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Correspondence: Dr D Tang, Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA E-mail: [email protected]; Dr HJ Zeh, Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.

E-mail: [email protected]; Professor MT Lotze, University of Pittsburgh Cancer Institute, G.27A Hillman Cancer Center, 5117 Centre Avenue, Pittsburgh, PA 15213, USA.

These lead to inflammatory nucleosome release and propagate K-Ras-driven pancreatic tumorigenesis.

Extracellular nucleosomes promote interleukin 6 (IL-6) secretion by infiltrating macrophages/neutrophils and enhance oncogenic K-Ras signaling activation in pancreatic lesions.

Conditional genetic ablation of either single or both alleles of HMGB1 in the pancreas renders mice extremely sensitive to oncogenic K-Ras-driven initiation of precursor lesions at birth, including pancreatic intraepithelial neoplasms, intraductal papillary mucinous neoplasms, and mucinous cystic neoplasms.

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