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Jochen Hess

Researcher at German Cancer Research Center

Publications -  125
Citations -  6990

Jochen Hess is an academic researcher from German Cancer Research Center. The author has contributed to research in topics: Head and neck squamous-cell carcinoma & Cancer. The author has an hindex of 39, co-authored 110 publications receiving 6071 citations. Previous affiliations of Jochen Hess include University of Würzburg & Heidelberg University.

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A pro-tumorigenic function of S100A8/A9 in carcinogen-induced hepatocellular carcinoma.

TL;DR: It is found that tumor cell proliferation was diminished in the absence of S100A8/A9, leading to significant reduction of tumor size, demonstrating that calprotectin is required for the progression of non- inflammation driven liver tumor and might represent a therapeutic target for the treatment of HCC formed in non-cirrhotic liver.
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Integrative Analysis of Multi-omics Data Identified EGFR and PTGS2 as Key Nodes in a Gene Regulatory Network Related to Immune Phenotypes in Head and Neck Cancer.

TL;DR: The data highlight a complex interplay between genetic and epigenetic events in the establishment of the tumor immune phenotype and provide compelling experimental evidence that a patient with squamous cell carcinoma of the head and neck at higher risk for ICI treatment failure might benefit from a combination with EGFR inhibition.
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Efficient keratinocyte differentiation strictly depends on JNK-induced soluble factors in fibroblasts

TL;DR: Results imply that mesenchymal JNK has a pivotal role in the paracrine cross talk between dermal fibroblasts and epidermal keratinocytes during wound healing, and demonstrate that efficient keratinocyte terminal differentiation requires constant presence of JNK-dependent and fibroblast-derived soluble factors.
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Keratinocyte-specific deletion of the receptor RAGE modulates the kinetics of skin inflammation in vivo.

TL;DR: It is shown that RAGE expression in cutaneous keratinocytes modulates the strength and kinetics of acute inflammation and supports the maintenance of epidermal keratinocyte activation, and the central role of RAGE in paracrine communication between Keratinocytes and stromal immune cells is supported.