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Pathogenetic model of survivin-dependent molecular signalling pathways in tumorigenesis of oral cancer and precursor lesions
BACKGROUND: p53 tumour suppressor gene limits unchecked cellular growth in response to DNA damage, by causing G1 arrest and the activation of apoptosis. Inhibitors of apoptosis include survivin which acts by inhibition of caspases. Survivin has a significant role as a cell cycle modulator and is onl...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer - Medknow
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10581315/ https://www.ncbi.nlm.nih.gov/pubmed/37854918 http://dx.doi.org/10.4103/jomfp.jomfp_5_23 |
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author | Aggarwal, Dipanshu Shetty, Devi Charan Jain, Anshi Gulati, Nikita Juneja, Saurabh |
author_facet | Aggarwal, Dipanshu Shetty, Devi Charan Jain, Anshi Gulati, Nikita Juneja, Saurabh |
author_sort | Aggarwal, Dipanshu |
collection | PubMed |
description | BACKGROUND: p53 tumour suppressor gene limits unchecked cellular growth in response to DNA damage, by causing G1 arrest and the activation of apoptosis. Inhibitors of apoptosis include survivin which acts by inhibition of caspases. Survivin has a significant role as a cell cycle modulator and is only minimally present in mature tissues. Aberrant expression of p53 and survivin has been evaluated in various carcinomas. Thus, the objective of this research was to elucidate the co-expression of p53 and survivin in tissue samples of Oral Potentially Malignant Disorders (OPMDs) and Oral Squamous Cell Carcinoma (OSCCs). METHOD: Thirty tissue samples of OPMDs and 30 tissue samples of OSCCs taken from department archives were used in the study. Expression of p53 and survivin was analyzed in the study groups by the help of immunohistochemistry. Also, co-expression of both the markers was evaluated. RESULTS: The expression of p53 and survivin in the oral epithelium of patients with OSCCs was significantly higher than that in patients with OPMDs (P value ≤0.05). CONCLUSION: Our results provide insights into the altered survivin and p53 co-expression with significant immunoexpression within the study groups. Therefore, survivin and p53 could be better markers for identifying cell proliferation and apoptotic pathway. Also, malignant transformation rate of OPMD increases with increased expression of these markers. |
format | Online Article Text |
id | pubmed-10581315 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Wolters Kluwer - Medknow |
record_format | MEDLINE/PubMed |
spelling | pubmed-105813152023-10-18 Pathogenetic model of survivin-dependent molecular signalling pathways in tumorigenesis of oral cancer and precursor lesions Aggarwal, Dipanshu Shetty, Devi Charan Jain, Anshi Gulati, Nikita Juneja, Saurabh J Oral Maxillofac Pathol Original Article BACKGROUND: p53 tumour suppressor gene limits unchecked cellular growth in response to DNA damage, by causing G1 arrest and the activation of apoptosis. Inhibitors of apoptosis include survivin which acts by inhibition of caspases. Survivin has a significant role as a cell cycle modulator and is only minimally present in mature tissues. Aberrant expression of p53 and survivin has been evaluated in various carcinomas. Thus, the objective of this research was to elucidate the co-expression of p53 and survivin in tissue samples of Oral Potentially Malignant Disorders (OPMDs) and Oral Squamous Cell Carcinoma (OSCCs). METHOD: Thirty tissue samples of OPMDs and 30 tissue samples of OSCCs taken from department archives were used in the study. Expression of p53 and survivin was analyzed in the study groups by the help of immunohistochemistry. Also, co-expression of both the markers was evaluated. RESULTS: The expression of p53 and survivin in the oral epithelium of patients with OSCCs was significantly higher than that in patients with OPMDs (P value ≤0.05). CONCLUSION: Our results provide insights into the altered survivin and p53 co-expression with significant immunoexpression within the study groups. Therefore, survivin and p53 could be better markers for identifying cell proliferation and apoptotic pathway. Also, malignant transformation rate of OPMD increases with increased expression of these markers. Wolters Kluwer - Medknow 2023 2023-07-13 /pmc/articles/PMC10581315/ /pubmed/37854918 http://dx.doi.org/10.4103/jomfp.jomfp_5_23 Text en Copyright: © 2023 Journal of Oral and Maxillofacial Pathology https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. |
spellingShingle | Original Article Aggarwal, Dipanshu Shetty, Devi Charan Jain, Anshi Gulati, Nikita Juneja, Saurabh Pathogenetic model of survivin-dependent molecular signalling pathways in tumorigenesis of oral cancer and precursor lesions |
title | Pathogenetic model of survivin-dependent molecular signalling pathways in tumorigenesis of oral cancer and precursor lesions |
title_full | Pathogenetic model of survivin-dependent molecular signalling pathways in tumorigenesis of oral cancer and precursor lesions |
title_fullStr | Pathogenetic model of survivin-dependent molecular signalling pathways in tumorigenesis of oral cancer and precursor lesions |
title_full_unstemmed | Pathogenetic model of survivin-dependent molecular signalling pathways in tumorigenesis of oral cancer and precursor lesions |
title_short | Pathogenetic model of survivin-dependent molecular signalling pathways in tumorigenesis of oral cancer and precursor lesions |
title_sort | pathogenetic model of survivin-dependent molecular signalling pathways in tumorigenesis of oral cancer and precursor lesions |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10581315/ https://www.ncbi.nlm.nih.gov/pubmed/37854918 http://dx.doi.org/10.4103/jomfp.jomfp_5_23 |
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