2015
DOI: 10.1016/j.oooo.2014.06.017
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MutSα and MutLα immunoexpression analysis in diagnostic grading of oral epithelial dysplasia and squamous cell carcinoma

Abstract: Conclusion:The results suggest a diagnostic role for MMR proteins in OED and OSCC.

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Cited by 23 publications
(24 citation statements)
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“…This initial observation was subsequently confirmed by Jessri et al (19) that revealed a progressive reduction of hMLH1, hMSH2, and hPMS2 from mild, moderate, and severe dysplasia to OSCC. In a following study, Jessri et al (25) further confirmed the lower expression of hMLH1, hMSH2, hPMS2, and hMSH6 in more dysplastic OL and even more in OSCC, also highlighting the diagnostic utility of hMSH6 in the identification of carcinoma in situ.…”
Section: Mmr Expression In Oral Squamous Cell Carcinomasupporting
confidence: 54%
See 1 more Smart Citation
“…This initial observation was subsequently confirmed by Jessri et al (19) that revealed a progressive reduction of hMLH1, hMSH2, and hPMS2 from mild, moderate, and severe dysplasia to OSCC. In a following study, Jessri et al (25) further confirmed the lower expression of hMLH1, hMSH2, hPMS2, and hMSH6 in more dysplastic OL and even more in OSCC, also highlighting the diagnostic utility of hMSH6 in the identification of carcinoma in situ.…”
Section: Mmr Expression In Oral Squamous Cell Carcinomasupporting
confidence: 54%
“…These results were confirmed by the same group that showed a lower expression of hMLH1 in more dysplastic OL, also revealing an inverse correlation with p53 and AgNOR expression (18). These authors suggested that hMLH1 alterations would represent an early molecular event in oral carcinogenesis, what was supported by Jessri et al (19) who confirmed a reduced expression of hMLH1, hPMS2, and hMSH2 in OL and in OSCC when compared to normal oral mucosa, also attributing a diagnostic role for these proteins.…”
Section: Mmr Expression In Oral and Lip Potentially Malignant Lesionsmentioning
confidence: 55%
“…The incidence of male and female HPV‐related oropharyngeal cancers in Australia has significantly increased annually across both genders in line with global trends . Alternative theories for this increase relate to the importance of individual genetic variation with data suggesting a role for common polymorphisms in DNA repair enzymes among others …”
Section: Introductionmentioning
confidence: 96%
“…24,25 Alternative theories for this increase relate to the importance of individual genetic variation with data suggesting a role for common polymorphisms in DNA repair enzymes among others. [26][27][28][29] To date, however, there are no data assessing patient awareness, knowledge of risk factors, actual risk factors, patient delay, professional delay, diagnostic delay and access to health practitioners for oral cancer in the Australian health system. A key aim is to identify whether asymptomatic diagnosis is possible by analysing if these patients presented to any health professionals in the preceding months to years before symptoms began, suggesting missed opportunities for early diagnosis of malignant lesions or OPMDs.…”
mentioning
confidence: 99%
“…Continues)All the reviewed works were unanimous in recognizing the veracity and complexity of the Genomic Repair System, also called Mismatch Repair System (MMR), confirming the participation of repair gene proteins (such as hMSH2 and hMSH6) in patients with oral cancer and even of lesions that are susceptible to malignization [8][9][10][11][12][13][14][15]. To test the participation of hMSH2 and hMSH6 repair genes, some authors used immunohistochemical analysis as the technique, which evidenced the presence of different levels of these proteins, in different oral lesions prone to malignancy and/or malignant oral lesions, with variable laboratory and clinical significance 12,14,15. Thus, Pimenta et al,9 through this evaluation, verified that there is, even if reduced, a small expression of the hMSH2 protein in oral lichen planus when compared with normal oral mucosal epithelial tissue; this reduction of expression may suggest a greater susceptibility of lichen planus to mutation and, therefore, to differentiate into oral squamous cell carcinoma.…”
mentioning
confidence: 99%