Ricerc@Sapienza

While accumulating literature is demonstrating the role of the dopamine transporter (DAT) in predicting emotional–behavioural difficulties in adults of at risk populations, only few studies have focused on the possible association between the methylation status of the DAT promoter and the psychopathological risk of mothers, fathers and children in normative samples.

In the wake of multiple observations arising from diverse corners of physiological and molecular genetics, the onslaught of
epigenetic changes, gene x environment interaction, under current appearances requires rendition for purposes of displaying
both performance augmentation, amelioration of structural-functional impairment and the promotion of resilience manifested
by the lasting health benefits that arise from regular and consistent physical exercise. The notion that individuals, who

Background: The effect of gene polymorphisms and promoter methylation, associated with maladaptive developmental outcomes, vary depending on environmental factors (e.g., parental psychopathology). Most studies have focused on 0- to 5-year-old children, adolescents, or adults, whereas there is dearth of research on school-age youths and pre-adolescents.

Parental psychopathological risk is considered as one of the most crucial features associated with epigenetic modifications in o↵spring, which in turn are thought to be related to their emotional/behavioral profiles. The dopamine active transporter (DAT) gene is suggested to play a significant role in a↵ective/behavioral regulation.

Background: BRCA1 methylation has been associated with homologous recombination deficiency, a biomarker of platinum sensitivity. Studies evaluating BRCA1-methylated tubal/ovarian cancer (OC) do not consistently support improved survival following platinum chemotherapy. We examine the characteristics of BRCA1-methylated OC in a meta-analysis of individual participant data.

Epigenetic alterations have been associated with both pathogenesis and progression of cancer. By screening of library compounds, we identified a novel hybrid epi-drug MC2884, a HAT/EZH2 inhibitor, able to induce bona fide cancer-selective cell death in both solid and hematological cancers in vitro, ex vivo and in vivo xenograft models. Anticancer action was due to an epigenome modulation by H3K27me3, H3K27ac, H3K9/14ac decrease, and to caspase-dependent apoptosis induction. MC2884 triggered mitochondrial pathway apoptosis by up-regulation of cleaved-BID, and strong down-regulation of BCL2.