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Overexpression of Survivin and Caspase 3 in Oral Carcinogenesis

Overexpression of Survivin and Caspase 3 in Oral Carcinogenesis RESEARCH ARTICLE Overexpression of Survivin and Caspase 3 in Oral Carcinogenesis Sopee Poomsawat, DDS, MSc, PhD,* Jirapa Punyasingh, DDS, MS,* and Paisarn Vejchapipat, MD, PhDw that can inhibit (eg, Bcl-2, Bcl-x, mutant p53, survivin) or 1,2 Abstract: Survivin is an inhibitor of apoptosis protein that in- promote (eg, Bax, caspase) cell death. Genetic alter- hibits caspase 3 function. While cytoplasmic survivin suppresses ations or changes in the proteins in the component of the apoptosis, nuclear survivin regulates cell division. Little is apoptotic pathway contribute to the development of known about the subcellular localization of survivin in oral many cancer types. For example, follicular lymphomas carcinogenesis. This study examined the subcellular distribution show overexpression of Bcl-2 protein, which protects of these 2 proteins in oral squamous cell carcinoma (OSCC) and lymphocytes from apoptosis and allows them to survive premalignant lesions including oral leukoplakia (OL) with and for long periods. This process leads to a steady accumu- without dysplasia. Expression of survivin and caspase 3 were lation of B lymphocytes and finally to marrow infiltra- immunohistochemically analyzed in 114 samples including tion. Mutation in the gene encoding caspase 8 has been OSCC, OL with and without dysplasia, and normal oral mucosa http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Applied Immunohistochemistry & Molecular Morphology Wolters Kluwer Health

Overexpression of Survivin and Caspase 3 in Oral Carcinogenesis

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Copyright
Copyright © 2013 by Lippincott Williams & Wilkins
ISSN
1541-2016
DOI
10.1097/PAI.0b013e31828a0d0c
pmid
23531848
Publisher site
See Article on Publisher Site

Abstract

RESEARCH ARTICLE Overexpression of Survivin and Caspase 3 in Oral Carcinogenesis Sopee Poomsawat, DDS, MSc, PhD,* Jirapa Punyasingh, DDS, MS,* and Paisarn Vejchapipat, MD, PhDw that can inhibit (eg, Bcl-2, Bcl-x, mutant p53, survivin) or 1,2 Abstract: Survivin is an inhibitor of apoptosis protein that in- promote (eg, Bax, caspase) cell death. Genetic alter- hibits caspase 3 function. While cytoplasmic survivin suppresses ations or changes in the proteins in the component of the apoptosis, nuclear survivin regulates cell division. Little is apoptotic pathway contribute to the development of known about the subcellular localization of survivin in oral many cancer types. For example, follicular lymphomas carcinogenesis. This study examined the subcellular distribution show overexpression of Bcl-2 protein, which protects of these 2 proteins in oral squamous cell carcinoma (OSCC) and lymphocytes from apoptosis and allows them to survive premalignant lesions including oral leukoplakia (OL) with and for long periods. This process leads to a steady accumu- without dysplasia. Expression of survivin and caspase 3 were lation of B lymphocytes and finally to marrow infiltra- immunohistochemically analyzed in 114 samples including tion. Mutation in the gene encoding caspase 8 has been OSCC, OL with and without dysplasia, and normal oral mucosa

Journal

Applied Immunohistochemistry & Molecular MorphologyWolters Kluwer Health

Published: Jan 1, 2014

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