Expression of survivin in dysplasia and different grades of oral squamous cell carcinoma

Deo, Priya Nimish; Deshmukh, Revati

doi:10.1177/2057178x17710147

Cited by 4 publications

(6 citation statements)

References 12 publications

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“…In the present study, the overall expression of survivin is positive in both metastatic and nonmetastatic OSCCs. The moderately differentiated squamous cell carcinomas of metastatic and nonmetastatic cases showed significantly increased survivin expression, which was similar to the study conducted by Deo et al 9 This result is in contrast to the study conducted by Kulkarni et al, 21 where the survivin expression is high in poorly differentiated squamous cell carcinoma cases.…”

Section: Discussionsupporting

confidence: 87%

“…5 Survivin is a multifunctional protein involved in regulation of cytokinesis and cell cycle progression, and participation in a variety of pathways such as the p53, Wnt, hypoxia, TGF, and Notch signaling pathways. [6][7][8] Survivin is considered to be good prognostic marker of OSCC 9 and is highly expressed in most human tumors of the oral cavity, lung, colon, breast, liver, gastrointestinal, and prostate. 8 In this study, investigation of immunohistochemical expression of survivin in metastatic and nonmetastatic tumors is done.…”

Section: Introductionmentioning

confidence: 99%

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Survivin Expression in Metastatic and Nonmetastatic Oral Squamous Cell Carcinoma: A Comparative Study

Balakrishnan

Ambika

Saranyan

et al. 2020

Journal of Advanced Oral Research

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Aim: Survivin is a multifunctional protein chiefly involved in apoptosis and cell cycle regulation. Increased expression of survivin in tumors and fetal tissue determines its antiapoptotic activity. The aim of the study is to identify the immunoexpression of survivin in metastatic and nonmetastatic oral squamous cell carcinoma (OSCC) and also to evaluate and compare the expression of survivin in metastatic and nonmetastatic OSCC of buccal mucosa. Materials and Methods: In total, 40 histopathologically proven cases of OSCC, including 20 metastatic and 20 nonmetastatic cases, are selected. Among the 20 metastatic and nonmetastatic cases, 10 well-differentiated and 10 moderately differentiated squamous cell carcinoma cases were included and were subjected to immunohistochemical staining for survivin expression. The results were analyzed by SPSS version 11.5 using chi-square test. Results: The expression of survivin in metastatic and nonmetastatic tumors is 15%–70% and 15%–60%, respectively. When comparing the cases of moderately differentiated squamous cell carcinoma in metastatic and nonmetastatic tumors, 70% cases show moderate staining intensity. Conclusion: The survivin expression was comparatively high in metastatic OSCC. Also based on the aforementioned results, survivin expression was high in increasing grades of OSCC.

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Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Survivin Expression in Metastatic and Nonmetastatic Oral Squamous Cell Carcinoma: A Comparative Study

Balakrishnan

Ambika

Saranyan

et al. 2020

Journal of Advanced Oral Research

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“…Several molecules potentially represent the loss of functioning tumour suppressors genes, cell cycle regulators, or apoptosis regulators, which results in an imbalanced cell growth and/or death process . [ 12 ] To recognize oral precancerous lesions prone to invasive transformation, new biological predictors of malignant development are required.…”

Section: Discussionmentioning

confidence: 99%

“…[ 18 ] Survivin's differential expression makes it a desirable target for the selection of patients for molecularly based cancer therapy, and it can be employed as a prognostic indicator for proliferation and invasion. [ 12 ]…”

Section: Discussionmentioning

confidence: 99%

Pathogenetic model of survivin-dependent molecular signalling pathways in tumorigenesis of oral cancer and precursor lesions

Aggarwal,

Shetty,

Jain

et al. 2023

Journal of Oral and Maxillofacial Pathology

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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.

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“…In relation to Wnt/β-catenin target genes, reports have explored their expressions in oral cancer, with data showing abnormal expressions in a subset of those genes [ 112 , 113 , 114 , 115 ]. For example, high levels of cyclin D1, survivin and c-myc, which are classical Wnt/β-catenin targets, have been detected in OSCC samples when compared with control groups [ 76 , 116 , 117 , 118 , 119 , 120 ], indicating that Wnt/β-catenin target genes might be upregulated in oral cancer, contributing to cell migration and invasion.…”

Section: Altered Wnt/β-catenin Signaling In Oral Carcinogenesismentioning

confidence: 99%

Wnt/β-Catenin Signaling in Oral Carcinogenesis

Reyes

Flores

Betancur

et al. 2020

IJMS

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Oral carcinogenesis is a complex and multifactorial process that involves cumulative genetic and molecular alterations, leading to uncontrolled cell proliferation, impaired DNA repair and defective cell death. At the early stages, the onset of potentially malignant lesions in the oral mucosa, or oral dysplasia, is associated with higher rates of malignant progression towards carcinoma in situ and invasive carcinoma. Efforts have been made to get insights about signaling pathways that are deregulated in oral dysplasia, as these could be translated into novel markers and might represent promising therapeutic targets. In this context, recent evidence underscored the relevance of the Wnt/β-catenin signaling pathway in oral dysplasia, as this pathway is progressively “switched on” through the different grades of dysplasia (mild, moderate and severe dysplasia), with the consequent nuclear translocation of β-catenin and expression of target genes associated with the maintenance of representative traits of oral dysplasia, namely cell proliferation and viability. Intriguingly, recent studies provide an unanticipated connection between active β-catenin signaling and deregulated endosome trafficking in oral dysplasia, highlighting the relevance of endocytic components in oral carcinogenesis. This review summarizes evidence about the role of the Wnt/β-catenin signaling pathway and the underlying mechanisms that account for its aberrant activation in oral carcinogenesis.

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Expression of survivin in dysplasia and different grades of oral squamous cell carcinoma

Cited by 4 publications

References 12 publications

Survivin Expression in Metastatic and Nonmetastatic Oral Squamous Cell Carcinoma: A Comparative Study

Survivin Expression in Metastatic and Nonmetastatic Oral Squamous Cell Carcinoma: A Comparative Study

Pathogenetic model of survivin-dependent molecular signalling pathways in tumorigenesis of oral cancer and precursor lesions

Wnt/β-Catenin Signaling in Oral Carcinogenesis

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