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PubMed1996

Polysomies of chromosomes 7 and 17 in head and neck squamous cell carcinomas.

OBJECTIVE: To determine the polysomies (ie, cells with > or = 3 chromosome copies) of chromosomes 7 and 17 in tumor tissue, histologically normal epithelia adjacent to the tumor (tumor-adjacent epithelia), and buccal epithelia distant from the tumor (tumor-distant epithelia) of head and neck squamous cell carcinomas. DESIGN: Nonfluorescent, nonisotopic, in situ hybridization using chromosome-specific centromeric DNA probes for chromosomes 7 and 17 was performed on the formalin-fixed, paraffin-embedded specimens from tumor and tumor-adjacent and tumor-distant epithelia of 19 patients with head and neck squamous cell carcinomas and from buccal epithelia of cancer-free control subjects who smoked and did not smoke cigarettes. MAIN OUTCOME MEASURES: Four hundred nuclei in tumor tissue and 200 nuclei in histologically normal epithelia were scored for hybridized signals in each sample. RESULTS: Buccal epithelia of cancer-free control subjects who smoked and did not smoke cigarettes showed no difference in the polysomies of chromosomes 7 and 17, respectively. The polysomies of chromosomes 7 and 17 in the tumor cells were higher than those in the tumor-adjacent epithelia (P < .001 for both), tumor-distant epithelia (P < .001 for both), and buccal epithelia of cancer-free control subjects who smoked and did not smoke cigarettes (P < .001 for both). The polysomies of chromosomes 7 and 17 in the tumor-adjacent epithelia were higher than those in the tumor-distant epithelia (P < .001 for both) and the control buccal epithelia (P = .002 and P < .001, respectively). The tumor-distant epithelia and the control buccal epithelia for the polysomies of chromosomes 7 and 17 had no differences. CONCLUSIONS: The finding of genotypic abnormalities in the tumor-adjacent epithelia supports the concept of field cancerization. Such genotypic parameters may provide a genetic basis for the development of an early recurrence or second primary tumors after therapeutic treatment of head and neck squamous cell carcinomas.

Aged↗
PubMed1999

Promotional effects of CO2 laser on DMBA-induced hamster buccal pouch carcinogenesis as shown by immunohistochemistry of the placental form of glutathione S-transferase.

BACKGROUND AND OBJECTIVE: The purpose of the present study was to investigate the kinetics of the expression of the placental form of glutathione S-transferase (GST-P), a useful marker of premalignant lesions, and cell proliferation after CO2 laser surgery on the carcinogen-initiated epithelium. STUDY DESIGN/MATERIALS AND METHODS: CO2 laser incisions were made on buccal pouch epithelium of 36 hamsters after initiation by 9,10-dimethyl-1,2-benzanthracene (DMBA) (group 1, G1), and scalpel incisions were similarly made on 33 animals (group 2, G2). Twenty animals not treated further after initiation were used as DMBA-treated controls. Incidence of malignant transformation, expression of GST-P, and cell proliferation were examined. RESULTS: The incidence of malignant transformation in G1 and G2 increased significantly (G1: P < 0.001; G2: P < 0.05) compared with that in DMBA-treated controls. GST-P expression of hyperplasia in G1 and G2 decreased significantly (P < 0.001) compared with that in DMBA-treated controls. In hyperplasia, cell proliferation of the GST-P-negative area was significantly (P < 0.001) higher than that of the GST-P-positive area. CONCLUSION: The incisions, particularly by the CO2 laser, on the initiated areas made expression of GST-P decrease and cell proliferation increase in the GST-P-negative areas. These incisions may serve to promote malignant transformation.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1996

The localization of p34cdc2 in the cells of normal, hyperplastic, and malignant epithelial and lymphoid tissues of the oral cavity.

The expression of p34cdc2 has been examined in normal, hyperplastic, and malignant oral epithelia and lymphoid tissues. Four monoclonal antibodies were prepared against Xenopus p34cdc2, three of which react specifically with human p34cdc2 and not with p33cdk2. These produced similar patterns of staining in both fixed and frozen sections of human material. Staining occurred mainly in the proliferative compartments of normal and hyperplastic tissues. In normal oral epithelia, parabasal and basal cells were the most strongly stained, with lighter cytoplasmic staining in lower prickle cells. In tonsillar germinal centres, a high proportion of cells was stained, with fewer positive cells in interfollicular zones, a distribution in keeping with the known pattern of cell proliferation. In normal cells, the intracellular location of p34cdc2 was cytoplasmic until early prophase, but in oral squamous cell carcinomas and lymphomas, it was located in both cytoplasm and nucleus during interphase and a larger fraction of cells was positive than in the equivalent normal tissues. Higher-grade neoplasms showed both a higher intensity of staining and a higher proportion of p34cdc2-positive cells.

Antibodies, Monoclonal↗
PubMed1998

Immunohistochemical study of desmosomes in oral squamous cell carcinoma: correlation with cytokeratin and E-cadherin staining, and with tumour behaviour.

Reduction or loss of the intercellular junctions known as desmosomes may contribute to the invasive and metastatic behaviour of various carcinomas. Previous studies have shown that metastasis of oral squamous cell carcinomas of the head and neck correlates with a reduction in immunohistochemical staining for desmoplakin and desmoglein at the invasion front. The primary aim of the present study was to extend these observations to include a third component of desmosomes, the glycoprotein desmocollin. An additional aim was to determine whether the differentiation status of tumours is reflected in their staining for cytokeratins 1, 13, and 19, and, if so, whether these parameters correlate with desmosomal staining and/or metastasis. The study included 54 primary tumours of which 28 showed lymph node metastases. The results of this investigation show that tumours can be divided into three groups according to whether they have lost staining for no, one or more than one desmosomal component. A statistically significant correlation was found between the number of desmosomal components lost and metastasis. Tumours could also be divided into five groups according to their staining for different combinations of cytokeratins. Furthermore, differentiation status as indicated both histologically and by cytokeratin staining correlated with reduced desmosomal staining and metastasis. Tumours were also examined for intensity of staining for the adhesion molecule E-cadherin. Reduction in E-cadherin staining was correlated with mode of invasion and with reduction in desmosomal staining, but not with poor differentiation as indicated by cytokeratin staining. The results of this extensive study reinforce the view that adhesive junctions and adhesion molecules contribute to the suppression of tumour invasion and metastasis.

Adult↗
PubMed1999

Prevalence of Epstein-Barr virus in oral squamous cell carcinoma.

Forty-six samples of oral squamous cell carcinoma (OSCC) were evaluated for the prevalence of Epstein-Barr virus (EBV) infection by the polymerase chain reaction (PCR), Southern blot hybridization, and in situ hybridization (ISH). EBV DNA was detected in 7 (15.2 per cent) out of 46 samples by a combination of PCR and Southern blot hybridization methods. All seven positive samples showed well-differentiated carcinoma, thus suggesting a possible relationship between EBV infection and the degree of differentiation of carcinoma tissue. Latent infection membrane protein 1 (LMP1) was detected immunohistochemically in six of the EBV-positive OSCCs. However, no signal of the EBV-encoded small RNA (EBER)-1 was demonstrated by the ISH method. No significant relationship was observed between EBV infection and lymph node metastasis. A follow-up study (range from 4.4 to 79 months; mean 34.9 months) showed no recurrence or death to occur in the EBV-positive patients, which thus suggested a good prognosis for EBV-positive OSCC patients.

Adult↗
PubMed1999

Synthesis and protein distribution of the unspliced large tenascin-C isoform in oral squamous cell carcinoma.

The inclusion or omission of the alternatively spliced region in the tenascin-C (Tn-C) mRNA gives rise to the large (Tn-C(L)) or small (Tn-C(S)) variant, respectively. Tn-C(L) is thought to be a typical component of provisional extracellular matrices (ECMs) and is expressed during tumour stroma remodelling. Tn-C(L) synthesis has been studied using RNA/RNA in situ hybridization, and Tn-C(L) protein distribution, using immunohistochemistry (clone BC-2), in 18 oral squamous cell carcinomas (OSCCs) of different grades of malignancy. While the Tn-C(L) protein was demonstrated within the whole stromal compartment regardless of grade of malignancy, the majority of the Tn-C(L) mRNA signal-bearing cells were carcinoma cells. Only a few stromal myofibroblasts were able to synthesize Tn-C(L), as revealed by alpha-smooth muscle actin double staining. In well-differentiated carcinomas (G1), the Tn-C(L) synthesizing carcinoma cells were localized as a single positive cell layer in the tumour stroma interface, particularly in invasive areas. A higher grade of malignancy (G2/G3) is associated with a significantly increased number of Tn-C(L) synthesizing carcinoma cells randomly distributed within the invading tumour areas. Double-staining experiments (Tn-C(L) mRNA ISH/BC-2 immunohistochemistry) indicate that these cells are capable of organizing and depositing a three-dimensional Tn-C(L) matrix. Even though an instructive and/or inductive role of the carcinoma cells in tumour stroma formation cannot be excluded, these results demonstrate that carcinoma cells can directly produce the ECM components of tumour stroma.

Basement Membrane↗
PubMed2000

Immunohistochemical study of MUC1 mucin in premalignant oral lesions and oral squamous cell carcinoma: association with disease progression, mode of invasion, and lymph node metastasis.

BACKGROUND: MUC1 mucin is a transmembrane, mucin-like glycoprotein encoded by the MUC1 gene. Although MUC1 expression has been identified in a variety of neoplastic tissues, to the authors' knowledge, few studies have examined MUC1 expression in premalignant and malignant oral lesions. METHODS: A total of 36 specimens of oral epithelial dysplasia, 12 carcinoma in situ (CIS) specimens and 77 specimens of oral squamous cell carcinoma (OSCC), were examined by both light and electron microscopy using immunohistochemical staining of MUC1 mucin. Relations between staining patterns and clinicopathologic findings also were examined. RESULTS: Distinct membrane MUC1 mucin staining patterns were identified in epithelial dysplasia (33.0%), CIS (50.0%), and OSCC (59.7%) cases. A predominantly cytoplasmic staining pattern was detected in epithelial dysplasia (5.6%), CIS (41.7%), and OSCC (32.5%) cases. Significant positive correlations were found between MUC1 mucin membranous immunoreactivity and disease progression from epithelial dysplasia to OSCC (P < 0.01), mode of tumor invasion (P < 0.02), and lymph node metastasis (P < 0.01). Furthermore, the malignant transformation of oral epithelium, tumor invasion, and tumor metastasis were associated with higher MUC1 mucin expression in the cytoplasm (P < 0.01). In addition to the usual cell surface expression, cytoplasmic expression of MUC1 mucin was confirmed by colloidal gold labeling with transmission electron microscopy. CONCLUSIONS: The results of the current study suggest that determination of MUC1 mucin expression may be a parameter in the diagnosis of premalignant and malignant lesions arising in the oral cavity and that this expression may affect the malignant behavior of OSCC. MUC1 mucin expression may be a useful diagnostic marker for prediction of the invasive/metastatic potential of OSCC.

Carcinoma, Squamous Cell↗
PubMed1996

Altered expression of CD44 isoforms in squamous-cell carcinomas and cell lines derived from them.

CD44 is a transmembrane glycoprotein that binds hyaluronan, extracellular matrix proteins and growth factors. Multiple isoforms of CD44 are generated by alternative splicing of 10 separate exons (V1-V10). Expression of the variable exons has been correlated with tumour progression and metastasis in a range of cell types. However, multiple CD44 isoforms are expressed by normal stratified squamous epithelia, such as the epidermis and the lining of the oral cavity. The purpose of our study was to examine CD44 expression in squamous-cell carcinomas (SCC). By immunofluorescence we found reduced expression of one or more of the variant exons in a series of 13 oral SCC, with loss being most common in poorly differentiated tumours. Of the exons we examined, V3 was lost most frequently, but otherwise there was no consistent pattern as to which exons (V4/5, 6, 8) were missing. We also studied CD44 expression in a range of SCC lines, using Western blotting and semi-quantitative RT-PCR. All lines showed reduced expression of the terminal differentiation marker involucrin. Two lines showed selective loss of the largest forms of CD44 and one failed to express any of the variant exons. These cell lines, therefore, provide a useful experimental model with which to study the biological significance of exon loss in SCC.

Alternative Splicing↗
PubMed2000

Paan without tobacco: an independent risk factor for oral cancer.

Oral cancer is the second most common cancer in women and the third most common in men in Pakistan. Tobacco is smoked and chewed extensively in Pakistan. Paan is a quid of piper betel leaf that contains areca nut, lime, condiment, sweeteners, and sometimes tobacco, which is also used extensively. We did this study to clarify the independent association of paan and oral cancer. Between July 1996 and March 1998, we recruited biopsy-proven, primary cases of oral squamous-cell carcinoma, from 3 tertiary teaching centers in Karachi, Pakistan, and controls pair-matched for age, gender, hospital and time of occurrence, excluding persons with a past or present history of any malignancy. There were 79 cases and 149 controls. Approximately 68% of the cases were men, 49 years old on average, the youngest being 22 years old and the eldest 80. People with oral submucous fibrosis were 19.1 times more likely to develop oral cancer than those without it, after adjusting for other risk factors. People using paan without tobacco were 9.9 times, those using paan with tobacco 8.4 times, more likely to develop oral cancer as compared with non-users, after adjustment for other covariates. This study identifies an independent effect of paan without tobacco in the causation of oral cancer. Its findings may be of significance in South Asian communities where paan is used, and among health-care providers who treat persons from South Asia.

Adolescent↗
PubMed1997

Quantification of surgical margin shrinkage in the oral cavity.

BACKGROUND: Obtaining adequate surgical margins, free of tumor, is crucial for success in oncologic surgery. The head and neck surgeon often finds that the tumor-free margin reported from histopathologic measurement is significantly smaller than the margin measured in-situ. It was the purpose of this study to quantify the change in size of mucosal and muscle surgical margins following excision, formalin fixation, and slide preparation of tongue and labiobuccal tissue in a canine model. METHODS: Ten mongrel dogs under general anesthesia for a concurrent project were used in this study. Changes in mucosal and muscle dimensions around custom-made brass disks, one with a needle depth gauge, were measured immediately following excision after formalin fixation and after slide preparation. RESULTS: The mean shrinkage from initial resection to final microscopic assessment of the lingual surface mucosal margins was 30.7% (p < 0.0001). The deep tongue margin shrank 34.5% (p < 0.0001). The mean shrinkage of the labiobuccal mucosal margin was 47.3% (p < 0.0001). In all cases, the greatest proportion of shrinkage occurred immediately upon resection. CONCLUSIONS: From the in-situ measurement by the surgeon to final pathologic evaluation on the microscope slide, the measured dimensions of oral cavity mucosal and tongue muscle margins shrink significantly. To obtain 5 mm of pathologically clear margin an in-situ margin of resection of at least 8 to 10 mm needs to be taken. Studies reporting clinical correlation of recurrence and survival information with surgical margin status should include a detailed description of the technique used to determine the reported surgical margin status.

Animals↗
PubMed1997

Early genetic and functional events in the pathogenesis of oral cancer.

Oral squamous cell carcinoma (SCC) is a major world health problem, but the changes leading to the development of malignancy remain essentially unknown. Early changes are thought to include the loss of tumour suppressor genes on chromosomes 3p, 9p, and 17p. Although what genes are involved on chromosome 3 remains speculative, p16 (9p21) and p53 (17p13) are inactivated in a high proportion of oral dysplastic lesions and carcinomas. SCC-derived cell lines are immortal, have decreased growth requirements in vitro, and show a variable capacity to form tumours in athymic mice. Normal oral keratinocytes and cells from potentially malignant lesions invariably senesce at early culture passage, have strict growth requirements in vitro, and are nontumorigenic in vivo. By contrast to normal oral keratinocytes, cells from potentially malignant lesions are defective in their capacity to terminally differentiate in suspension culture. Loss of cellular senescence and gain of the immortal phenotype is associated with inactivation of p16 and p53.

Animals↗
PubMed2001

Histological grading of oral epithelial dysplasia: revisited.

Treatment of oral precancer is largely based on histological grading of epithelial dysplasia, despite the fact that this estimation is subjective and therefore carries a low reproducibility. The grade of epithelial dysplasia may not be proportional to the risk of malignant potential and clinical characteristics may complement therapeutic decisions. Molecular genetic changes found in oral epithelial dysplasia remain unclear and at present lack clinical significance. Genomic and proliferation markers are likely to be associated with histopathological parameters, but their relationship with the grading of dysplasia remains uncertain. They are potential biomarker candidates but their utility in prognosis of oral precancer deserves further study.

Biomarkers↗