Clinical implications of p53 alterations in oral cancer progression: a review from India

p53 plays a central role in prevention of normal cell from the development of the malignant phenotype. Somatic alterations (mutations, loss of heterozygosity, deletions) in p53 are a hallmark of most human cancers and cause defects in normal p53 function. However, in the tumors harboring wild-type p53, there are alterations in the regulation of the p53. Thus, understanding why p53 is unable to perform its role as a tumor suppressor in these wild-type tumors is very crucial. Germ-line polymorphisms in p53 are also anticipated to cause measurable disturbance in p53 function. Over-expression as well as polymorphic variants of MDM2 might have effects on cancer development. In addition, degradation of p53 by E6 protein of high risk human papillomavirus is also suggested as one of the mechanisms which attenuate p53 responses in oral carcinogenesis. p53 has also been demonstrated to mediate cellular responses upon various DNA damaging cancer therapies, importantly, apoptosis. These responses have been implicated in an individual’s ability to respond to these cancer therapies. Thus, exploring mechanisms by which normal function of p53 is affected in the comprehensive way in oral cancer might aid in the identification of tumor characteristics, prognosis and thus in the development of a new approach to treat the oral cancer

CLINICAL IMPLICATIONS OF p53 ALTERATIONS IN ORAL CANCER PROGRESSION: A REVIEW FROM INDIA

p53 plays a central role in prevention of normal cell from the development of the malignant phenotype. Somatic alterations (mutations, loss of heterozygosity, deletions) in p53 are a hallmark of most human cancers and cause defects in normal p53 function. However, in the tumors harboring wild-type p53, there are alterations in the regulation of the p53. Thus, understanding why p53 is unable to perform its role as a tumor suppressor in these wild-type tumors is very crucial. Germ-line polymorphisms in p53 are also anticipated to cause measurable disturbance in p53 function. Over-expression as well as polymorphic variants of MDM2 might have effects on cancer development. In addition, degradation of p53 by E6 protein of high risk human papillomavirus is also suggested as one of the mechanisms which attenuate p53 responses in oral carcinogenesis. p53 has also been demonstrated to mediate cellular responses upon various DNA damaging cancer therapies, importantly, apoptosis. These responses have been implicated in an individual’s ability to respond to these cancer therapies. Thus, exploring mechanisms by which normal function of p53 is affected in the comprehensive way in oral cancer might aid in the identification of tumor characteristics, prognosis and thus in the development of a new approach to treat the oral cancer

Performance anchored score normalization for multi-biometric fusion

This work presents a family of novel normalization techniques for score-level multi-biometric fusion. The proposed normalization is not only concerned to bring comparison scores to a common range and scale, it also focuses in bringing certain operational performance points in the distribution into alignment. The Performance Anchored Normalization (PAN) algorithms discussed here were tested on the extended Multi Modal Verification for Teleservices and Security applications database (XM2VTS) and proved to outperform conventional score normalization techniques in most tests. The tests were performed with combination fusion rules and presented as biometric verification performance measures

Stability Comparison Of Two Different Dentoalveolar Expansion Treatment Protocols

Objective: The aim of this study was to compare the longitudinal stability of the conventional straight-wire system after the use of a quad-helix appliance with Damon self-ligating system in patients with Class I malocclusion. Methods: 27 adolescent patients were evaluated at three different periods: pre-treatment (T1), post-treatment (T2) and three years post-treatment (T3). Group 1 included 12 patients (with a mean age of 14.65 year) treated with Damon 3MX bracket system; and Group 2 included 15 patients (with a mean age of 14.8 year) who underwent orthodontic treatment with Roth prescribed brackets after expansion with Quad-Helix appliance. Relapse was evaluated with dental cast examination and cephalometric radiograph tracings. Statistical analysis was performed with IBM-SPSS for Windows software, version 21 (SPSS Inc., Chicago, IL). A p-value smaller than 0.05 was considered statistically significant. Results: There were significant increases in all transverse dental and postero-anterior measurements (except for UL6-ML mm in Group 1) with active treatment. There was some significant relapse in the long-term in inter-canine width in both groups and in the inter-first premolar width in Group 2 (p< 0.05). Significant decrease in all frontal measurements from T2 to T3 was seen for both groups. Upper and lower incisors significantly proclined in T1-T2 (p< 0.05), however no relapse was found for both groups. When two systems were compared, there was no significant difference for the long-term follow-up period. Conclusion: Conventional (quad-helix appliance with conventional brackets) and Damon systems were found similar with regard to the long-term incisor positions and transverse dimension changes of maxillary arch.PubMedScopu