• Asian Pacific Journal of Cancer Prevention
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• 제13권12호
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• pp.6109-6113
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• 2012

Background: Oral cancer has become one of the most prevalent cancers worldwide and human Papillomavirus is one of the risk factors for developing oral cancer. For this study HPV18 was chosen as it is one of the high risk HPV types and may lead to carcinogenesis. However, prevalence of HPV18 infection in Oral Squamous Cell Carcinoma in Malaysia remains unclear. Objective: This study aimed to investigate the viral load of HPV18 DNA in OSCC and potentially malignant lesions using saliva samples. Materials and Methods: Genomic DNAs of thirty saliva samples of normal subjects and thirty saliva samples compromised of 16 samples from potentially malignant lesions and 14 of OSCC patients were amplified for HPV18 DNA using a nested polymerase chain reaction analysis. All PCR products were then analyzed using the Bioanalyzer to confirm presence of HPV18 DNA. Result: From thirty patients examined, only one of 30 (3.3%) cases was found to be positive for HPV18 in this study. Conclusion: The finding of this study revealed that there is a low viral detection of HPV18 in Malaysian OSCC by using saliva samples, suggesting that prevalence of HPV18 may not be important in this group of Malaysian OSCC.

• Asian Pacific Journal of Cancer Prevention
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• 제14권2호
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• pp.781-784
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• 2013

Aim: The purpose of this study was to determine whether susceptibility to oral tongue squamous cell carcinoma (OSCC) is related to polymorphisms in the u-PA gene. Methods: We examined the rs2227564 C/T and rs2227562 G/A single nucleotide polymorphisms (SNPs) in 196 OSCC patients and 201 age- and gender-matched controls via direct sequencing and PCR-RFLP methods. Results: Significant differences were found in allelic and genotypic distributions of the rs2227564 and rs2227562 loci when comparing cases and controls. In addition, logistic analyses indicated that the rs2227564 C/T genotype was related to a 1.52-fold increased risk of developing OSCC (adjusted OR=1.521, 95%CI: 1.144~2.022, P=0.004). Linkage disequilibrium analysis was conducted and no association between the two loci was found (D'=0.031, $r^2$=0.000). Conclusions: Our findings provide evidence that the rs2227564 C/T SNP in the u-PA gene is associated with the development of OSCC.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제28권2호
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• pp.155-160
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• 2002

Oral squamous cell carcinoma (OSCC), the most common head and neck cancer, shows poor prognosis as a result of frequent local invasion and lymph node metastasis that is mediated by multiple proteolytic enzymes and angiogenesis. In recent reports, angiogenesis is known to play an important role in tumor invasion and metastasis. The purpose of this study was to determine the role of angiogenesis in OSCCs, particularly with respect to the invasive and the metastatic potential. The microvessel density (CD31) in 34 human OSCC cases were investigated by immunohistochemistry, and reviewed with respect to the invasiveness and the presence of lymph node metastasis and following results were obtained. The blood vessel density $(28.8{\pm}7.9)$ in the strong invasive cases were significantly higher than those $(23.3{\pm}6.9)$ in the weak invasive cases. (p<0.05) In the 14 cases with lymph node metastasis, the average blood vessel density was $28.5{\pm}9.6$. On the other hand, in the 20 cases without lymph node metastasis, the blood vessel density was $25.2{\pm}6.4$. The blood vessel density was not statistically related to lymph node metastasis. (p>0.05) These results suggest that angiogenesis may be related to the local invasion of OSCC and further research will be needed to investigate the possibility that antiangiogenic agent can be used as an anticancer agent for OSCC.

• Biomolecules & Therapeutics
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• 제30권3호
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• pp.284-290
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• 2022

Oral squamous cell carcinoma (OSCC) is mostly diagnosed at an advanced stage, with local and/or distal metastasis. Thus, locoregional and/or local control of the primary tumor is crucial for a better prognosis in patients with OSCC. Platelets have long been considered major players in cancer metastasis. Traditional antiplatelet agents, such as aspirin, are thought to be potential chemotherapeutics, but they need to be used with caution because of the increased bleeding risk. Podoplanin (PDPN)-expressing cancer cells can activate platelets and promote OSCC metastasis. However, the reciprocal effect of platelets on PDPN expression in OSCC has not been investigated. In this study, we found that direct contact with platelets upregulated PDPN and integrin β1 at the protein level and promoted invasiveness of human OSCC Ca9.22 cells that express low levels of PDPN. In another human OSCC HSC3 cell line that express PDPN at an abundant level, silencing of the PDPN gene reduced cell invasiveness. Analysis of the public database further supported the co-expression of PDPN and integrin β1 and their increased expression in metastatic tissues compared to normal and tumor tissues of the oral cavity. Taken together, these data suggest that PDPN is a potential target to regulate platelet-tumor interaction and metastasis for OSCC treatment, which can overcome the limitations of traditional antiplatelet drugs.

• International Journal of Oral Biology
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• 제46권1호
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• pp.30-38
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• 2021

Cudraxanthone D (CD) is a natural xanthone compound derived from the root barks of Cudrania tricuspidata. However, the biological functions of CD in human metabolism have been rarely reported until now. Autophagy is the self-degradation process related to cancer cell metastasis. Here, we elucidated the effects of CD on human oral squamous cell carcinoma (OSCC) cells' metastatic ability. We confirmed that CD effectively decreased the proliferation and viability of SCC25 human OSCC cells in time- and dose-dependent manners. Also, the metastasis phenotype of the SCC25 cell (migration, invasion, and epithelial-mesenchymal transition [EMT]) was inhibited by CD. To further investigate the mechanism by which CD inhibited the metastatic capacity, we detected the relationship between EMT and autophagy in the SCC25 cells. The results revealed that CD inhibited the metastasis of the SCC25 cells by attenuating autophagy. Thus, our findings produced a potential novel agent for the treatment of human OSCC metastasis.

• Asian Pacific Journal of Cancer Prevention
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• 제17권11호
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• pp.5037-5040
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• 2016

Objectives: To determine the frequency of delayed diagnosis of oral squamous cell carcinoma in our setup; highlighting factors responsible for any delay and their possible relevance to demographic and diagnostic features. Methods: This cross sectional study of six months duration was conducted in the Oral and Maxillofacial Surgery Department of the Armed Forces Institute of Dentistry, Rawalpindi, Pakistan. A total of 246 patients, both male and female, having a biopsy proven definitive diagnosis of OSCC were included using a consecutive sampling technique. Delay in diagnosis was assessed from the stated period of time from when the patient first noticed symptoms of disease until a definitive diagnosis was made. We concluded delayed diagnosis if this was more than 40 days. Results: The ages of patients ranged from 27 to 60 years with a mean of $46.7{\pm}10.2$ years and a marked male predominance (3.7:1). Delayed diagnosis was observed in 91.5% of cases. However, statistically no significant differences were found with age, gender, marital, education status, household income and time of biopsy. Conclusion: Our primary finding of delayed diagnosis with no prior contact with any health care professional clearly reflects a need of taking urgent measures to avoid serious impacts on morbidity and mortality associated with OSCC.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제27권6호
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• pp.511-518
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• 2001

The effect of mycolactone, a recently reported apoptosis-inducing factor, was investigated in SCC15 oral squamous cell carcinoma(OSCC) cell line. Mycolactone rapidly induced cell death in OSCC cells in 2days, which was similar to that found in apoptotic cell such as detaching from culture plate and rounding-up of cells. Apoptotic cells were increased 4hrs after mycolactone treatment and more than half of cells showed apoptosis after 72hrs. Caspase 3 activation a biochemical evidence of apoptosis, was determined by Western blotting. Caspase 3 activation was started at 2hrs that lasted until 8hrs after mycolactone treatment. The expression of bcl-2 family genes was determined to explain the mechanism of apoptosis found in OSCC cells. The expressions of bad, bak, and bax (pro-apoptotic genes) and bcl-w and bcl-2 genes (anti-apoptotic genes) were not changed by mycolactone treatment. The expression of bcl-xi was decreased 8 hrs after mycolactone treatment. Mcl-1 expression was initially increased at 2 hrs which was decreased 8 hrs after mycolactone treatment. The down-regulation of these two anti-apoptotic genes might explain the mycolactone-induced apoptosis in OSCC cells. In this study, mycholactone was revealed to induce cell death in OSCC cells apoptosis and the apoptosis mechanism of OSCC cells was shown to be down-regulation of anti-apoptotic genes, bcl-xi and mcl-1. These results suggested the applicability of mycolactone for the development of an anti-cancer drug candidate by inducing apoptosis of OSCC cancer cell.

• Maxillofacial Plastic and Reconstructive Surgery
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• 제31권1호
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• pp.8-17
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• 2009

Purpose: We determined the therapeutic effect of an epidermal growth factor receptor (EGFR)-specific monoclonal antibody (mAb), cetuximab (Erbitux) on the growth of oral squamous cell carcinoma (OSCC) xenografted in athymic nude mice. Experimental Design: We induced subcutaneous tumors by inoculating human tumor cell suspension into the right flank of nude mice. Nude mice with subcutaneous tumors were randomized to receive cetuximab alone, paclitaxel alone, cetuximab plus paclitaxel, or a placebo (control). Antitumor mechanisms of cetuximab were determined by immunohistochemical and apoptosis assays. Results: Cetuximab, paclitaxel, and cetuximab/paclitaxel combined therapy resulted in 50%, 52%, 67% in vivo inhibition of tumor proliferation, respectively. Tumors of mice treated with cetuximab plus paclitaxel demonstrated decreased PCNA-positive tumor cells and increased apoptotic tumor cells, which slowed growth of the murine tumors. Conclusion: These data show that EGFR can be a molecular target for the treatment of OSCC. And combination therapy with cetuximab and paclitaxel warrants further clinical study.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제34권2호
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• pp.135-140
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• 2008

Loss of E-cadherin (E-cad) expression has been found in multiple cancers and is postulated to facilitate tumor cell dissociation and metastais. Promotor methylation may provides an alternative pathway for loss of gene function. This study evaluated the role of hypermethylation in the down-regulation of E-cad in oral squamous cell carcinoma (OSCC). We examined the E-cad expression by immunohistochemical staining and detected methylation status by methylation-specific polymerase chain reaction (MSP) in 20 OSCC tissues. Overally, 12 (60%) cases of hypermethylation of E-cad were detected and we found there were no correlation between methylation and age, histologic grade, lympn node metastasis, tumor size and clinical stage. However, Eleven (73.3%) of 15 samples which was negative for E-cad staining showed hypermethylation of E-cad promotor region. On the other hand, only one (20%) of 5 E-cad positive sample was observed with methylated status. The underexpression of E-cad was found to be related to promotor hypermethylation (p=0.035). In conclusion, we suggest that hypermethylation play a role in inactivation of E-cad gene and may be a appreciable biomarker for diagnosis and treatment of OSCC.

• Asian Pacific Journal of Cancer Prevention
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• 제16권13호
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• pp.5489-5492
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• 2015

Background: Gradual loss of cytokeratin 13 (CK13) may be linked with the severity of dysplastic changes and transformation to malignancy. In this study we assessed the differential expression of CK13 in normal, hyperplastic, dysplastic and cancerous oral mucosa. Materials and Methods: A total of 93 oral biopsies were collected during the 2011-2014 period. The biopsies were characterized as normal (19), hyperplastic (21), severely dysplastic/carcinoma in situ (16) and invasive oral squamous cell carcinoma (OSCC) (37) after morphological assessment. Formalin fixed paraffin embedded sections were stained with a monoclonal antibody against CK13 using the Envision technique. Immunohistochemically stained slides were then analyzed for CK13 expression. Results: CK13 was consistently and diffusely expressed in all normal and hyperplastic tissue biopsies from oral mucosa. Severely dysplastic/carcinoma in situ biopsies showed complete loss in 50% of cases, while in the remaining 50% expression was very focal and weak. OSCC cases showed complete or near complete loss of CK13 in all cases. Few cases showed weak expression in keratin pearls only. Conclusions: This study validates the utility of CK13 IHC as a useful immunohistochemical marker in routine diagnostic practice to make distinction between non-neoplastic from dysplastic and neoplastic (malignant) oral lesions.