A Cross-Cultural Principle Of Temporal Spatialization

The Temporal Focus Hypothesis proposes that a person’s tendency to conceptualize either the past or the future as beinglocated in front of them depends on their temporal focus: the balance of attention paid to the past (tradition) and thefuture (progress). How general is the TFH and to what extent can cultures and subcultures be placed on a single linerelating time spatialization and temporal focus in spite of stark differences in language, religion, history, and economicdevelopment? Data from 10 Western and Middle Eastern (sub)cultural groups (N=1198) were used to derive a linearmodel relating aggregated temporal focus and proportion of future-in-front responses. This model then successfully fittednine independently collected (sub)cultural groups in China and Vietnam (N=841). A logistic mixed model computedover the whole dataset (N=2039) showed that the group-level relation arose at the individual level and allowed precisequantification of its influence. Temporal focus shapes how people around the world think of time in spatial terms

Does time extend asymmetrically towards the past and the future? Across-cultural study

Is the human representation of time symmetrical or asymmetrical toward the past and the future? Some studies suggestthat we perceive the future as being closer, more attended and more valued than the past (indicating a future asymmetry).By contrast, asymmetries toward the past have been found in past-focused cultures. Yet, available evidence is still limitedand mixed. In the present work we searched for asymmetry in several temporal tasks (temporal distance, time discounting,temporal depth, and self-continuity) in a set of cultures that vary widely in their temporal focus (American, Spanish,Turkish, Chinese, Moroccan, Serbian, Bosniak and Croatian; total N=1075). The results supported an overall asymmetrytoward the future in all tasks, although it failed to be significant in most cultures when considered on their own. However,only self-continuity showed variations that can be explained by the contrast between past-focused versus future-focusedcultures

Epigenetic modulation of cytokine expression in gastric cancer: influence on angiogenesis, metastasis and chemoresistance

Cytokines are proteins that act in the immune response and inflammation and have been associated with the development of some types of cancer, such as gastric cancer (GC). GC is a malignant neoplasm that ranks fifth in incidence and third in cancer-related mortality worldwide, making it a major public health issue. Recent studies have focused on the role these cytokines may play in GC associated with angiogenesis, metastasis, and chemoresistance, which are key factors that can affect carcinogenesis and tumor progression, quality, and patient survival. These inflammatory mediators can be regulated by epigenetic modifications such as DNA methylation, histone protein modification, and non-coding RNA, which results in the silencing or overexpression of key genes in GC, presenting different targets of action, either direct or mediated by modifications in key genes of cytokine-related signaling pathways. This review seeks insight into the relationship between cytokine-associated epigenetic regulation and its potential effects on the different stages of development and chemoresistance in GC

Landscape of Genome-Wide DNA Methylation of Colorectal Cancer Metastasis.

Colorectal cancer is a heterogeneous disease caused by both genetic and epigenetics factors. Analysing DNA methylation changes occurring during colorectal cancer progression and metastasis formation is crucial for the identification of novel epigenetic markers of patient prognosis. Genome-wide methylation sequencing of paired samples of colon (normal adjacent, primary tumour and lymph node metastasis) showed global hypomethylation and CpG island (CGI) hypermethylation of primary tumours compared to normal. In metastasis we observed high global and non-CGI regions methylation, but lower CGI methylation, compared to primary tumours. Gene ontology analysis showed shared biological processes between hypermethylated CGIs in metastasis and primary tumours. After complementary analysis with The Cancer Genome Atlas (TCGA) cohort, FIGN, HTRA3, BDNF, HCN4 and STAC2 genes were found associated with poor survival. We mapped the methylation landscape of colon normal tissues, primary tumours and lymph node metastasis, being capable of identified methylation changes throughout the genome. Furthermore, we found five genes with potential for methylation biomarkers of poor prognosis in colorectal cancer patients

Genome-wide and gene-specific epigenomic platforms for hepatocellular carcinoma biomarker development trials

The majority of the epigenomic reports in hepatocellular carcinoma have focused on identifying novel differentially methylated drivers or passengers of the oncogenic process. Few reports have considered the technologies in place for clinical translation of newly identified biomarkers. The aim of this study was to identify epigenomic technologies that need only a small number of samples to discriminate HCC from non-HCC tissue, a basic requirement for biomarker development trials. To assess that potential, we used quantitative Methylation Specific PCR, oligonucleotide tiling arrays, and Methylation BeadChip assays. Concurrent global DNA hypomethylation, gene-specific hypermethylation, and chromatin alterations were observed as a hallmark of HCC. A global loss of promoter methylation was observed in HCC with the Illumina BeadChip assays and the Nimblegen oligonucleotide arrays. HCC samples had lower median methylation peak scores and a reduced number of significant promoter-wide methylated probes. Promoter hypermethylation of RASSF1A, SSBP2, and B4GALT1 quantified by qMSP had a sensitivity ranging from 38% to 52%, a specificity of 100%, and an AUC from 0.58 to 0.75. A panel combining these genes with HCC risk factors had a sensitivity of 87%, a specificity of 100%, and an AUC of 0.91

Genome-Wide and Gene-Specific Epigenomic Platforms for Hepatocellular Carcinoma Biomarker Development Trials

The majority of the epigenomic reports in hepatocellular carcinoma have focused on identifying novel differentially methylated drivers or passengers of the oncogenic process. Few reports have considered the technologies in place for clinical translation of newly identified biomarkers. The aim of this study was to identify epigenomic technologies that need only a small number of samples to discriminate HCC from non-HCC tissue, a basic requirement for biomarker development trials. To assess that potential, we used quantitative Methylation Specific PCR, oligonucleotide tiling arrays, and Methylation BeadChip assays. Concurrent global DNA hypomethylation, gene-specific hypermethylation, and chromatin alterations were observed as a hallmark of HCC. A global loss of promoter methylation was observed in HCC with the Illumina BeadChip assays and the Nimblegen oligonucleotide arrays. HCC samples had lower median methylation peak scores and a reduced number of significant promoter-wide methylated probes. Promoter hypermethylation of RASSF1A, SSBP2, and B4GALT1 quantified by qMSP had a sensitivity ranging from 38% to 52%, a specificity of 100%, and an AUC from 0.58 to 0.75. A panel combining these genes with HCC risk factors had a sensitivity of 87%, a specificity of 100%, and an AUC of 0.91

Novel Methylation Biomarkers for Colorectal Cancer Prognosis

Colorectal cancer (CRC) comprises the third most common cancer worldwide and the second regarding number of deaths. In order to make a correct and early diagnosis to predict metastasis formation, biomarkers are an important tool. Although there are multiple signaling pathways associated with cancer progression, the most recognized are the MAPK pathway, p53 pathway, and TGF-β pathway. These pathways regulate many important functions in the cell, such as cell cycle regulation, proliferation, differentiation, and metastasis formation, among others. Changes in expression in genes belonging to these pathways are drivers of carcinogenesis. Often these expression changes are caused by mutations; however, epigenetic changes, such as DNA methylation, are increasingly acknowledged to play a role in the deregulation of oncogenic genes. This makes DNA methylation changes an interesting biomarkers in cancer. Among the newly identified biomarkers for CRC metastasis INHBB, SMOC2, BDNF, and TBRG4 are included, all of which are highly deregulated by methylation and closely associated with metastasis. The identification of such biomarkers in metastasis of CRC may allow a better treatment and early identification of cancer formation in order to perform better diagnostics and improve the life expectancy

Long Non-Coding RNAs (lncRNAs) as Regulators of the PI3K/AKT/mTOR Pathway in Gastric Carcinoma

Gastric cancer (GC) represents ~10% of the global cancer-related deaths, increasingly affecting the younger population in active stages of life. The high mortality of GC is due to late diagnosis, the presence of metastasis and drug resistance development. Additionally, current clinical markers do not guide the patient management adequately, thereby new and more reliable biomarkers and therapeutic targets are still needed for this disease. RNA-seq technology has allowed the discovery of new types of RNA transcripts including long non-coding RNAs (lncRNAs), which are able to regulate the gene/protein expression of many signaling pathways (e.g., the PI3K/AKT/mTOR pathway) in cancer cells by diverse molecular mechanisms. In addition, these lncRNAs might also be proposed as promising diagnostic or prognostic biomarkers or as potential therapeutic targets in GC. This review describes important topics about some lncRNAs that have been described as regulators of the PI3K/AKT/mTOR signaling pathway, and hence, their potential oncogenic role in the development of this malignancy