Role of DNA methylation in head and neck cancer

Head and neck cancer (HNC) is a heterogenous and complex entity including diverse anatomical sites and a variety of tumor types displaying unique characteristics and different etilogies. Both environmental and genetic factors play a role in the development of the disease, but the underlying mechanism is still far from clear. Previous studies suggest that alterations in the genes acting in cellular signal pathways may contribute to head and neck carcinogenesis. In cancer, DNA methylation patterns display specific aberrations even in the early and precancerous stages and may confer susceptibility to further genetic or epigenetic changes. Silencing of the genes by hypermethylation or induction of oncogenes by promoter hypomethylation are frequent mechanisms in different types of cancer and achieve increasing diagnostic and therapeutic importance since the changes are reversible. Therefore, methylation analysis may provide promising clinical applications, including the development of new biomarkers and prediction of the therapeutic response or prognosis. In this review, we aimed to analyze the available information indicating a role for the epigenetic changes in HNC

Epigenetic mechanisms in virus-induced tumorigenesis

About 15–20% of human cancers worldwide have viral etiology. Emerging data clearly indicate that several human DNA and RNA viruses, such as human papillomavirus, Epstein–Barr virus, Kaposi’s sarcoma-associated herpesvirus, hepatitis B virus, hepatitis C virus, and human T-cell lymphotropic virus, contribute to cancer development. Human tumor-associated viruses have evolved multiple molecular mechanisms to disrupt specific cellular pathways to facilitate aberrant replication. Although oncogenic viruses belong to different families, their strategies in human cancer development show many similarities and involve viral-encoded oncoproteins targeting the key cellular proteins that regulate cell growth. Recent studies show that virus and host interactions also occur at the epigenetic level. In this review, we summarize the published information related to the interactions between viral proteins and epigenetic machinery which lead to alterations in the epigenetic landscape of the cell contributing to carcinogenesis

Planobispora takensis sp. nov., isolated from soil

A novel Gram-stain-positive, filamentous bacterial strain (A-T 7458<sup>T</sup>) was isolated from soil collected from hill evergreen forest in Thailand. The strain developed cylindrical sporangia containing a longitudinal pair of motile spores, on short ramifications of aerial mycelia. From a taxonomic study using a polyphasic approach, strain A-T 7458<sup>T</sup>had typical characteristics of members of the genus Planobispora. 16S rRNA gene sequence analysis indicated that the isolate was closely related to Planobispora siamensis A-T 4600<sup>T</sup>(98.5 %), Planobispora rosea JCM 3166<sup>T</sup>(97.6 %) and Planobispora longispora NBRC 13918<sup>T</sup>(97.6 %). The DNA-DNA relatedness values, which differentiated the novel strain from the closest species, were significantly below 70 %. The cell-wall peptidoglycan contained meso-diaminopimelic acid. The whole-cell sugars contained ribose, madurose, mannose and glucose. The predominant menaquinone was MK-9(H<sub>2</sub>). The diagnostic phospholipids were diphosphatidylglycerol, phosphatidylglycerol, phosphatidylethanolamine, phosphatidylmethylethanolamine, phosphatidylinositol, phosphatidylinositol-mannoside and aminophosphoglycolipid. The predominant cellular fatty acids were unsaturated C<sub>17:1</sub> and C<sub>18:1</sub>, and saturated C<sub>16:0</sub> and C<sub>17:0</sub>. Following an evaluation of phenotypic, chemotaxonomic and genotypic characteristics, the novel isolate is proposed to represent a novel species of the genus Planobispora, to be named Planobispora takensis sp. nov. The type strain is A-T 7458<sup>T</sup>(=BCC 48396<sup>T</sup>=NBRC 109077<sup>T</sup>). 2014 IUM