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Fulltext Aberrant expression of the S1P regulating enzymes, SPHK1 and SGPL1, contributes to a migratory phenotype in OSCC mediated through S1PR2

Patmanathan SN, Johnson SP, Lai SL, Panja Bernam S, Lopes V, Wei W, et al.

Sci Rep, 2016 05 10;6:25650.
PMID: 27160553 DOI: 10.1038/srep25650

Oral squamous cell carcinoma (OSCC) is a lethal disease with a 5-year mortality rate of around 50%. Molecular targeted therapies are not in routine use and novel therapeutic targets are required. Our previous microarray data indicated sphingosine 1-phosphate (S1P) metabolism and signalling was deregulated in OSCC. In this study, we have investigated the contribution of S1P signalling to the pathogenesis of OSCC. We show that the expression of the two major enzymes that regulate S1P levels were altered in OSCC: SPHK1 was significantly upregulated in OSCC tissues compared to normal oral mucosa and low levels of SGPL1 mRNA correlated with a worse overall survival. In in vitro studies, S1P enhanced the migration/invasion of OSCC cells and attenuated cisplatin-induced death. We also demonstrate that S1P receptor expression is deregulated in primary OSCCs and that S1PR2 is over-expressed in a subset of tumours, which in part mediates S1P-induced migration of OSCC cells. Lastly, we demonstrate that FTY720 induced significantly more apoptosis in OSCC cells compared to non-malignant cells and that FTY720 acted synergistically with cisplatin to induce cell death. Taken together, our data show that S1P signalling promotes tumour aggressiveness in OSCC and identify S1P signalling as a potential therapeutic target.

Matched MeSH terms: Mouth Neoplasms
Goniothalamin induces cell cycle arrest and apoptosis in H400 human oral squamous cell carcinoma: A caspase-dependent mitochondrial-mediated pathway with downregulation of NF-κβ

Li LK, Rola AS, Kaid FA, Ali AM, Alabsi AM

Arch Oral Biol, 2016 Apr;64:28-38.
PMID: 26752226 DOI: 10.1016/j.archoralbio.2015.12.002

Goniothalamin is a natural occurring styryl-lactone compound isolated from Goniothalamus macrophyllus. It had been demonstrated to process promising anticancer activity on various cancer cell lines. However, little study has been carried out on oral cancer. The aim of this study was to determine the cytotoxic effects of goniothalamin against H400 oral cancer cells and its underlying molecular pathways. Results from MTT assay demonstrated that goniothalamin exhibited selective cytotoxicity as well as inhibited cells growth of H400 in dose and time-dependent manner. This was achieved primarily via apoptosis where apoptotic bodies and membrane blebbing were observed using AO/PI and DAPI/Annexin V-FITC fluorescence double staining. In order to understand the apoptosis mechanisms induced by goniothalamin, apoptosis assessment based on mitochondrial membrane potential assay and cytochrome c enzyme-linked immunosorbent assay were carried out. Results demonstrated that the depolarization of mitochondrial transmembrane potential facilitated the release of mitochondrial cytochrome c into cytosol. Caspases assays revealed the activation of initiator caspase-9 and executioner caspase-3/7 in dose-dependent manners. This form of apoptosis was closely associated with the regulation on Bcl-2 family proteins, cell cycle arrest at S phase and inhibition of NF-κβ translocation from cytoplasm to nucleus. Conclusion, goniothalamin has the potential to act as an anticancer agent against human oral squamous cell carcinoma (H400 cells).

Matched MeSH terms: Mouth Neoplasms
Oral mucosal lesions associated with betel quid, areca nut and tobacco chewing habits: consensus from a workshop held in Kuala Lumpur, Malaysia, November 25-27, 1996

Zain RB, Ikeda N, Gupta PC, Warnakulasuriya S, van Wyk CW, Shrestha P, et al.

J Oral Pathol Med, 1999 Jan;28(1):1-4.
PMID: 9890449

A variety of betel/areca nut/tobacco habits have been reviewed and categorized because of their possible causal association with oral cancer and various oral precancerous lesions and conditions, and on account of their widespread occurrence in different parts of the world. At a recent workshop in Kuala Lumpur it was recommended that "quid" be defined as "a substance, or mixture of substances, placed in the mouth or chewed and remaining in contact with the mucosa, usually containing one or both of the two basic ingredients, tobacco and/or areca nut, in raw or any manufactured or processed form." Clear delineations on contents of the quid (areca nut quid, tobacco quid, and tobacco and areca nut quid) are recommended as absolute criteria with finer subdivisions to be added if necessary. The betel quid refers to any quid wrapped in betel leaf and is therefore a specific variety of quid. The workshop proposed that quid-related lesions should be categorized conceptually into two categories: first, those that are diffusely outlined and second, those localized at the site where a quid is regularly placed. Additional or expanded criteria and guidelines were proposed to define, describe or identify lesions such as chewer's mucosa, areca nut chewer's lesion, oral submucous fibrosis and other quid-related lesions. A new clinical entity, betel-quid lichenoid lesion, was also proposed to describe an oral lichen planus-like lesion associated with the betel quid habit.

Matched MeSH terms: Mouth Neoplasms/classification; Mouth Neoplasms/etiology; Mouth Neoplasms/pathology
HPV infection and the alterations of the pRB pathway in oral carcinogenesis

Lim KP, Hamid S, Lau SH, Teo SH, Cheong SC

Oncol Rep, 2007 Jun;17(6):1321-6.
PMID: 17487385 DOI: 10.3892/or.17.6.1321

Inactivation of the retinoblastoma (pRB) pathway is a common event in oral squamous cell carcinoma particularly through the aberrant expression of the components within this pathway. This study examines the alterations of molecules within the pRB pathway by looking at the presence of homozygous deletions in p16(INK4A) and the expression patterns of pRB, cyclin D1 and CDK4, as well as the presence of human papillomavirus (HPV) in our samples. In our study, 5/20 samples demonstrated deletions of p16(INK4A) exon 1alpha. pRB overexpression was found in 20/20 samples, the expression was mainly observed in all layers of the epithelia, particularly in the basal layer where cells are actively dividing and aberrant pRB expression was found in 12/20 samples. Cyclin D1 and CDK4 overexpression was detected in 6/20 and 2/20 samples respectively in comparison to hyperplasias where both proteins were either not expressed or expressed at minimal levels (<10%). Strikingly, HPV was found to be present in all of our samples, suggesting that HPV plays a significant role in driving oral carcinogenesis. Notably, 17/20 of our samples showed more than one alteration in the pRB pathway, however, we did not find any significant relationship between the presence of HPV, homozygous deletion of p16(INK4A) and overexpression of pRB, cyclin D1 and CDK4. Collectively, this data demonstrates that alterations in the pRB pathway are a common event and involve the aberration of more than one molecule within the pathway. Furthermore, the involvement of HPV in all our samples suggests that HPV infection may play an important role in oral carcinogenesis.

Matched MeSH terms: Mouth Neoplasms/etiology*; Mouth Neoplasms/metabolism; Mouth Neoplasms/virology
Establishment and characterization of Asian oral cancer cell lines as in vitro models to study a disease prevalent in Asia

Hamid S, Lim KP, Zain RB, Ismail SM, Lau SH, Mustafa WM, et al.

Int J Mol Med, 2007 Mar;19(3):453-60.
PMID: 17273794

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 papilloma-virus (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 p16INK4a 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.

Matched MeSH terms: Mouth Neoplasms/epidemiology*; Mouth Neoplasms/pathology*; Mouth Neoplasms/virology
Fulltext Deregulation of lysophosphatidic acid metabolism in oral cancer promotes cell migration via the up-regulation of COX-2

Abdul Rahman M, Tan ML, Johnson SP, Hollows RJ, Chai WL, Mansell JP, et al.

PeerJ, 2020;8:e10328.
PMID: 33240646 DOI: 10.7717/peerj.10328

Oral squamous cell carcinoma (OSCC) is the sixth most common cancer worldwide and accounts for 300,000 new cases yearly. The five-year survival rate is approximately 50% and the major challenges to improving patient prognosis include late presentation, treatment resistance, second primary tumours and the lack of targeted therapies. Therefore, there is a compelling need to develop novel therapeutic strategies. In this study, we have examined the effect of lysophosphatidic acid (LPA) on OSCC cell migration, invasion and response to radiation, and investigated the contribution of cyclooxygenase-2 (COX-2) in mediating the tumour promoting effects of LPA. Using the TCGA data set, we show that the expression of the lipid phosphate phosphatases (LPP), LPP1 and LPP3, was significantly down-regulated in OSCC tissues. There was no significant difference in the expression of the ENPP2 gene, which encodes for the enzyme autotaxin (ATX) that produces LPA, between OSCCs and control tissues but ENPP2 levels were elevated in a subgroup of OSCCs. To explore the phenotypic effects of LPA, we treated OSCC cell lines with LPA and showed that the lipid enhanced migration and invasion as well as suppressed the response of the cells to irradiation. We also show that LPA increased COX-2 mRNA and protein levels in OSCC cell lines and inhibition of COX-2 activity with the COX-2 inhibitor, NS398, attenuated LPA-induced OSCC cell migration. Collectively, our data show for the first time that COX-2 mediates some of the pro-tumorigenic effects of LPA in OSCC and identifies the ATX-LPP-LPA-COX-2 pathway as a potential therapeutic target for this disease.

Matched MeSH terms: Mouth Neoplasms
Fulltext Cisplatin-Resistance in Oral Squamous Cell Carcinoma: Regulation by Tumor Cell-Derived Extracellular Vesicles

Khoo XH, Paterson IC, Goh BH, Lee WL

Cancers (Basel), 2019 Aug 14;11(8).
PMID: 31416147 DOI: 10.3390/cancers11081166

Drug resistance remains a severe problem in most chemotherapy regimes. Recently, it has been suggested that cancer cell-derived extracellular vesicles (EVs) could mediate drug resistance. In this study, the role of EVs in mediating the response of oral squamous cell carcinoma (OSCC) cells to cisplatin was investigated. We isolated and characterized EVs from OSCC cell lines showing differential sensitivities to cisplatin. Increased EV production was observed in both de novo (H314) and adaptive (H103/cisD2) resistant lines compared to sensitive H103 cells. The protein profiles of these EVs were then analyzed. Differences in the proteome of EVs secreted by H103 and H103/cisD2 indicated that adaptation to cisplatin treatment caused significant changes in the secreted nanovesicles. Intriguingly, both resistant H103/cisD2 and H314 cells shared a highly similar EV protein profile including downregulation of the metal ion transporter, ATP1B3, in the EVs implicating altered drug delivery. ICP-MS analysis revealed that less cisplatin accumulated in the resistant cells, but higher levels were detected in their EVs. Therefore, we inhibited EV secretion from the cells using a proton pump inhibitor and observed an increased drug sensitivity in cisplatin-resistant H314 cells. This finding suggests that control of EV secretion could be a potential strategy to enhance the efficacy of cancer treatment.

Matched MeSH terms: Mouth Neoplasms
miRNA for the assessment of lymph node metastasis in patients with oral squamous cell carcinoma: Systematic review and metanalysis

Jadhav KB, Nagraj SK, Arora S

J Oral Pathol Med, 2020 Nov 21.
PMID: 33220092 DOI: 10.1111/jop.13134

BACKGROUND: miRNA is one of the advanced epigenetic molecular markers correlating with lymph node metastasis in patients with Oral squamous cell carcinoma (OSCC). Numerous published papers are showing correlation of miRNA with metastasis. There is a need to analyze and validate such correlation.
METHOD: English language literature in major databases from the last 20 years was searched using controlled vocabulary and keywords. Strict inclusion and exclusion criteria were followed for selection of studies. The quality assessment was done as per the QUADAS tool 2 by three independent reviewers. The metanalysis was performed by using random effect model. Standardized mean difference (SMD) was considered as the effect measure. Statistical software used was STATA version 13.1.
RESULTS: With all inclusion and exclusion criteria, eight studies could qualify for metanalysis. The pooled estimate is found to be 0.13 (-0.35, 0.62), P = .585, which is statistically not significant. This indicates that there is a no significant difference in the fold change between metastasis and no metastasis groups. P-value of chi-square statistic for heterogeneity is

Matched MeSH terms: Mouth Neoplasms
Effectiveness of "OralDETECT": a Repetitive Test-enhanced, Corrective Feedback Method Competency Assessment Tool for Early Detection of Oral Cancer

Zain RB, Pateel DGS, Ramanathan A, Kallarakkal TG, Wong GR, Yang YH, et al.

J Cancer Educ, 2020 Aug 21.
PMID: 32821988 DOI: 10.1007/s13187-020-01814-1

Early diagnosis of oral cancer results in less aggressive treatment and improves the quality of life and overall 5-year survival rate. Well-trained dental professionals can play a crucial role in the early detection of oral cancers. The present study aims to determine the effectiveness of the training program "OralDETECT", a spaced repetitive, test-enhanced learning tool with a corrective feedback mechanism for early detection of oral cancer. Thirty-two dentists and 259 dental students from three Malaysian dental schools were involved in this study. All participants were trained and calibrated to recognize oral potentially malignant disorders (OPMD) and oral cancer using "OralDETECT", which is comprised of a series of pre-test, lecture, post-tests and review sessions. The percentage of correct answers (scores) for each test given by the participants was calculated and analysed using a paired t test. It was found that the overall percentage of diagnostic accuracy for both dental professionals and student groups increased to above 80% from the pre-tests to the final post-tests. There was a significant improvement in overall scores between the pre-tests and all three post-tests for the dental professional groups and the student groups. The diagnostic accuracy for individual OPMD and lesions suspicious of oral cancer also increased to above 80% for both groups. The results of our study demonstrate that the "OralDETECT" is an efficient and effective competency tool which can be used to train dental professionals and students for the early detection of OPMD and oral cancer.

Matched MeSH terms: Mouth Neoplasms
Fulltext The 4717C > G polymorphism in periplakin modulates sensitivity to EGFR inhibitors

Lee HM, Kelly GM, Zainal NS, Yee PS, Fadlullah MZH, Lee BKB, et al.

Sci Rep, 2019 02 20;9(1):2357.
PMID: 30787334 DOI: 10.1038/s41598-019-38742-0

The use of EGFR inhibitors on oral squamous cell carcinoma (OSCC) as monotherapy yielded modest clinical outcomes and therefore would benefit from biomarkers that could predict which patient subsets are likely to respond. Here, we determined the efficacy of erlotinib in OSCC cell lines, and by comparing sensitive and resistant lines to identify potential biomarkers. We focused on the 4717C > G polymorphism in periplakin (PPL) where the CC genotype was associated with erlotinib resistance. To validate this, erlotinib-resistant cell lines harbouring CC genotype were engineered to overexpress the GG genotype and vice versa. Isogenic cell lines were then studied for their response to erlotinib treatment. We demonstrated that overexpression of the GG genotype in erlotinib-resistant lines sensitized them to erlotinib and inhibition of AKT phosphorylation. Similarly, the expression of the CC genotype conferred resistance to erlotinib with a concomitant increase in AKT phosphorylation. We also demonstrated that cell lines with the CC genotype generally are more resistant to other EGFR inhibitors than those with the GG genotype. Overall, we showed that a specific polymorphism in the PPL gene could confer resistance to erlotinib and other EGFR inhibitors and further work to evaluate these as biomarkers of response is warranted.

Matched MeSH terms: Mouth Neoplasms
Synergistic Growth Inhibition by Afatinib and Trametinib in Preclinical Oral Squamous Cell Carcinoma Models

Yee PS, Zainal NS, Gan CP, Lee BKB, Mun KS, Abraham MT, et al.

Target Oncol, 2019 04;14(2):223-235.
PMID: 30806895 DOI: 10.1007/s11523-019-00626-8

BACKGROUND: Given that aberrant activation of epidermal growth factor receptor family receptors (ErbB) is a common event in oral squamous cell carcinoma, and that high expression of these receptor proteins is often associated with poor prognosis, this rationalizes the approach of targeting ErbB signaling pathways to improve the survival of patients with oral squamous cell carcinoma. However, monotherapy with the ErbB blocker afatinib has shown limited survival benefits.
OBJECTIVES: This study was performed to identify mechanisms of afatinib resistance and to explore potential afatinib-based combination treatments with other targeted inhibitors in oral squamous cell carcinoma.
METHODS: We determined the anti-proliferative effects of afatinib on a panel of oral squamous cell carcinoma cell lines using a crystal violet-growth inhibition assay, click-iT 5-ethynyl-2'-deoxyuridine staining, and cell-cycle analysis. Biochemical assays were performed to study the underlying mechanism of drug treatment as a single agent or in combination with the MEK inhibitor trametinib. We further evaluated and compared the anti-tumor effects of single agent and combined treatment by using oral squamous cell carcinoma xenograft models.
RESULTS: In this study, we showed that afatinib inhibited oral squamous cell carcinoma cell proliferation via cell-cycle arrest at the G0/G1 phase, and inhibited tumor growth in xenograft mouse models. Interestingly, we demonstrated reactivation of the mitogen-activated protein kinase (ERK1/2) pathway in vitro, which possibly reduced the effects of ErbB inhibition. Concomitant treatment of oral squamous cell carcinoma cells with afatinib and trametinib synergized the anti-tumor effects in oral squamous cell carcinoma-bearing mouse models.
CONCLUSIONS: Our findings provide insight into the molecular mechanism of resistance to afatinib and support further clinical evaluation into the combination of afatinib and MEK inhibition in the treatment of oral squamous cell carcinoma.

Matched MeSH terms: Mouth Neoplasms/drug therapy*; Mouth Neoplasms/metabolism; Mouth Neoplasms/pathology
Cytotoxic constituent of Melicope latifolia (DC.) T. G. Hartley

Lim PC, Ali Z, Khan IA, Khan SI, Kassim NK, Awang K, et al.

Nat Prod Res, 2021 Feb 12.
PMID: 33576269 DOI: 10.1080/14786419.2021.1885031

An undescribed conjugated sesquiterpene, amelicarin (1), together with nine known compounds (2-10) were isolated for the first time from Melicope latifolia. Their structures were elucidated by extensive NMR spectroscopic and mass spectrometric methods. The conjugated sesquiterpene possesses a unique 6/6/9/4-ring fused tetracyclic skeleton. The proposed biosynthesis pathway of 1 consist of three reactions steps: (1) polyketide formation, (2) cyclisation and (3) addition to form the conjugated sesquiterpenoid as final metabolite. Out of the ten isolated metabolites, amelicarin (1) showed activity against 4 cancerous cell lines namely SK-MEL skin cancer, KB oral cancer, BT-549 breast cancer, and SK-OV-3 ovarian cancer with IC50 values between 15 and 25 µg/mL.

Matched MeSH terms: Mouth Neoplasms
Cancer-associated fibroblasts regulate keratinocyte cell-cell adhesion via TGF-β-dependent pathways in genotype-specific oral cancer

Cirillo N, Hassona Y, Celentano A, Lim KP, Manchella S, Parkinson EK, et al.

Carcinogenesis, 2017 01;38(1):76-85.
PMID: 27803052 DOI: 10.1093/carcin/bgw113

The interrelationship between malignant epithelium and the underlying stroma is of fundamental importance in tumour development and progression. In the present study, we used cancer-associated fibroblasts (CAFs) derived from genetically unstable oral squamous cell carcinomas (GU-OSCC), tumours that are characterized by the loss of genes such as TP53 and p16INK4A and with extensive loss of heterozygosity, together with CAFs from their more genetically stable (GS) counterparts that have wild-type TP53 and p16INK4A and minimal loss of heterozygosity (GS-OSCC). Using a systems biology approach to interpret the genome-wide transcriptional profile of the CAFs, we show that transforming growth factor-β (TGF-β) family members not only had biological relevance in silico but also distinguished GU-OSCC-derived CAFs from GS-OSCC CAFs and fibroblasts from normal oral mucosa. In view of the close association between TGF-β family members, we examined the expression of TGF-β1 and TGF-β2 in the different fibroblast subtypes and showed increased levels of active TGF-β1 and TGF-β2 in CAFs from GU-OSCC. CAFs from GU-OSCC, but not GS-OSCC or normal fibroblasts, induced epithelial-mesenchymal transition and down-regulated a broad spectrum of cell adhesion molecules resulting in epithelial dis-cohesion and invasion of target keratinocytes in vitro in a TGF-β-dependent manner. The results demonstrate that the TGF-β family of cytokines secreted by CAFs derived from genotype-specific oral cancer (GU-OSCC) promote, at least in part, the malignant phenotype by weakening intercellular epithelial adhesion.

Matched MeSH terms: Mouth Neoplasms/genetics; Mouth Neoplasms/metabolism; Mouth Neoplasms/pathology*
Fulltext The role of treating nicotine addiction prior to treatment of periodontal diseases

Nurul Asyikin Yahya, Amer Siddiq Amer Nordin

ASEAN Journal of Psychiatry, 2011;12(1):0-0.
MyJurnal

Introduction and Objective: Tobacco use is a significant risk factor for oral diseases. Periodontal disease has been known to be associated with tobacco use for over twenty years. Despite that, dentists and particularly periodontist does not include tobacco use cessation as part of their initial treatment in treating periodontal disease or placing implants in patients who use tobacco. The increase in prevalence and severity of periodontitis among smokers
cannot be explained by differences in the amount of plaque between smokers and nonsmokers. A possible explanation is that smoking may alter the quality of the flora. Dental professionals also have a crucial role to play in tobacco cessation counseling, particularly for patients with chronic periodontitis. More patients will be affected by periodontitis than will ever be affected by oral cancer. Methods and Results: Reviews of literatures were
done on a clearly formulated question on the need of smoking cessation intervention to increase positive outcome of treatment on periodontal disease. Conclusion: Various epidemiological studies strongly suggest that tobacco use cessation is beneficial to patients following periodontal treatments for a better outcome.

Matched MeSH terms: Mouth Neoplasms
Fulltext Absence of nucleotide alteration in region of exon 34 of NOTCH1 and NOTCH2 receptor genes analysed in oral cancer samples: a preliminary observation

Nor Nasyitah Ismail, Khairani Idah Mokhtar

Archives of Orofacial Sciences, 2010;5(1):17-23.
MyJurnal

Oral cancer is one of the common cancer cases identified in the developing countries. Genetic mutation and overexpression of certain genes and proteins have been associated in the development of this cancer. Notch signalling pathway is normally involved in controlling the development process of vertebrates and invertebrates; however, deregulation of this pathway was found to be responsible in the formation of certain cancers including oral cancers. Activation of this pathway requires binding of the ligands to its receptors. Four NOTCH receptors (NOTCH 1, 2, 3 and 4) have been identified in mammals. Disruptions within these molecules might interfere with the normal functions of Notch signalling pathway. Hence, this study was conducted to detect mutations of NOTCH1 and NOTCH2 receptor genes which might be occurring in the oral cancer cases obtained from the local population. DNA extracted from fresh-frozen tissue biopsy of the tongue and buccal mucosa from 10 confirmed cases of oral cancer were subjected for polymerase chain reaction (PCR) amplification using the specific sets of primers. The PCR products were sent for sequencing before final results were analysed.
Due to time and cost limitation, only two out of four NOTCH receptor genes; NOTCH1 and NOTCH2, were used in this analysis. The results revealed absence of nucleotide changes for both NOTCH receptor genes amplified from these oral cancer samples. More samples and further analysis looking into other regions in these genes are required to conclude the involvement of NOTCH receptor genes mutation in causing oral cancer.

Matched MeSH terms: Mouth Neoplasms
Fulltext Effects of tobacco use on oral health - an overview

Awan, K.H.

Ann Dent, 2011;18(1):18-23.
MyJurnal

Tobacco use is linked with many serious illnesses, such as cancer, cardiopulmonary diseases, as well as with many health problems. Every year, the use of tobacco products causes a heavy toll of deaths and severe human disease worldwide. One of the many health problems linked to tobacco use is its detrimental impact on oral health. Tobacco causes a whole series of oral health problems, ranging from life-threatening (precancerous changes leading to oral cancer) and serious (periodontal disease, teeth decay) to social (bad breath). Tobacco is consumed through the mouth in a variety of forms, varied from smoked tobacco to smokeless tobacco chewing on itself or combined with areca nut. All these forms of tobacco have damaging effects on the oral health. The most significant preventive measure to prevent the oral health problems caused by tobacco use is to stop using tobacco products. The risk of developing oral cancer drops rapidly when a smoker ceases tobacco use. After ten years of not using tobacco, an ex-smoker/user's risk of oral cancers is about the same as that for someone who has never smoked. To stop using tobacco products is not an easy task. Fortunately, there are a number of therapies available to assist in quitting of tobacco. It is important to remember that, while it will be difficult, ceasing to use tobacco has immediate health benefits, including increased life expectancy and reduced risk of tobacco related diseases and conditions.

Matched MeSH terms: Mouth Neoplasms
Fulltext Case series analysis of oral cancer and their risk factors

Khan, A.R., Anwar, N., Manan, A.H.B., Narayan, K.A.

Malaysian Dental Journal, 2008;29(1):46-50.
MyJurnal

Cancer causes approximately 12% of all deaths throughout the world and is the third leading cause of death in developing countries. In Malaysia, Indians have the highest incidence of mouth cancer compared to other races, and females are more affected compared to males.
Objective: The main objective of this study was to analyze the cases of oral cancer treated in the dental department of Penang hospital, Malaysia and to determine the risk factors associated with oral cancer.

Methodology: We reviewed the medical reports of all the patients with oral cancer treated in the dental department of Penang General Hospital from 1994 to 2004.

Results: There were 46 cases of oral cancer treated by the dental department of Penang General Hospital during this time period. 22 were males and 24 females. The mean age of the patients was 61.2 years old. Indians comprised the majority of the cases (n=23; 50%) followed by Malays (n=12; 26.1%) and Chinese (n=11; 23.9%). Of these cases, 54.3% (n=25) had used quid, 39.1% (n=18) smoked cigarettes and 32.6% (n=15) consumed alcohol. Indians made up 76% (n=19) of all quid users (p=

Matched MeSH terms: Mouth Neoplasms
Fulltext An immunohistochemical study of p53 in oral epithelium dysplasia and squamous cell carcinoma

Ma, M.S.

Malaysian Dental Journal, 2007;28(2):78-82.
MyJurnal

Squamous cell carcinoma (SCC) is the commonest cancer in the mouth. Multiple risk factors, such as smoking, alcohol consumption, irradiation, viruses infection and chronic irritation are thought to be responsible for the formation of oral squamous cell carcinoma. Although SCC can develop through a series of precancerous stages manifested as various degrees of epithelial dysplasia, this is not always the case. p53 is the commonest mutated gene in human cancers. Mis-sense mutation of the gene or complexing of the protein with viral or cellular proteins prolongs its half-life and leads to its detection by immunohistochemistry. This study was designed with the aim of demonstrating any possible relationship between p53 and oral squamous cell carcinoma by immunohistochemical staining techniques. A total of 66 specimens from the oral cavity (10 normal mucosa, 11 hyperkeratosis without dysplasia, 11 mild dysplasia, 11 moderate dysplasia, 10 severe dysplasia and 13 SCC) were examined for the presence of p53. The results show p53 was not expressed in normal mucosa, but was found with increasing frequency in increasingly severe dysplasia and SCC. In conclusion, this study shows p53 mutation is common in oral squamous cell carcinoma and probably occurs early in the multisteps of oral carcinogenesis.

Matched MeSH terms: Mouth Neoplasms
An overview of application of silver nanoparticles for biomaterials in dentistry

Bapat RA, Chaubal TV, Joshi CP, Bapat PR, Choudhury H, Pandey M, et al.

Mater Sci Eng C Mater Biol Appl, 2018 Oct 01;91:881-898.
PMID: 30033323 DOI: 10.1016/j.msec.2018.05.069

Oral cavity is a gateway to the entire body and protection of this gateway is a major goal in dentistry. Plaque biofilm is a major cause of majority of dental diseases and although various biomaterials have been applied for their cure, limitations pertaining to the material properties prevent achievement of desired outcomes. Nanoparticle applications have become useful tools for various dental applications in endodontics, periodontics, restorative dentistry, orthodontics and oral cancers. Off these, silver nanoparticles (AgNPs) have been used in medicine and dentistry due to its antimicrobial properties. AgNPs have been incorporated into biomaterials in order to prevent or reduce biofilm formation. Due to greater surface to volume ratio and small particle size, they possess excellent antimicrobial action without affecting the mechanical properties of the material. This unique property of AgNPs makes these materials as fillers of choice in different biomaterials whereby they play a vital role in improving the properties. This review aims to discuss the influence of addition of AgNPs to various biomaterials used in different dental applications.

Matched MeSH terms: Mouth Neoplasms
A hybrid prognostic model for oral cancer based on clinicopathologic and genomic markers

Chang SW, Merican AFMA, Rosnah Zain, Kareem SA

Sains Malaysiana, 2014;43:567-573.

There are very few prognostic studies that combine both clinicopathologic and genomic data. Most of the studies use only clinicopathologic factors without taking into consideration the tumour biology and molecular information, while some studies use genomic markers or microarray information only without the clinicopathologic parameters. Thus, these studies may not be able to prognoses a patient effectively. Previous studies have shown that prognosis results are more accurate when using both clinicopathologic and genomic data. The objectives of this research were to apply hybrid artificial intelligent techniques in the prognosis of oral cancer based on the correlation of clinicopathologic and genomic markers and to prove that the prognosis is better with both markers. The proposed hybrid model consisting of two stages, where stage one with ReliefF-GA feature selection method to find an optimal feature of subset and stage two with ANFIS classification to classify either the patients alive or dead after certain years of diagnosis. The proposed prognostic model was experimented on two groups of oral cancer dataset collected locally here in Malaysia, Group 1 with clinicopathologic markers only and Group 2 with both clinicopathologic and genomic markers. The results proved that the proposed model with optimum features selected is more accurate with the use of both clinicopathologic and genomic markers and outperformed the other methods of artificial neural network, support vector machine and logistic regression. This prognostic model is feasible to aid the clinicians in the decision support stage and to identify the high risk markers to better predict the survival rate for each oral cancer patient.

Matched MeSH terms: Mouth Neoplasms

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