The behaviour of human oral squamous cell carcinoma in cell culture (original) (raw)
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Pattern of keratinization in oral squamous cells during carcinogenesis
Background: Oral carcinogenesis is a multi-step process. Broadly, oral squamous cell carcinoma (OSCC) can be well-, moderately- or poorly-differentiated, and either keratinizing or non-keratinizing. Most cases are moderately to poorly-differentiated. Precursor lesions (dysplasia) can be categorized into mild, moderate, or severe (carcinoma in situ).In the present study, the pattern of keratin expression in oral squamous cells during carcinogenesis is vividly analysed. Materials and Methods: Samples in the form of scraped and exfoliated cytosmear were collected from the affected sites of the clinically diagnosed 136 oral cancer patients and were immediately fixed in acetoalcohol (1:3). The wet fixed smears were stained by routine Papanicolaou’s staining protocol and Giemsa’s solution. Stained tissues were studied under the microscope. Results: Cytological pleomorphism is a unique feature observed during carcinogenesis. There appears to be a spectrum of degrees of keratinization rather than distinct types, and the degree of keratinization is reflected in the degree of packing and orientation of keratin filaments. It is presumed that alteration in the architectural regularity of the cell membrane is an important aspect of keratinization which leads to cytological pleomorphism during oral carcinogenesis. Conclusion: Pattern of keratinization alongwith cytological pleomorphism in exfoliated epithelial squamous cells has a practical utility in the diagnosis and early detection of oral cancer during carcinogenesis. Keywords: Carcinogenesis, Keratinization, Keratins, Oral squamous cell carcinoma.
The American journal of pathology, 1994
Simple epithelial keratins K7, K8, and K18 are present in no more than trace amounts in normal stratified squamous epithelial but have been reported in squamous cell carcinomas. With the aim of determining the level at which keratin synthesis is regulated in vivo, we have compared the expression of mRNA by in situ hybridization and protein by immunohistochemistry for K7, K8, and K18 in a series of normal, dysplastic, and malignant oral epithelia. In normal epithelia mRNAs for K7, K8, and K18 were present in basal and lower spinous cells but adjacent sections were generally negative for the respective proteins. In severe dysplasia there was irregular suprabasal extension of K8 and K18 mRNAs in all cases and their proteins were expressed in more than half of the cases. The carcinomas expressed K8 and K18 mRNAs homogeneously and were strongly reactive for these keratin proteins but K7 expression appeared reduced in malignancy. These results are consistent with the post-transcriptional ...
Oral Oncology, 2011
To evaluate differential expressions for keratin (K) subtypes 13 and 17 in oral borderline malignancies, we examined 67 surgical specimens of the oral mucosa for their immunohistochemical profiles. From those specimens, 173 foci of epithelial dysplasia, 152 foci of carcinoma in situ (CIS), and 82 foci of squamous cell carcinoma (SCC) were selected according to our diagnostic criteria, along with 20 areas of normal epithelia. In normal epithelia, there was no K17 positivity (0%), whereas definite K13 positivity (100%) was observed. The same tendencies were obtained in mild (undefined) and moderate (true) epithelial dysplasias (K17: 0%; K13: 100%). In contrast, all CIS (100%) had K17 positivities, while K13 positivities were lost in many of them (7%). Similar tendencies were confirmed in invasive SCC (K17: 100%, K13: 4%). Simultaneous immunopositivities for K17 and K13 were found only in SCC (7%) and CIS (4%) foci with distinct keratinization. These foci also showed K10 positivities, though K10 positive areas were not identical to K13 positive areas. The results indicate that expressions of K17 and K13 are reciprocal in oral epithelial lesions and that the K17 emergence is related to malignancies.
Expression of biological markers in oral squamous cell carcinomas
Humberto Thomazi Gassen; Sergio Augusto Quevedo Miguens Jr.; Vanessa Costantin; Simone Marcia dos Santos Machado; Aurelício Novaes Silva-Junior; Pedro Antônio Gonzáles Hernández
Squamous cell carcinomas are the most commonly diagnosed oral malignancy, accounting for about 90% of all malignant oral lesions. Detection of the condition at early stages is rare; as a result, the clinical and histological characteristics and prognosis of this tumor have not been extensively investigated. The objective of this study was to evaluate clinical and microscopic features of squamous cell carcinomas using immunohistochemical analysis and assessing biological markers of angiogenesis and tumor vascular activity (anti-CD31, anti-CD34, Factor VIII), cell proliferation (Ki-67), and loss of cell suppression (p53). Tolonium chloride 1% was used to determine the optimal biopsy site. Six patients seen at the Stomatology Service of a university hospital in Canoas, southern Brazil, with a suspected diagnosis of squamous cell carcinoma were analyzed. All patients were male, with a mean age of 56.6 years, and four had a white skin color. Lesions were detected in the tongue (4) and tonsillar pillar (2). All diagnoses were confi rmed by microscopy (hematoxylin-eosin staining). Immunohistochemical analysis revealed p53 expression in 5 of the cases, Ki-67 in 6, and anti-CD34 in 1; anti-CD31 and Factor VIII were not detected in any patient. Our fi ndings suggest an important contribution of tumor markers in the diagnosis and prognosis of these malignancies, as well as in treatment planning.
Analysis of cell proliferation and pattern of invasion in oral squamous cell carcinoma
Journal of Oral Science, 2010
Cell proliferation markers play an important role in the biological behavior of neoplasms. This study investigated the immunohistochemical expression of PCNA, Ki-67 and Cyclin B1 proteins based on the pattern of cell invasion in oral squamous cell carcinoma (OSCC). A total of 39 OSCC specimens and 13 samples of normal oral mucosa (control) were immunohistochemically analyzed. Protein expression was evaluated according to World Health Organization-Histological Malignancy Grading (WHO-HMG) and a specific grading system for invasion, graded from 1 to 4, varying from a consistently well-defined "pushing" border to diffuse infiltration and cellular dissociation, and was then correlated with clinical features. We found higher expression of Ki-67 and Cyclin B1 in OSCC when compared with the control group. High Ki-67 expression levels were more commonly seen in the floor of the mouth than in the tongue (P = 0.009). Cyclin B1 showed a positive correlation with histological grade, according to WHO-HMG criteria (P = 0.01). Our results suggest that Cyclin B1 is a reliable proliferation marker for indicating degree of tumor proliferation. Correlations between PCNA, Ki-67, Cyclin B1 and invasive tumor front with overall survival were not observed. Further studies are needed in order to elucidate whether cell proliferation activity at the tumor invasion front is related to prognosis.
International Journal of Molecular Medicine, 2007
We have established 3 cell lines ORL-48,-115 and-136 from surgically resected specimens obtained from untreated primary human oral squamous cell carcinomas of the oral cavity. The in vitro growth characteristics, epithelial origin, in vitro anchorage independency, human papillomavirus (HPV) infection, microsatellite instability status, karyotype and the status of various cell cycle regulators and gatekeepers of these cell lines were investigated. All 3 cell lines grew as monolayers with doubling times ranging between 26.4 and 40.8 h and were immortal. Karyotyping confirmed that these cell lines were of human origin with multiple random losses and gains of entire chromosomes and regions of chromosomes. Immunohistochemistry staining of cytokeratins confirmed the epithelial origin of these cell lines, and the low degree of anchorage independency expressed by these cell lines suggests non-transformed phenotypes. Genetic analysis identified mutations in the p53 gene in all cell lines and hypermethylation of p16 INK4a in ORL-48 and-136. Analysis of MDM2 and EGFR expression indicated MDM2 overexpression in ORL-48 and EGFR overexpression in ORL-136 in comparison to the protein levels in normal oral keratinocytes. Analysis of the BAT-26 polyadenine repeat sequence and MLH-1 and MSH-2 repair enzymes demonstrated that all 3 cell lines were microsatellite stable. The role of HPV in driving carcinogenesis in these tumours was negated by the absence of HPV. Finally, analysis of the tissues from which these cell lines were derived indicated that the cell lines were genetically representative of the tumours, and, therefore, are useful tools in the understanding of the molecular changes associated with oral cancers.