Who Are the Workers Who Never Joined a Union? : Empirical Evidence from Western and Eastern Germany

"Using representative data from the German social survey ALLBUS 2002 and the European Social Survey 2002/03, this paper provides the first empirical analysis of trade union ‘never-membership’ in Germany. We show that between 54 and 59 percent of all employees in Germany have never been members of a trade union. In western Germany, individuals’ probability of ‘never-membership’ is significantly affected by their personal characteristics, their political orientation and (to a lesser degree) their family background. In addition, the presence of a union at the workplace plays a significant role. While the latter factor is also important in eastern Germany, many of the variables which are relevant for ‘never-membership’ in the west prove to be irrelevant in the east. This difference probably reflects the fact that most employees in eastern Germany did not really have a choice not to become union members during the communist regime." (author's abstract)"Mit Daten des ALLBUS 2002 und des European Social Survey 2002/03 analysiert diese Arbeit erstmalig die ‚Nie-Mitgliedschaft’ in deutschen Gewerkschaften. Wir zeigen, dass 54 bis 59 Prozent aller Beschäftigten in Deutschland niemals Mitglied einer Gewerkschaft waren. Die individuelle Wahrscheinlichkeit einer ‚Nie-Mitgliedschaft’ hängt in Westdeutschland signifikant mit persönlichen Merkmalen, der politischen Ausrichtung und (in geringerem Maße) dem familiären Hintergrund zusammen. Darüber hinaus spielt das Vorhandensein einer Gewerkschaft am Arbeitsplatz eine signifikante Rolle. Während letzteres auch in Ostdeutschland von Bedeutung ist, erweisen sich viele der im Westen relevanten Erklärungsvariablen im Osten als irrelevant. Dieser Unterschied spiegelt wahrscheinlich wider, dass die meisten Arbeitnehmer in Ostdeutschland während des SED-Regimes kaum die Wahl hatten, auf eine Gewerkschaftsmitgliedschaft zu verzichten." (Autorenreferat

Standardising RNA profiling based biomarker application in cancer - the need for robust control of technical variables

Histopathology-based staging of colorectal cancer (CRC) has utility in assessing the prognosis of patient subtypes, but as yet cannot accurately predict individual patient’s treatment response. Transcriptomics approaches, using array based or next generation sequencing (NGS) platforms, of formalin fixed paraffin embedded tissue can be harnessed to develop multi-gene biomarkers for predicting both prognosis and treatment response, leading to stratification of treatment. While transcriptomics can shape future biomarker development, currently < 1% of published biomarkers become clinically validated tests, often due to poor study design or lack of independent validation. In this review of a large number of CRC transcriptional studies, we identify recurrent sources of technical variability that encompass collection, preservation and storage of malignant tissue, nucleic acid extraction, methods to quantitate RNA transcripts and data analysis pipelines. We propose a series of defined steps for removal of these confounding issues, to ultimately aid in the development of more robust clinical biomarkers

The expression of RUNX3 in colorectal cancer is associated with disease stage and patient outcome

RUNX3 is believed to have tumour suppressor properties in several cancer types. Inactivation of RUNX3 has been shown to occur by methylation-induced transcriptional silencing and by mislocalization of the protein to the cytoplasm. The aim of this study was to examine the clinical significance of RUNX3 expression in a large series of colorectal cancers using immunohistochemistry and tissue arrays. With advancing tumour stage, expression of RUNX3 in the nucleus decreased, whereas expression restricted to the cytoplasmic compartment increased. Nuclear RUNX3 expression was associated with significantly better patient survival compared to tumours in which the expression of RUNX3 was restricted to the cytoplasm (P=0.025). These results support a role for RUNX3 as a tumour suppressor in colorectal cancer

Identification of rare cell phenotypes in Sarcoma H&E by a combination of deep learning and image processing approaches

Rare cells, i.e., those with a lower abundance within a population, play an important part in the conditions of health and disease of an organism. In Sarcoma, the presence of these cells can reveal the state of immune response or angiogenesis among other conditions [1]. Thus, its identification is crucial and one way to identify rare cells is through its phenotype [2]. Pooling of rare cells from large whole slide images (WSI) for training is tedious and time-consuming (Fig. 1). Deep learning techniques [3, 4] have been widely used for cellular segmentation and identification. However, an important pre-requisite of deep learning mandates large number of manually annotated training data, which is not always available

Gastrointestinal tissue‐based molecular biomarkers: A practical categorization based on the 2019 WHO Classification of Epithelial Digestive Tumours

Molecular biomarkers have come to constitute one of the cornerstones of oncological pathology. The method of classification not only directly affects the manner in which patients are diagnosed and treated, but also guides the development of drugs and of artificial intelligence tools. The aim of this article is to organise and update gastrointestinal molecular biomarkers in order to produce an easy-to-use guide for routine diagnostics. For this purpose, we have extracted and reorganised the molecular information on epithelial neoplasms included in the 2019 World Health Organization classification of tumours. Digestive system tumours, 5th edn

TRIP-Br2 promotes oncogenesis in nude mice and is frequently overexpressed in multiple human tumors

<p>Abstract</p> <p>Background</p> <p>Members of the TRIP-Br/SERTAD family of mammalian transcriptional coregulators have recently been implicated in E2F-mediated cell cycle progression and tumorigenesis. We, herein, focus on the detailed functional characterization of the least understood member of the TRIP-Br/SERTAD protein family, TRIP-Br2 (SERTAD2).</p> <p>Methods</p> <p>Oncogenic potential of TRIP-Br2 was demonstrated by (1) inoculation of NIH3T3 fibroblasts, which were engineered to stably overexpress ectopic TRIP-Br2, into athymic nude mice for tumor induction and (2) comprehensive immunohistochemical high-throughput screening of TRIP-Br2 protein expression in multiple human tumor cell lines and human tumor tissue microarrays (TMAs). Clinicopathologic analysis was conducted to assess the potential of TRIP-Br2 as a novel prognostic marker of human cancer. RNA interference of <it>TRIP-Br2 </it>expression in HCT-116 colorectal carcinoma cells was performed to determine the potential of TRIP-Br2 as a novel chemotherapeutic drug target.</p> <p>Results</p> <p>Overexpression of TRIP-Br2 is sufficient to transform murine fibroblasts and promotes tumorigenesis in nude mice. The transformed phenotype is characterized by deregulation of the E2F/DP-transcriptional pathway through upregulation of the key E2F-responsive genes <it>CYCLIN E</it>, <it>CYCLIN A2</it>, <it>CDC6 </it>and <it>DHFR</it>. TRIP-Br2 is frequently overexpressed in both cancer cell lines and multiple human tumors. Clinicopathologic correlation indicates that overexpression of TRIP-Br2 in hepatocellular carcinoma is associated with a worse clinical outcome by Kaplan-Meier survival analysis. Small interfering RNA-mediated (siRNA) knockdown of TRIP-Br2 was sufficient to inhibit cell-autonomous growth of HCT-116 cells <it>in vitro</it>.</p> <p>Conclusion</p> <p>This study identifies <it>TRIP-Br2 </it>as a <it>bona-fide </it>protooncogene and supports the potential for TRIP-Br2 as a novel prognostic marker and a chemotherapeutic drug target in human cancer.</p

Identification of a BRCA1-mRNA Splicing Complex Required for Efficient DNA Repair and Maintenance of Genomic Stability

Mutations within BRCA1 predispose carriers to a high risk of breast and ovarian cancers. BRCA1 functions to maintain genomic stability through the assembly of multiple protein complexes involved in DNA repair, cell-cycle arrest, and transcriptional regulation. Here, we report the identification of a DNA damage-induced BRCA1 protein complex containing BCLAF1 and other key components of the mRNA-splicing machinery. In response to DNA damage, this complex regulates pre-mRNA splicing of a number of genes involved in DNA damage signaling and repair, thereby promoting the stability of these transcripts/proteins. Further, we show that abrogation of this complex results in sensitivity to DNA damage, defective DNA repair, and genomic instability. Interestingly, mutations in a number of proteins found within this complex have been identified in numerous cancer types. These data suggest that regulation of splicing by the BRCA1-mRNA splicing complex plays an important role in the cellular response to DNA damage