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Aim: The purpose of this study was to determine theDNA yield and quality from different non-invasivesampling methods and to identify the method whichgave the highest DNA yield. Method: Thirty-eightvolunteers had been recruited in this study whereblood, buccal cells and saliva were collected usingvarious collection techniques. Buccal cells werecollected by 1) cytobrush and 2) saline mouth rinsingor “swish”. Meanwhile saliva was collected by passivedrooling method. Upon processing the white bloodcell (WBC), buccal cells and saliva samples, DNAextraction was performed according to themanufacturer’s protocol. Quantification and quality(DNA ratio at A260/A280) of the extracted DNA weredetermined using NanoDropND-1000®. T-test wasperformed to compare means between DNA obtainedfrom various collection methods. Results: DNA yieldsfrom buccal cells collected with cytobrush, “swish”,saliva and WBC (mean ± SD) were (8.2 ± 5.9)ng/μl,(28.2 ± 14.9)ng/μl, (5.9 ± 9.5)ng/μl and (105.3 ±75.0)ng/μl respectively. Meanwhile the mean DNAratio at A260/A280 for cytobrush, “swish”, saliva andWBC were 2.3, 2.0, 1.7 and 1.8 respectively. Post hoctest with Bonferroni correction suggested that DNAyield from “swish” technique exhibited the least meandifferent as compared to the DNA extracted from WBC(p<0.05). There was no significant difference in themean quality of the DNA extracted from WBC, salivaand buccal cells collected in these non-invasivemethods (p=0.323). Conclusion: The “swish”technique of obtaining buccal cells yielded thehighest amount of DNA and was of the quality of DNAextracted from blood sample.Key words: buccal cells; non-invasive methods;cytobrush; “swish”; saliva; DNA yield; DNA quality
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Background: MDM2 and p53 are involved in a negative feedback loop where p53 regulates MDM2 at the transcriptional level. MDM2, in turn, downregulates p53. This co-ordinated interaction between these proteins is set to play an important role in the regulation of cell cycle progression following DNA damage to cells. The over-expression of both p53 and MDM2 has been reported in various cancers. However there are only few studies discussing the co-expression of MDM2 with p53 in oral squamous cell carcinoma Aim: The purpose of this study was to determine the correlation of co-expression of p53, MDM2, and Ki-67 proteins with clinico-pathological factors in oral squamous cell carcinoma (OSCC) and to conduct a systematic review of the co-expression of p53/MDM2. Method: This is a retrospective descriptive study and a systematic review. Formalin-fixed paraff inembedded tissues from 45 OSCC cases were stained by immunohistochemistry (IHC) for p53, MDM2, and Ki-67 proteins. Results: Immuno-reactivity for p53, MDM2, and Ki-67 was seen in 75.6%, 97.8%, and 62.2% cases of OSCC respectively. The co-expression of p53 and MDM2 (p53/MDM2) was detected in 97.1%, however there was no signif icant correlation between p53 and MDM2 expression. Notably, p53/MDM2 coexpression was significantly associated with tumour differentiation (p-value = 0.045). The Ki-67LI was not signif icantly associated with neither MDM2 nor p53/MDM2 co-expression (p-value = 0.268, 0.916 respectively). Conclusion: The expression of MDM2 was not signif icantly associated with p53 expression suggesting that MDM2 expression is mediated by p53-independent pathways or mutated p53 could not induce the expression of MDM2 in this set of OSCCs. The only clinico-pathological parameter that correlates significantly with co-expression of p53/MDM2 is tumour differentiation where it is suggestive that the co-expression of these 2 proteins is indicative of aggressive tumour behavior.
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Langerhans Cell Histiocytosis (LCH) refers to a group of lesions presenting with a spectrum of clinical. features but sharing similar histology. These lesions are rare and treatment has been quite variable with current treatment protocol recommended being dependent on whether it is a unifocal or multi focal bone disease or a multi focal multisystem disease. However, the clinical presentations of LCH are variable and the decision to place into the appropriate clinical types may sometimes be masked by the non-discovery of all the lesions. In the oral maxillofacial area, the clinical features of these lesions may further pose a problem by nondescript manifestations as dental/periodontal/oral mucosal disorders. These oral findings may sometimes lead to inappropriate choice of treatment and delay in the diagnosis of all the lesions involved. This paper describes one such case where LCH manifest itself as a periodontal disease thus leading to delay in identifying all the sites involved and consequently a delay in id~ntifying the appropriate clinical type.