Displaying publications 1 - 20 of 47 in total

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  1. Goot-Heah K, Kwai-Lin T, Froemming GR, Abraham MT, Nik Mohd Rosdy NM, Zain RB
    Asian Pac J Cancer Prev, 2012;13(12):6109-13.
    PMID: 23464414
    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.

    Matched MeSH terms: Mouth Neoplasms/genetics
  2. Salahshourifar I, Vincent-Chong VK, Kallarakkal TG, Zain RB
    Oral Oncol, 2014 May;50(5):404-12.
    PMID: 24613650 DOI: 10.1016/j.oraloncology.2014.02.005
    Oral cancer is a multifactorial disease in which both environmental and genetic factors contribute to the aetiopathogenesis. Oral cancer is the sixth most common cancer worldwide with a higher incidence among Melanesian and South Asian countries. More than 90% of oral cancers are oral squamous cell carcinoma (OSCC). The present study aimed to determine common genomic copy number alterations (CNAs) and their frequency by including 12 studies that have been conducted on OSCCs using array comparative genomic hybridization (aCGH). In addition, we reviewed the literature dealing with CNAs that drive oral precursor lesions to the invasive tumors. Results showed a sequential accumulation of genetic changes from oral precursor lesions to invasive tumors. With the disease progression, accumulation of genetic changes increases in terms of frequency, type and size of the abnormalities, even on different regions of the same chromosome. Gains in 3q (36.5%), 5p (23%), 7p (21%), 8q (47%), 11q (45%), 20q (31%) and losses in 3p (37%), 8p (18%), 9p (10%) and 18q (11%) were the most common observations among those studies. However, losses are less frequent than gains but it appears that they might be the primary clonal events in causing oral cancer.
    Matched MeSH terms: Mouth Neoplasms/genetics*
  3. Chang SW, Abdul-Kareem S, Merican AF, Zain RB
    BMC Bioinformatics, 2013;14:170.
    PMID: 23725313 DOI: 10.1186/1471-2105-14-170
    Machine learning techniques are becoming useful as an alternative approach to conventional medical diagnosis or prognosis as they are good for handling noisy and incomplete data, and significant results can be attained despite a small sample size. Traditionally, clinicians make prognostic decisions based on clinicopathologic markers. However, it is not easy for the most skilful clinician to come out with an accurate prognosis by using these markers alone. Thus, there is a need to use genomic markers to improve the accuracy of prognosis. The main aim of this research is to apply a hybrid of feature selection and machine learning methods in oral cancer prognosis based on the parameters of the correlation of clinicopathologic and genomic markers.
    Matched MeSH terms: Mouth Neoplasms/genetics
  4. Siow MY, Ng LP, Vincent-Chong VK, Jamaludin M, Abraham MT, Abdul Rahman ZA, et al.
    Oral Dis, 2014 May;20(4):345-51.
    PMID: 23651447 DOI: 10.1111/odi.12118
    To identify differentially expressed miRNA between oral squamous cell carcinoma (OSCC) and non-cancer (NC) and to associate these with clinico-pathological parameters.
    Matched MeSH terms: Mouth Neoplasms/genetics*
  5. Vincent-Chong VK, Salahshourifar I, Razali R, Anwar A, Zain RB
    Head Neck, 2016 04;38 Suppl 1:E783-97.
    PMID: 25914319 DOI: 10.1002/hed.24102
    BACKGROUND: This purpose of this meta-analysis study was to identify the most frequent and potentially significant copy number alteration (CNA) in oral carcinogenesis.

    METHODS: Seven oral squamous cell carcinoma (OSCC)-related publications, corresponding to 312 samples, were identified for this meta-analysis. The data were analyzed in a 4-step process that included the genome assembly coordination of multiple platforms, assignment of chromosomal position anchors, calling gains and losses, and functional annotation analysis.

    RESULTS: Gains were more frequent than losses in the entire dataset. High-frequency gains were identified in chromosomes 5p, 14q, 11q, 7p, 17q, 20q, 8q, and 3q, whereas high-frequency losses were identified in chromosomes 3p, 8p, 6p, 18q, and 4q. Ingenuity pathway analysis showed that the top biological function was associated with immortalization of the epithelial cells (p = 1.93E-04).

    CONCLUSION: This study has identified multiple recurrent CNAs that are involved in various biological annotations associated with oral carcinogenesis. © 2015 Wiley Periodicals, Inc. Head Neck 38: E783-E797, 2016.

    Matched MeSH terms: Mouth Neoplasms/genetics*
  6. Salahshourifar I, Vincent-Chong VK, Chang HY, Ser HL, Ramanathan A, Kallarakkal TG, et al.
    Clin Oral Investig, 2015 Dec;19(9):2273-83.
    PMID: 25846277 DOI: 10.1007/s00784-015-1467-7
    OBJECTIVES: This study includes the direct sequencing of cornulin (CRNN) gene to elucidate the possible mechanism of CRNN downregulation and explore the genetic imbalances at 1q21.3 across oral squamous cell carcinoma (OSCC) samples.

    MATERIALS AND METHODS: In mutation screening of CRNN gene, gDNA from OSCC tissues were extracted, amplified, and followed by direct sequencing. OSCC samples were also subjected to fragment analysis on CRNN gene to investigate its microsatellite instability (MSI) and loss of heterozygosity (LOH). Immunohistochemistry was performed to validate CRNN downregulation in OSCC samples.

    RESULTS: No pathogenic mutation was found in CRNN gene, while high frequency of allelic imbalances was found at 1q21.3 region. MSI was found more frequent (25.3 %) than LOH (9.3 %). Approximately 22.6 % of cases had high MSI which reflects higher probability of inactivation of DNA mismatch repair genes. MSI showed significant association with no betel quid chewing (p = 0.003) and tongue subsite (p = 0.026). LOH was associated with ethnicity (p = 0.008) and advanced staging (p = 0.039). The LOH at 1q21.3 was identified to be as an independent prognostic marker in OSCC (HRR = 7.15 (95 % CI, 1.41-36.25), p = 0.018). Downregulation of CRNN was found among MSI-positive OSCCs and was associated with poor prognosis (p = 0.044).

    CONCLUSION: This study showed a significant correlation between LOH/MSI at 1q21.3 with clinical outcomes and that downregulation of CRNN gene could be considered as a prognostic marker of OSCC.

    CLINICAL RELEVANCE: Insights of the downregulation mode of CRNN gene lays the basis of drug development on this gene as well as revealing its prognostic value.

    Matched MeSH terms: Mouth Neoplasms/genetics*
  7. Chai AWY, Yee PS, Price S, Yee SM, Lee HM, Tiong VK, et al.
    Elife, 2020 09 29;9.
    PMID: 32990596 DOI: 10.7554/eLife.57761
    New therapeutic targets for oral squamous cell carcinoma (OSCC) are urgently needed. We conducted genome-wide CRISPR-Cas9 screens in 21 OSCC cell lines, primarily derived from Asians, to identify genetic vulnerabilities that can be explored as therapeutic targets. We identify known and novel fitness genes and demonstrate that many previously identified OSCC-related cancer genes are non-essential and could have limited therapeutic value, while other fitness genes warrant further investigation for their potential as therapeutic targets. We validate a distinctive dependency on YAP1 and WWTR1 of the Hippo pathway, where the lost-of-fitness effect of one paralog can be compensated only in a subset of lines. We also discover that OSCCs with WWTR1 dependency signature are significantly associated with biomarkers of favorable response toward immunotherapy. In summary, we have delineated the genetic vulnerabilities of OSCC, enabling the prioritization of therapeutic targets for further exploration, including the targeting of YAP1 and WWTR1.
    Matched MeSH terms: Mouth Neoplasms/genetics*
  8. Jayaraj R, Kumaraswamy C, Raymond G, Ravishankar Ram M, Govind SK, Chandramoorthy HC, et al.
    Oral Oncol, 2020 10;109:104634.
    PMID: 32171663 DOI: 10.1016/j.oraloncology.2020.104634
    Matched MeSH terms: Mouth Neoplasms/genetics*
  9. Vincent-Chong VK, Salahshourifar I, Woo KM, Anwar A, Razali R, Gudimella R, et al.
    PLoS One, 2017;12(4):e0174865.
    PMID: 28384287 DOI: 10.1371/journal.pone.0174865
    BACKGROUND: Cancers of the oral cavity are primarily oral squamous cell carcinomas (OSCCs). Many of the OSCCs present at late stages with an exceptionally poor prognosis. A probable limitation in management of patients with OSCC lies in the insufficient knowledge pertaining to the linkage between copy number alterations in OSCC and oral tumourigenesis thereby resulting in an inability to deliver targeted therapy.

    OBJECTIVES: The current study aimed to identify copy number alterations (CNAs) in OSCC using array comparative genomic hybridization (array CGH) and to correlate the CNAs with clinico-pathologic parameters and clinical outcomes.

    MATERIALS AND METHODS: Using array CGH, genome-wide profiling was performed on 75 OSCCs. Selected genes that were harboured in the frequently amplified and deleted regions were validated using quantitative polymerase chain reaction (qPCR). Thereafter, pathway and network functional analysis were carried out using Ingenuity Pathway Analysis (IPA) software.

    RESULTS: Multiple chromosomal regions including 3q, 5p, 7p, 8q, 9p, 10p, 11q were frequently amplified, while 3p and 8p chromosomal regions were frequently deleted. These findings were in confirmation with our previous study using ultra-dense array CGH. In addition, amplification of 8q, 11q, 7p and 9p and deletion of 8p chromosomal regions showed a significant correlation with clinico-pathologic parameters such as the size of the tumour, metastatic lymph nodes and pathological staging. Co-amplification of 7p, 8q, 9p and 11q regions that harbored amplified genes namely CCND1, EGFR, TPM2 and LRP12 respectively, when combined, continues to be an independent prognostic factor in OSCC.

    CONCLUSION: Amplification of 3q, 5p, 7p, 8q, 9p, 10p, 11q and deletion of 3p and 8p chromosomal regions were recurrent among OSCC patients. Co-alteration of 7p, 8q, 9p and 11q was found to be associated with clinico-pathologic parameters and poor survival. These regions contain genes that play critical roles in tumourigenesis pathways.

    Matched MeSH terms: Mouth Neoplasms/genetics*
  10. Pentenero M, Bowers L, Jayasinghe R, Cheong SC, Farah CS, Kerr AR, et al.
    Oral Dis, 2019 Jun;25 Suppl 1:79-87.
    PMID: 31140691 DOI: 10.1111/odi.13051
    Long non-coding RNAs (lncRNA) modulate gene expression at the epigenetic, transcriptional and post-transcriptional levels and are involved in tumorigenesis. They can form complex secondary and tertiary structures and have been shown to act as precursors, enhancers, reservoirs and decoys in the complex endogenous RNA network. They were first reported in relation to oral squamous cell carcinoma (OSCC) in 2013. Here, we summarise the functional roles and pathways of the most commonly studied lncRNAs in OSCC. Existing research demonstrates the involvement of lncRNA within pivotal pathways leading to the development and spread of OSCC, including interactions with key cancer-associated microRNAs such as miR-21. The number of studies on lncRNA and OSCC remains limited in this new field. As evidence grows, the tissue-specific expression patterns of lncRNAs should further advance our understanding of the altered regulatory networks in OSCC and possibly reveal new biomarkers and therapeutic targets.
    Matched MeSH terms: Mouth Neoplasms/genetics*
  11. Prime SS, Cirillo N, Cheong SC, Prime MS, Parkinson EK
    Cancer Lett, 2021 10 10;518:102-114.
    PMID: 34139286 DOI: 10.1016/j.canlet.2021.05.025
    This study reviews the molecular landscape of oral potentially malignant disorders (OPMD). We examine the impact of tumour heterogeneity, the spectrum of driver mutations (TP53, CDKN2A, TERT, NOTCH1, AJUBA, PIK3CA, CASP8) and gene transcription on tumour progression. We comment on how some of these mutations impact cellular senescence, field cancerization and cancer stem cells. We propose that OPMD can be monitored more closely and more dynamically through the use of liquid biopsies using an appropriate biomarker of transformation. We describe new gene interactions through the use of a systems biology approach and we highlight some of the first studies to identify functional genes using CRISPR-Cas9 technology. We believe that this information has translational implications for the use of re-purposed existing drugs and/or new drug development. Further, we argue that the use of digital technology encompassing clinical and laboratory-based data will create relevant datasets for machine learning/artificial intelligence. We believe that therapeutic intervention at an early molecular premalignant stage should be an important preventative strategy to inhibit the development of oral squamous cell carcinoma and that this approach is applicable to other aerodigestive tract cancers.
    Matched MeSH terms: Mouth Neoplasms/genetics*
  12. Pentenero M, Bowers LM, Jayasinghe R, Yap T, Cheong SC, Kerr AR, et al.
    Oral Dis, 2019 Jun;25 Suppl 1(Suppl 1):88-101.
    PMID: 31140697 DOI: 10.1111/odi.13076
    BACKGROUND: Long non-coding RNAs (lncRNAs) have important roles in regulating gene expression pertaining to cell proliferation, survival, migration and genomic stability. Dysregulated expression of lncRNAs is implicated in cancer initiation, progression and metastasis.

    OBJECTIVES: To explore, map and summarize the extent of evidence from clinical studies investigating the differential expression of lncRNAs in oral/tongue squamous cell carcinoma.

    METHODS: PubMed, Scopus and Web of Science were used as search engines. Clinical, full-length, English language studies were included. PRISMA-ScR protocol was used to evaluate and present results. The present scoping review summarizes relationships of the differential expression of lncRNAs with the presence of tumour and with clinicopathological features including survival.

    RESULTS: Almost half of the investigated transcripts have been explored in more than one study, yet not always with consistent results. The collected data were also compared to the limited studies investigating oral epithelial dysplasia. Data are not easily comparable, first because of different methods used to define what differential expression is, and second because only a limited number of studies performed multivariate analyses to identify clinicopathological features associated with the differentially expressed lncRNAs.

    CONCLUSIONS: Standard methods and more appropriate data analyses are needed in order to achieve reliable results from future studies.

    Matched MeSH terms: Mouth Neoplasms/genetics*
  13. Khor GH, Froemming GR, Zain RB, Abraham MT, Thong KL
    Asian Pac J Cancer Prev, 2014;15(20):8957-61.
    PMID: 25374236
    BACKGROUND: Promoter hypermethylation leads to altered gene functions and may result in malignant cellular transformation. Thus, identification of biomarkers for hypermethylated genes could be useful for diagnosis, prognosis, and therapeutic treatment of oral squamous cell carcinoma (OSCC).

    OBJECTIVES: To screen hypermethylated genes with a microarray approach and to validate selected hypermethylated genes with the methylation-specific polymerase chain reaction (MSPCR).

    MATERIALS AND METHODS: Genome-wide analysis of normal oral mucosa and OSCC tissues was conducted using the Illumina methylation microarray. The specified differential genes were selected and hypermethylation status was further verified with an independent cohort sample of OSCC samples. Candidate genes were screened using microarray assay and run by MSPCR analysis.

    RESULTS: TP73, PIK3R5, and CELSR3 demonstrated high percentages of differential hypermethylation status.

    CONCLUSIONS: Our microarray screening and MSPCR approaches revealed that the signature candidates of differentially hypermethylated genes may possibly become potential biomarkers which would be useful for diagnostic, prognostic and therapeutic targets of OSCC in the near future.

    Matched MeSH terms: Mouth Neoplasms/genetics*
  14. Saeed AA, Sims AH, Prime SS, Paterson I, Murray PG, Lopes VR
    Oral Oncol, 2015 Mar;51(3):237-46.
    PMID: 25560800 DOI: 10.1016/j.oraloncology.2014.12.004
    It is well recognized that oral squamous cell carcinoma (OSCC) cases from Asia that are associated with betel quid chewing are phenotypically distinct to those from Western countries that are predominantly caused by smoking/drinking, but the molecular basis of these differences are largely unknown. The aim of this study is to examine gene expression, related carcinogenic pathways and molecular processes that might be responsible for the phenotypic heterogeneity of OSCC between UK and Sri Lankan population groups.
    Matched MeSH terms: Mouth Neoplasms/genetics*
  15. Sam KK, Gan CP, Yee PS, Chong CE, Lim KP, Karen-Ng LP, et al.
    Oral Oncol, 2012 Nov;48(11):1128-35.
    PMID: 22705356 DOI: 10.1016/j.oraloncology.2012.05.016
    The presence of a variety of MDM2 splice variants has been reported in a range of different tumor types and is associated with poor patient prognosis. Furthermore, several MDM2 variants have been shown to have oncogenic properties. Despite this, MDM2 splice variants have not been comprehensively characterized in oral squamous cell carcinoma (OSCC).
    Matched MeSH terms: Mouth Neoplasms/genetics*
  16. Ashazila MJ, Kannan TP, Venkatesh RN, Hoh BP
    Oral Oncol, 2011 May;47(5):358-64.
    PMID: 21450513 DOI: 10.1016/j.oraloncology.2011.03.005
    Loss of heterozygosity (LOH) and microsatellite instability (MSI) have been documented as important events in oral squamous cell carcinoma (OSCC). Five microsatellite markers D3S192, D3S966, D3S647, D3S1228 and D3S659 were selected on chromosome 3p because of high frequency of alterations reported in head and neck squamous cell carcinoma and the involvement of von Hippel Lindau (VHL) at 3p25-26 and the fragile histidine triad (FHIT) at 3p14.2 genes proven in many tumour types. A total of 50 archival tissue samples of OSCC and corresponding normal samples were analyzed for LOH and MSI status. The overall LOH for the markers selected on 3p was 56 out of 189 informative cases (29.6%). The most frequent LOH was identified for the marker D3S966 which was 18/42 (42.8%) of informative cases suggesting the presence of putative tumour suppressor genes (TSGs) in this loci. In this study, high frequency of microsatellite instability was found in D3S966 which was 28.6% of informative cases; this reveals the possibility of mutations of MMR genes in this region. Frequent microsatellite alterations (MA) were observed in 3 markers D3S966 (71.4%), D3S1228 (56.7%) and D3S192 (41.0%). There was no significant association between LOH with gender, tumour stages and differentiation grades. However, there was a significant association between tumour stage and differentiation grades with MSI status in OSCC in Malaysian population with p values of 0.002 and 0.035, respectively. There was also a significant association between MA and differentiation grades (p=0.041).
    Matched MeSH terms: Mouth Neoplasms/genetics*
  17. Saleh A, Zain RB, Hussaini H, Ng F, Tanavde V, Hamid S, et al.
    Oral Oncol, 2010 May;46(5):379-86.
    PMID: 20371203 DOI: 10.1016/j.oraloncology.2010.02.022
    Despite the advances in cancer treatment, the 5-year survival rate for oral cancer has not changed significantly for the past 40 years and still remains among the worst of all anatomic sites. Gene expression microarrays have been used successfully in the identification of genetic alterations in cancer development, however, these have hitherto been limited by the need for specimens with good quality intact RNA. Here, we demonstrated the use of formalin-fixed paraffin-embedded tissues in microarray experiments to identify genes differentially expressed between cancerous and normal oral tissues. Forty-three tissue samples were macrodissected and gene expression analyses were conducted using the Illumina DASL assay. We report RNA yield of 2.4 and 0.8 microg/mm(3) from tumour and normal tissues, respectively and this correlated directly with the tissue volume used for RNA extraction. Using unsupervised hierarchical clustering, distinct gene expression profiles for tumour and normal samples could be generated, and differentially expressed genes could be identified. The majority of these genes were involved in regulation of apoptosis and cell cycle, metastasis and cell adhesion including BCL2A1, BIRC5, MMP1, MMP9 and ITGB4. Representative genes were further validated in independent samples suggesting that these genes may be directly associated with oral cancer development. The ability to conduct microarrays on formalin-fixed paraffin-embedded specimens represents a significant advancement that could open up avenues for finding genes that could be used as prognostication and predictive tools for cancer.
    Matched MeSH terms: Mouth Neoplasms/genetics*
  18. Amtha R, Ching CS, Zain R, Razak IA, Basuki B, Roeslan BO, et al.
    Asian Pac J Cancer Prev, 2009 Jan-Mar;10(1):21-6.
    PMID: 19469619
    PURPOSE: to investigate genetic polymorphisms in GSTM1, GSTT1 and CYP1A1 and the association with the risk of oral cancer in the Jakarta population.
    METHOD: A total of 81 cases and 162 controls matched for age and sex were selected from 5 hospitals in Jakarta. Sociodemographic data using questionnaires were obtained and peripheral blood samples were collected with informed consent for PCR-RFLP assay. Conditional logistic regression analysis was performed to obtain the association between the risk of oral cancer and GSTM1, GSTT1 and CYP1A1 polymorphisms.
    RESULTS: GSTM1 and GSTT1 null were slightly overrepresented among cases (60.5% and 45.7% respectively) compared to controls (55.6% and 41.4% respectively), but no statistically significant differences were observed. In contrast, the distribution of CYP1A1 polymorphism was higher among controls compared to cases (52.5 % versus 42.4 %). The odds ratio of null GSTM1 and GSTT1 genotypes was slightly higher compared to wild type genotypes (OR 1.19, 95% CI 0.70-2.02 and OR 1.19, 95% CI 0.72-2.05 respectively). Furthermore, the presence of CYP1A1 polymorphism did not increase the risk of oral cancer (OR 0.70, 95% 0.39-1.25).
    CONCLUSION: Genetic polymorphisms of GSTM1, GSTT1 and CYP1A1 may not be risk factors for oral cancer in the Jakarta population.
    Matched MeSH terms: Mouth Neoplasms/genetics*
  19. Hamid S, Yang YH, Peng KN, Ismail SM, Zain RB, Lim KP, et al.
    Oral Oncol, 2009 Jun;45(6):496-500.
    PMID: 18804411 DOI: 10.1016/j.oraloncology.2008.06.003
    The MDM2 SNP309 has been associated with increased expression of the protein which could suppress p53 function, and has been shown to modulate risk to cancer. We have previously shown that overexpression of MDM2 is a common event in oral cancers. In the present study, we determined the association between the MDM2 SNP309 polymorphism and oral cancer in 207 oral cancer patients and 116 normal subjects. We genotyped the MDM2 SNP309 by PCR-RFLP. Logistic regression was adapted to calculate odds ratios for MDM2 SNP309 polymorphism from univariate and multivariable adjusted models. Our results suggest that MDM2 SNP309 does not confer increased risk to oral cancer (OR=1.55, 95% CI=0.77-3.11). However, the GG/TG genotype was associated with later disease onset in women above 55 years of age. Collectively, our data suggests that MDM2 SNP309 may modulate the risk to oral cancer and is a modifier of the age at oral cancer onset in women above the age of 55 years.
    Matched MeSH terms: Mouth Neoplasms/genetics*
  20. Khor GH, Froemming GR, Zain RB, Abraham TM, Lin TK
    Asian Pac J Cancer Prev, 2016;17(1):219-23.
    PMID: 26838213
    BACKGROUND: Promoter hypermethylation is a frequent epigenetic mechanism for gene transcription repression in cancer and is one of the hallmarks of the disease. Cadherin EGF LAG seven-pass G-type receptor 3 (CELSR3) contributes to cell contact-mediated communication. Dysregulation of promoter methylation has been reported in various cancers.

    OBJECTIVES: The objectives of this study were to investigate the CELSR3 hypermethylation level in oral squamous cell carcinomas (OSCCs) using methylation-sensitive high-resolution melting analysis (MS-HRM) and to correlate CELSR3 methylation with patient demographic and clinicopathological parameters.

    MATERIALS AND METHODS: Frozen tissue samples of healthy subjects' normal mucosa and OSCCs were examined with regard to their methylation levels of the CELSR3 gene using MS-HRM.

    RESULTS: MS-HRM analysis revealed a high methylation level of CELSR3 in 86% of OSCC cases. Significant correlations were found between CELSR3 quantitative methylation levels with patient ethnicity (P=0.005), age (P=0.024) and pathological stages (P=0.004). A moderate positive correlation between CELSR3 and patient age was also evident (R=0.444, P=0.001).

    CONCLUSIONS: CELSR3 promoter hypermethylation may be an important mechanism involved in oral carcinogenesis. It may thus be used as a biomarker in OSCC prognostication.

    Matched MeSH terms: Mouth Neoplasms/genetics*
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