying mechanisms of chromosome instability (CIN) in OSCC.

METHODSFormalin-fixed, paraffin-embedded tissues of 8 cases of normal oral epithelium and 32 cases of OSCC were examined for centrosome status by using indirect immunofluorescence staining, and chromosome instability (aneuploidy) in some tissues were detected by flow cytometry. The correlation between centrosome abnormalities and aneuploidy in OSCC was statistically analyzed by SPSS12.0.

RESULTSNormal oral epithelium showed normal size and number of centrosomes in epithelium cells, while 25 out of 32 cases of OSCC showed the evident centrosome amplification characterized by huge size and/or supernumerary centrosomes in a fraction of tumor cells, and 21 out of 32 cases were aneuploidy. The percentage of cases with abnormal centrosomes in aneuploid OSCC (19/21) was significantly higher than that in diploid OSCC(6/11) (P =0.032). Centrosome abnormality was significantly correlated with aneuploidy (Spearman r = 0.413, P = 0.047), and a positive correlation was found between the degree of centrosome amplification and the degree of DNA ploidy abnormality (Pearson r = 0.364, P = 0.041).

CONCLUSIONSCentrosome abnormality may be a contributing factor for chromosome instability in OSCC.

Aneuploidy ; Carcinoma, Squamous Cell ; genetics ; pathology ; Centrosome ; pathology ; Chromosomal Instability ; Humans ; Mouth Mucosa ; pathology ; Mouth Neoplasms ; genetics ; pathology

OBJECTIVEIt is currently considered that the defect of mitotic spindle caused by centrosome abnormalities may be one of the reasons for the development of aneuploidy in tumors. This study attempted to elucidate the possible role of centrosome defects in the development and progression of OSCC by investigating the frequency of centrosome amplification in oral precancerous lesions and OSCC.

METHODSFormalin-fixed, paraffin-embedded tissues of 12 cases of normal oral epithelium, 22 case of dysplasia with different degree epithelium dysplasia and 32 cases of OSCC with different differentiation were investigated for centrosome status by using indirect immunofluorescence double staining with antibodies to centrosome protein gamma-tubulin and cytokeratin. The differences and the change trend of centrosome status in these groups were statistically analyzed by SPSS10.0.

RESULTSNormal oral epithelium showed normal centrosomes in epithelium cells, while 16 of 22 cases (72.73%) of dysplasia (DYS) and 27 of 32 cases (84.38%) of OSCC showed the evidence of centrosome amplification and morphological abnormalities characterized by huge size, clump or supernumerary centrosomes in a fraction of epithelium or tumor cells. The percentage of cells with abnormal centrosomes increased gradually from mild-dysplasia epithelium to poorly differentiated OSCC, which positively correlated with the histologicalcytologic grade of oral precancerous lesions and OSCC (P < 0.01).

CONCLUSIONCentrosome amplification was an early event and that might play a role in the establishment and perhaps the progression of OSCC. There might be some direct relationship between centrosome defects and the cellular morphological phenotype characteristics of dysplasia and OSCC. Centrosome amplification could be served as an alternative diagnostic indicator of dysplasia and the intervention of centrosome cycle might serve as a particular way for the prevention and treatment of OSCC in the future.

Carcinoma, Squamous Cell ; genetics ; pathology ; Centrosome ; pathology ; Humans ; Mouth Mucosa ; pathology ; Mouth Neoplasms ; genetics ; pathology ; Precancerous Conditions ; pathology

Biomarkers, Tumor ; Humans ; Mouth Neoplasms ; chemistry ; genetics ; Precancerous Conditions ; chemistry ; genetics

OBJECTIVEThe purpose of this study was to investigate the transcription and expression levels of human leukocyte antigen-DR at different stages of oral squamous cell carcinomas.

METHODSThe specific monoclonal antibody and beta-locus specific oligonucleotide probes of human leukocyte antigen-DR were employed in this study. A total of 32 primary oral squamous cell carcinomas, 15 metastatic focuses and 26 histologically normal oral epithelia, were detected for the presence of the human leukocyte antigen-DR molecule by using immunohistochemistry and in situ hybridization.

RESULTSThe human leukocyte antigen-DR expression of the primary focuses was significantly higher than that of the normal epithelia (P < 0.05), but their expression did not show statistically difference between the metastatic focuses and the normal epithelia. The immunohistochemistric results were identical with those of in situ hybridization.

CONCLUSIONThe abnormal higher expression of the HLA-DR is a common character of primary oral squamous cell carcinomas, but it may be not relevant to the metastasis of tumors.

Carcinoma, Squamous Cell ; genetics ; immunology ; HLA-DR Antigens ; biosynthesis ; genetics ; Humans ; Immunohistochemistry ; In Situ Hybridization ; Mouth Mucosa ; immunology ; Mouth Neoplasms ; genetics ; immunology

OBJECTIVETo determine the difference in the gene expression between human oral verrucous carcinoma (OVC) and oral squamous cell carcinoma (OSCC).

METHODScDNA chip was used to detect the mRNA of cancer tissue from 4 OVC and 4 OSCC. After profile blotted and handled by bioinformation, the gene expression of these two kinds of lesions was examined.

RESULTSUsing the BioStarH-40 profile, 593 different expression of genes was found. The rate of different genes was 15.2%, of which the expression of 283 genes increased (59 genes significantly increased) and 310 genes decreased (98 genes significantly decreased) in OVC tissue than that in OSCC.

CONCLUSIONSThe gene expression of OVC and OSCC was different, which many contribute to the different biological behavior of these two kinds of lesions.

Carcinoma, Squamous Cell ; genetics ; Carcinoma, Verrucous ; genetics ; Gene Expression Profiling ; Humans ; Mouth Neoplasms ; genetics ; Oligonucleotide Array Sequence Analysis

OBJECTIVETo investigate the gene mutation in D-loop region of mitochondrial DNA (mtDNA) in oral squamous cell carcinoma (OSCC) tissue and to explore the role of the gene mutation in D-loop region in the OSCC tumorigenesis.

METHODSmtDNA was obtained from cancer, paracancerous and normal mucosa tissues of thirty patients with OSCC. The D-loop regions of mtDNA were amplified with PCR, sequencing and then analyzed by Chromas software and BLAST to identify the mutation site.

RESULTSMutation in the D-loop region was found in eight cases, with the mutation rate of 27%. There were nine mutations totally, including one point mutation, two base deletions, three insertion mutations, three heterozygous mutations. In these mutations, base deletions were different from each other and heterozygous mutations had no same mutation form, while the three insertion mutations were same, the insertion of base C. One case had T/A heterozygous mutation and base C insertion at the same time.

CONCLUSIONSThere were mutations in mtDNA D-loop in OSCC, but the relationship between occurrence of OSCC and mutation of mtDNA needs further study.

Adult ; Aged ; Carcinoma, Squamous Cell ; genetics ; DNA, Mitochondrial ; genetics ; Female ; Humans ; Male ; Middle Aged ; Mouth Neoplasms ; genetics ; Mutation

The p16/INK4A is one of the major target genes in carcinogenesis and its inactivation has frequently been reported in other types of tumors. The purpose of this study is to evaluate inactivation patterns of p16/INK4A in oral squamous cell carcinoma. Six different oral cancer cell lines, SCC-4, SCC-9, SCC-15, SCC-25, KB, and SNUDH- 379 were examined for inactivation of p16/INK4A genes. In the analysis of p16/INK4A gene inactivation, PCR amplification, direct sequencing, and methylation-specific PCR methods were adopted for evaluation of homozygous deletion, point mutation, and promoter hypermethylation, respectively. Homozygous deletion was detected in SCC-25 and SCC-9. SCC-15 showed hypermethylated promoter region within p16/INK4A gene. It is suggestive in the present study that inactivation patterns of p16/INK4A were mainly homozygous deletion, promoter methylation rather than point mutation in oral squamous cancer cell lines, so treatment modalities of oral squamous cell carcinoma should be focused on these types of inactivation.
Carcinoma, Squamous Cell/*genetics ; Cell Line, Tumor ; DNA Methylation ; *Gene Silencing ; Homozygote ; Humans ; Mouth Neoplasms/*genetics ; Point Mutation ; Promoter Regions (Genetics)/genetics ; Protein p16/*genetics

OBJECTIVETo study the differently expressed genes of oral squamous cell carcinoma (OSCC) tissue.

METHODSGene expression datasets related to oral squamous cell carcinoma in the gene expression omnibus (gene expression omnibus, GEO) repository were retrieved. Datasets were merged by normalization.Significantly expressed genes were obtained by statistical methods, and genes' functions, interactions, signaling pathways were analyzed accordingly.

RESULTSIn GEO, there were 1 125 records related to OSCC, and four of them were selected and merged to a super array data, within the super array data, 233 genes were significantly expressed (P < 0.05) , and the top 100 significantly expressed genes were selected as signature genes.Signature genes were more related to cell surface or cell-cell interactive activities. Clusters of interactive signature genes and the related signaling pathways were related with mitosis process.

CONCLUSIONSOSCC signature genes and the corresponding signaling pathways will provide not only an important clue for further research of the disease, but also reference for diagnosis and treatment.

Carcinoma, Squamous Cell ; genetics ; Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Mouth Neoplasms ; genetics ; Signal Transduction

OBJECTIVEThe purpose of this study was to examine the expression of human major histocompatibility complex-I at different degrees of dysplasia leukoplakia, and to investigate local immune status and discuss their associations with oral leukoplakia.

METHODSThe monoclonal antibody of MHC class I antigen was employed in this study. There were 55 oral leukoplakias, 31 primary oral squamous cell carcinomas and 28 histologically normal oral epithelia were detected for the presence of the MHC class I molecule by using immunohistochemistry method.

RESULTSThe MHC class I antigen expression of the severe dysplasia and oral squamous cell carcinoma was significantly lower than that of the normal epithelia (P < 0.05). But their expression did not show statistically difference between the normal epithelia and other groups of oral leukoplakia (P > 0.05).

CONCLUSIONThe expression levels of the MHC class I antigen is reduced in oral leukoplakia, particularly in severe dysplasia oral leukoplakia, it is relevant to the degree of dysplasia.

Antibodies, Monoclonal ; Carcinoma, Squamous Cell ; genetics ; Genes, MHC Class I ; Histocompatibility Antigens Class I ; genetics ; Humans ; Immunohistochemistry ; Leukoplakia, Oral ; genetics ; Mouth Neoplasms ; genetics