Heparin-binding epidermal growth factor-like growth factor eliminates constraints on activated Kras to promote rapid onset of pancreatic neoplasia. - Wikidata - awgldk - TriplyDB

Heparin-binding epidermal growth factor-like growth factor eliminates constraints on activated Kras to promote rapid onset of pancreatic neoplasia.

Heparin-binding epidermal growth factor-like growth factor eliminates constraints on activated Kras to promote rapid onset of pancreatic neoplasia.

http://www.wikidata.org/entity/Q41966212

about

Utilizing past and present mouse systems to engineer more relevant pancreatic cancer models The secret origins and surprising fates of pancreas tumors Mutant KRAS-induced expression of ICAM-1 in pancreatic acinar cells causes attraction of macrophages to expedite the formation of precancerous lesions.Smoking accelerates pancreatic cancer progression by promoting differentiation of MDSCs and inducing HB-EGF expression in macrophages.BAG3 promotes pancreatic ductal adenocarcinoma growth by activating stromal macrophages.Myeloid cells are required for PD-1/PD-L1 checkpoint activation and the establishment of an immunosuppressive environment in pancreatic cancer Fibrogenesis in pancreatic cancer is a dynamic process regulated by macrophage-stellate cell interaction.A microRNA signature in circulating exosomes is superior to exosomal glypican-1 levels for diagnosing pancreatic cancer.Identification of M2 macrophages in anterior pituitary glands of normal rats and rats with estrogen-induced prolactinoma.New Insights into Diabetes Cell Therapy.The impact of hypoxia in pancreatic cancer invasion and metastasis.Loss of HNF6 expression correlates with human pancreatic cancer progression.The Arkadia-ESRP2 axis suppresses tumor progression: analyses in clear-cell renal cell carcinoma HBEGF promotes gliomagenesis in the context of Ink4a/Arf and Pten loss.Epithelial-Myeloid cell crosstalk regulates acinar cell plasticity and pancreatic remodeling in mice.Oncogenic KRAS and the EGFR loop in pancreatic carcinogenesis-A connection to licensing nodes.Myeloid-derived macrophages and secreted HSP90α induce pancreatic ductal adenocarcinoma development.[Cellular therapy of diabetes: focus on the latest developments].

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Heparin-binding epidermal growth factor-like growth factor eliminates constraints on activated Kras to promote rapid onset of pancreatic neoplasia.

http://www.wikidata.org/entity/Q41966212

description

2013 nî lūn-bûn

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name

Heparin-binding epidermal grow ...... onset of pancreatic neoplasia.

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Heparin-binding epidermal grow ...... onset of pancreatic neoplasia.

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Heparin-binding epidermal grow ...... onset of pancreatic neoplasia.

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Heparin-binding epidermal grow ...... onset of pancreatic neoplasia

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A L Means

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C J Weaver

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F L Revetta

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H C Crawford

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L R Bridges

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M K Washington

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P2860

The role of the transcriptional regulator Ptf1a in converting intestinal to pancreatic progenitors

Activation of HER4 by heparin-binding EGF-like growth factor stimulates chemotaxis but not proliferation

A heparin-binding growth factor secreted by macrophage-like cells that is related to EGF

Lessons from hereditary colorectal cancer

Most human carcinomas of the exocrine pancreas contain mutant c-K-ras genes

EGF receptor is required for KRAS-induced pancreatic tumorigenesis

CD40 agonists alter tumor stroma and show efficacy against pancreatic carcinoma in mice and humans

Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice

Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse

Beta-catenin blocks Kras-dependent reprogramming of acini into pancreatic cancer precursor lesions in mice.

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10.1038/ONC.2013.3

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M Elizabeth Moss

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