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Klaus-Peter Janssen

Researcher at Technische Universität München

Publications -  143
Citations -  11627

Klaus-Peter Janssen is an academic researcher from Technische Universität München. The author has contributed to research in topics: Medicine & Wnt signaling pathway. The author has an hindex of 45, co-authored 124 publications receiving 8982 citations. Previous affiliations of Klaus-Peter Janssen include Centre national de la recherche scientifique & Curie Institute.

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Cell-of-Origin Patterns Dominate the Molecular Classification of 10,000 Tumors from 33 Types of Cancer.

Katherine A Hoadley, +738 more
- 05 Apr 2018 - 
TL;DR: Molecular similarities among histologically or anatomically related cancer types provide a basis for focused pan-cancer analyses, such as pan-gastrointestinal, Pan-gynecological, pan-kidney, and pan-squamous cancers, and those related by stemness features, which may inform strategies for future therapeutic development.
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Integrated Genomic Characterization of Pancreatic Ductal Adenocarcinoma

Benjamin J. Raphael, +265 more
- 14 Aug 2017 - 
TL;DR: An integrated multi-platform analysis of 150 pancreatic ductal adenocarcinoma specimens reveals a complex molecular landscape of PDAC and provides a roadmap for precision medicine.
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Tissue-specific and inducible cre-mediated recombination in the gut epithelium

TL;DR: Transgenic mice bearing a tamoxifen‐dependent Cre recombinase (vil‐Cre‐ERT2) expressed under the control of the villin promoter were created to perform targeted spatiotemporally controlled somatic recombination of target genes in the mouse digestive epithelium.
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Genomic and Functional Approaches to Understanding Cancer Aneuploidy

Alison M. Taylor, +732 more
- 09 Apr 2018 - 
TL;DR: The genomic and phenotypic correlates of cancer aneuploidy are defined and genome engineering is applied to delete 3p in lung cells, causing decreased proliferation rescued in part by chromosome 3 duplication.
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Induction of HDAC2 expression upon loss of APC in colorectal tumorigenesis.

TL;DR: Findings point toward HDAC2 as a particularly relevant potential target in cancer therapy because it is required for, and sufficient on its own to prevent, apoptosis of colonic cancer cells.