scholarly journals mRNA expression and hypermethylation of tumor suppressor genes apoptosis protease activating factor-1 and death-associated protein kinase in oral squamous cell carcinoma

2013 ◽  
Vol 6 (1) ◽  
pp. 280-286 ◽  
Author(s):  
CHUNYAN LI ◽  
LIN WANG ◽  
JING SU ◽  
RUHUI ZHANG ◽  
LI FU ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Protein Kinase ◽  
Tumor Suppressor ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Mrna Expression ◽  
Squamous Cell ◽  
Tumor Suppressor Genes ◽  
Suppressor Genes ◽  
Death Associated Protein Kinase

Oncogenes and Tumor Suppressor Genes Expression According to HPV Status in Oral Squamous Cell Carcinoma Affecting Young

2018 ◽  
Vol 126 (3) ◽  
pp. e148
Author(s):  
Marisol Miranda Galvis ◽  
Estela Kaminagakura ◽  
Alan Roger Santos-Silva ◽  
Felipe Paiva fonseca ◽  
Oslei P. Almeida ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Tumor Suppressor ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Tumor Suppressor Genes ◽  
Suppressor Genes ◽  
Genes Expression ◽  
Hpv Status

Molecular Pathogenesis of Oral Squamous Cell Carcinoma: Implications for Therapy

2008 ◽  
Vol 87 (1) ◽  
pp. 14-32 ◽  
Author(s):  
S. Choi ◽  
J.N. Myers
Keyword(s):  
Squamous Cell Carcinoma ◽  
Tumor Suppressor ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Tumor Suppressor Genes ◽  
Tumor Development ◽  
Genetic Alterations ◽  
Suppressor Genes ◽  
Promote Tumor Development

The development of oral squamous cell carcinoma (OSCC) is a multistep process requiring the accumulation of multiple genetic alterations, influenced by a patient’s genetic predisposition as well as by environmental influences, including tobacco, alcohol, chronic inflammation, and viral infection. Tumorigenic genetic alterations consist of two major types: tumor suppressor genes, which promote tumor development when inactivated; and oncogenes, which promote tumor development when activated. Tumor suppressor genes can be inactivated through genetic events such as mutation, loss of heterozygosity, or deletion, or by epigenetic modifications such as DNA methylation or chromatin remodeling. Oncogenes can be activated through overexpression due to gene amplification, increased transcription, or changes in structure due to mutations that lead to increased transforming activity. This review focuses on the molecular mechanisms of oral carcinogenesis and the use of biologic therapy to specifically target molecules altered in OSCC. The rapid progress that has been made in our understanding of the molecular alterations contributing to the development of OSCC is leading to improvements in the early diagnosis of tumors and the refinement of biologic treatments individualized to the specific characteristics of a patient’s tumor.

scholarly journals Death-Associated Protein Kinase is Underexpressed in High-Grade Oral Squamous Cell Carcinoma

2010 ◽  
Vol 28 (2) ◽  
Author(s):  
Ismário Silva de Meneses ◽  
Rafael Reis de Souza ◽  
Verónica de Lourdes Sierpe Jeraldo ◽  
Danielle Rodrigues Ribeiro Cavalcante ◽  
Francisco Prado Reis ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Protein Kinase ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
High Grade ◽  
Death Associated Protein Kinase

scholarly journals Frequently Methylated Tumor Suppressor Genes in Head and Neck Squamous Cell Carcinoma

2008 ◽  
Vol 68 (12) ◽  
pp. 4494-4499 ◽  
Author(s):  
Kristi L. Bennett ◽  
Matthew Karpenko ◽  
Mau-ting Lin ◽  
Rainer Claus ◽  
Khelifa Arab ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Tumor Suppressor ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Tumor Suppressor Genes ◽  
Neck Squamous Cell Carcinoma ◽  
Suppressor Genes
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