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Objective: To assess the psychosocial impact of malocclusion, establish its association with the severity of malocclusion and determine the effects of gender and age in such association. Basic research design: Cross-sectional study. Methods: 400 adolescents aged between 12-15 years were randomly selected. Each participant was examined for malocclusion and categorized according to Index of Orthodontic Treatment Need (IOTN) and Dental Aesthetic Index (DAI). The Psychosocial Impact of Dental Aesthetics Questionnaire (PIDAQ) was used to assess the psychosocial impact of malocclusion. Results: Significant differences were noted between PIDAQ subscales, and grades of malocclusion assessed by IOTN and DAI (p

Aberrant methylation is one of the driving forces of cancer genome development. Although the rate of methylation appears massively variable across the genome, it is mainly observed in histone modification, chromatin organization, DNA accessibility, or promoter sequence. Methylation of promoter sequence occurs mostly to cytosine nucleotides, which can affect transcription factors' binding affinities. In this study, we demonstrated that cytosine repeats (C types density), consisting of CC, CCC, CCCC, CCCCC, CCCCCC, CCCCCCC motifs and CpG islands density in 25 proto-oncogenes, tumor suppressor genes and control genes may play a role in the pathogenesis of acute myeloid leukemia. The promoter sequences were divided into a 100 nucleotide window from -500 to +100 nucleotides and 20 nucleotide window from -100 to +100. Each window is analyzed to find the higher C type and CpG islands density, which may cause the increased methylation in the promoter sequence. Our novel findings show that promoter sequence cytosine repeats and CpG density increase closer to transcription sites, especially just before and after the transcription start site (TSS). The results demonstrate that cytosine density increases while proto-oncogenes and TSG promoter sequences are closer to TSS 50.8% and 41.0% respectively, if (-500 to -200) and (-100 to +100) windows of the nucleotide sequences are compared. This proves that around TSS location has special nucleotide motifs and could be an important implication for our understanding of potential methylating locations in promoters.

Mixed lineage leukemias (MLL) express unique clinical and biological characteristics. MLL interacts with over 50 different genes resulting in expression of chimeric proteins whereby the MLL amino-terminal portion is fused to the carboxy-terminal portion of the partner. Chromosomal translocations t(9 ; 11), t(11 ; 19) and t(4 ; 11) leading to MLL-AF9, MLL-ENL and MLL-AF4 fusions are the most frequent. Leukemias with MLL rearrangements are mostly driven through dysregulation of a transforming gene expression program, making it a unique epigenetic model of leukemia. Using the whole genome profiling of acute myeloid leukemias (AMLs), we analysed the differential gene expression, methylation pattern, and mutational spectra between MLL and other AML types (n=197). We found that 120 genes were differentially expressed, with 36 genes characterized by more than twofold expression difference. In this study, we will present differently expressed genes with and their potential role in leukemogenesis. Since rearrangements of the MLL gene lead to aberrant methylation, we investigated differential methylation patterns among MLL and other AML types and identified affected methylation hotspots.