Article

Methylation-Mediated Molecular Dysregulation in Clinical Oral Malignancy

Department of Integrative Oncology, British Columbia Cancer Research Centre, 675 West 10th Avenue, Vancouver, BC, Canada V5Z 1L3.
Journal of Oncology 05/2012; 2012(4):170172. DOI: 10.1155/2012/170172
Source: PubMed

ABSTRACT

Herein we provide a concise review of the state of methylation research as it pertains to clinical oral cancerous and precancerous tissues. We provide context for ongoing research efforts in this field and describe technologies that are presently being applied to analyze clinical specimens. We also discuss the various recurrent methylation changes that have been reported for oral malignancy (including those genes frequently silenced by promoter methylation and the small RNAs with activity modulated by methylation changes) and describe surrogate disease markers identified via epigenetic analysis of saliva and blood specimens from patients with oral cancer.

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Available from: Cathie Garnis, Feb 19, 2015
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    • "Hypo-methylation of a CpG dinucleotide in the global DNA sequence causes activation of oncogenes such as genes in cell cycle signalling [7] [23]. DNA methylation patterns are reversible and dynamic to adapt with changes in the environment or treatment [18]. "
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    ABSTRACT: Oral squamous cell carcinoma (OSCC) is a category of aggressive malignancies that represent clinically, molecularly, and etiologically heterogeneous tumors. The majority of OSCCs are associated with tobacco and alcohol use, acting both independently and synergistically, which suggests that the environment plays an important role in carcinogenesis; however, the mechanisms associated with the development of OSCC are not well understood. It has been proposed that the epigenetic components could be implicated in the initiation and progression of OSCC. Primarily, aberrant DNA methylation patterns have been widely addressed in the study of OSCC. Diverse studies have proposed that other epigenetic processes such as post-translational histone modification, the deposition of histone variants, histone chaperones, and recently non-coding RNA, can be also involved in the development of oral cancer. In this review we focus on describing the new insights of the epigenetics processes that are related with OSCC as histones variants and long non-coding RNAs.
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