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Heidelberg University and BioQuant[Affi... Publications | LitMetric

8 results match your criteria: "Heidelberg University and BioQuant[Affiliation]"

Article Synopsis
  • The text discusses the introduction of "ehrapy," an open-source Python framework designed for comprehensive analysis of electronic health records (EHRs) and epidemiology data, addressing the lack of tools for heterogeneous data exploration.
  • ehrapy streamlines various analytical processes including data extraction, quality control, and statistical analysis, allowing researchers to explore patient-disease associations, compare patient groups, and analyze treatment impacts, among other features.
  • The framework is exemplified through six case studies, showcasing its application in patient stratification for pneumonia, survival analysis, cardiovascular risk evaluation, and bias detection in EHRs, with the goal of standardizing analysis pipelines in biomedical research.
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Interleukin-22 Promotes Cell Proliferation to Combat Virus Infection in Human Intestinal Epithelial Cells.

J Interferon Cytokine Res

October 2024

Department of Molecular Genetics and Microbiology, College of Medicine, University of Florida, Gainesville, Florida, USA.

Interferon lambdas (IFN-λs) are crucial to control virus infections at mucosal surfaces. Interleukin-22 (IL-22) was reported to help IFN-λ control rotavirus infection in the intestinal epithelium of mice either by aiding in the induction of interferon-stimulated genes (ISGs) or by increasing cell proliferation thereby clearing virally infected cells. We investigated whether IL-22 and IFN-λs exhibit similar synergistic effects in human intestinal epithelial cells (IECs) models.

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Superresolution microscopy localizes endogenous Dvl2 to Wnt signaling-responsive biomolecular condensates.

Proc Natl Acad Sci U S A

July 2022

Division of Signaling and Functional Genomics, German Cancer Research Center and Department of Cell and Molecular Biology, Heidelberg University and BioQuant, 69120 Heidelberg, Germany.

During organismal development, homeostasis, and disease, Dishevelled (Dvl) proteins act as key signaling factors in beta-catenin-dependent and beta-catenin-independent Wnt pathways. While their importance for signal transmission has been genetically demonstrated in many organisms, our mechanistic understanding is still limited. Previous studies using overexpressed proteins showed Dvl localization to large, punctate-like cytoplasmic structures that are dependent on its DIX domain.

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Here, as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, for which whole-genome and-for a subset-whole-transcriptome sequencing data from 2,658 cancers across 38 tumor types was aggregated, we systematically investigated potential viral pathogens using a consensus approach that integrated three independent pipelines. Viruses were detected in 382 genome and 68 transcriptome datasets. We found a high prevalence of known tumor-associated viruses such as Epstein-Barr virus (EBV), hepatitis B virus (HBV) and human papilloma virus (HPV; for example, HPV16 or HPV18).

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In this Article, author Benedikt Brors was erroneously associated with affiliation number '8' (Department of Developmental Neurobiology, St Jude Children's Research Hospital, Memphis, Tennessee, USA); the author's two other affiliations (affiliations '3' and '7', both at the German Cancer Research Center (DKFZ)) were correct. This has been corrected online.

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Pan-cancer analyses that examine commonalities and differences among various cancer types have emerged as a powerful way to obtain novel insights into cancer biology. Here we present a comprehensive analysis of genetic alterations in a pan-cancer cohort including 961 tumours from children, adolescents, and young adults, comprising 24 distinct molecular types of cancer. Using a standardized workflow, we identified marked differences in terms of mutation frequency and significantly mutated genes in comparison to previously analysed adult cancers.

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Leiomyosarcoma (LMS) is an aggressive mesenchymal malignancy with few therapeutic options. The mechanisms underlying LMS development, including clinically actionable genetic vulnerabilities, are largely unknown. Here we show, using whole-exome and transcriptome sequencing, that LMS tumors are characterized by substantial mutational heterogeneity, near-universal inactivation of TP53 and RB1, widespread DNA copy number alterations including chromothripsis, and frequent whole-genome duplication.

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