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Thomas Kirchner

Researcher at University of Erlangen-Nuremberg

Publications -  99
Citations -  8864

Thomas Kirchner is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Helicobacter pylori & Gastric mucosa. The author has an hindex of 40, co-authored 99 publications receiving 8517 citations. Previous affiliations of Thomas Kirchner include University of Würzburg.

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The Vienna classification of gastrointestinal epithelial neoplasia

TL;DR: The differences between Western and Japanese pathologists in the diagnostic classification of gastrointestinal epithelial neoplastic lesions can be resolved largely by adopting the proposed terminology, which is based on cytological and architectural severity and invasion status.
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Migrating cancer stem cells — an integrated concept of malignant tumour progression

TL;DR: An extended, integrated model that is consistent with all aspects of human tumour progression is suggested — the 'migrating cancer stem (MCS)-cell' concept.
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β-Catenin Regulates the Expression of the Matrix Metalloproteinase-7 in Human Colorectal Cancer

TL;DR: The identification of the matrix metalloproteinase MMP-7 as another target gene of β-catenin/TCF-4 is reported, indicating that defects in the APC tumor suppressor gene may also have an influence on later steps of colon tumor progression.
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Impaired uptake of apoptotic cells into tingible body macrophages in germinal centers of patients with systemic lupus erythematosus.

TL;DR: It is suggested that in a sub-group of SLE patients, apoptotic cells are not properly cleared by tingible body macrophages of the GCs, and nuclear autoantigens bind to FDCs and may thus provide survival signals for autoreactive B cells.
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Nuclear Overexpression of the Oncoprotein β-Catenin in Colorectal Cancer is Localized Predominantly at the Invasion Front

TL;DR: Using immunohistochemistry, the distribution of overexpressed beta-Catenin within individual colorectal carcinomas was investigated and it was found that surrounding tissue at the invasion front can give signals to the tumor cells, leading to a nuclear translocation of beta- Catenin, where it may play a direct role in tumor invasion processes.