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Objectives: Cancer is the product of alterations in oncogenes, tumour suppressor genes and most recently microRNA genes not as a single event or single change but rather as a multistep process. The role of microRNA genes in carcinogenesis is recently explored and appears to be an early event in the pathogenesis of this as well as other disease processes and occurs via gene regulation by their own products, the microRNAs.Material and Methods: A review of the available literature from 2000 to 2011 regarding the potential roles assumed by microRNAs in oral cancer was undertaken using PubMed, Medline, Scholar Google and Scopus. Keywords for the search were: microRNA and oral cancer and target genes, microRNA deregulation and oral cancer, microRNA and carcinogenesis in the head and neck/oral cavity. English language full length articles were reviewed.Results: Several microRNAs deregulated in oral cancer have been functionally validated and their exact target genes have been identified. Furthermore the carcinogenesis pathways impacted by these alterations has been proposed for some of these microRNAs.Conclusions: The expanding knowledge of specific roles of certain microRNAs is further contributing to our understanding of the complexity of tumour progression and behaviour. Consideration of this information and incorporation into treatment modalities through targeted therapy could potentially enhance our abilities to improve outcome especially when other established therapies have failed.

Abstract: Objective: To investigate effects on rat testes of radiofrequency radiation emitted from indoor Wi-Fi Internet access devices using 802.11.g wireless standards. Methods: Ten Wistar albino male rats were divided into experimental and control groups, with five rats per group. Standard wireless gateways communicating at 2.437 GHz were used as radiofrequency wave sources. The experimental group was exposed to radiofrequency energy for 24 h a day for 20 weeks. The rats were sacrificed at the end of the study. Intracardiac blood was sampled for serum 8-hydroxy-2′-deoxyguanosine levels. Testes were removed and examined histologically and immunohistochemically. Testis tissues were analyzed for malondialdehyde levels and prooxidant–antioxidant enzyme activities. Results: We observed significant increases in serum 8-hydroxy-2′-deoxyguanosine levels and 8-hydroxyguanosine staining in the testes of the experimental group indicating DNA damage due to exposure (p < 0.05). We also found decreased levels of catalase and glutathione peroxidase activity in the experimental group, which may have been due to radiofrequency effects on enzyme activity (p < 0.05). Conclusions: These findings raise questions about the safety of radiofrequency exposure from Wi-Fi Internet access devices for growing organisms of reproductive age, with a potential effect on both fertility and the integrity of germ cells. [Copyright &y& Elsevier]

Objectives: Head and neck/oral cancer, predominantly head and neck squamous cell carcinoma (HNSCC), is the sixth most common cancer in the world. While substantial advances have been made to define the genomic alterations associated with head and neck/oral cancer, most studies are focused on protein coding genes. The aim of this article is to review the current literature on identified genomic aberrations of non-coding genes (e.g., microRNA) in head and neck/oral cancer (HNOC), and their contribution to the initiation and progression of HNOC. Material and Methods: A comprehensive review of the available literature relevant to microRNA deregulation in HNSCC/HNOC, was undertaken using PubMed, Medline, Scholar Google and Scopus. Keywords for the search were: microRNA and oral cancer, microRNA and squamous cell carcinoma, microRNA deregulation and oral cancer, microRNA and carcinogenesis in the head and neck/oral cavity. Only full length articles in the English language were included. Results: We recently identified a panel of microRNA deregulations that were consistently observed in HNSCC [Chen et al., Oral Oncol. 2012;48(8):686-91], including 7 consistently up-regulated microRNAs (miR-21, miR-7, miR-155, miR-130b, miR-223, miR-34b), and 4 consistently down-regulated microRNAs (miR-100, miR-99a, miR-125b, miR-375). In this review, we will first provide an overview on microRNA and HNSCC. We will then provide a comprehensive review on the roles of microRNA deregulations in HNSCC. The functional significance of the identified HNSCC-associated microRNAs and a number of other relevant microRNAs (e.g., miR-138, miR-98, miR-137, miR-193a and miR-218) will be discussed in detail. Conclusions: Based on current literature, microRNA deregulation plays a major role in head and neck/oral cancer. [ABSTRACT FROM AUTHOR]

Objectives: Cancer is the product of alterations in oncogenes, tumour suppressor genes and most recently microRNA genes not as a single event or single change but rather as a multistep process. The role of microRNA genes in carcinogenesis is recently explored and appears to be an early event in the pathogenesis of this as well as other disease processes and occurs via gene regulation by their own products, the microRNAs. Material and Methods: A review of the available literature from 2000 to 2011 regarding the potential roles assumed by microRNAs in oral cancer was undertaken using PubMed, Medline, Scholar Google and Scopus. Keywords for the search were: microRNA and oral cancer and target genes, microRNA deregulation and oral cancer, microRNA and carcinogenesis in the head and neck/oral cavity. English language full length articles were reviewed. Results: Several microRNAs deregulated in oral cancer have been functionally validated and their exact target genes have been identified. Furthermore the carcinogenesis pathways impacted by these alterations has been proposed for some of these microRNAs. Conclusions: The expanding knowledge of specific roles of certain microRNAs is further contributing to our understanding of the complexity of tumour progression and behaviour. Consideration of this information and incorporation into treatment modalities through targeted therapy could potentially enhance our abilities to improve outcome especially when other established therapies have failed. [ABSTRACT FROM AUTHOR]