Luteolin inhibits pancreatitis‑induced acinar‑ductal metaplasia, proliferation and epithelial‑mesenchymal transition of acinar cells. (scientific article)

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MAPK signaling is required for dedifferentiation of acinar cells and development of pancreatic intraepithelial neoplasia in mice

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PI3K regulation of RAC1 is required for KRAS-induced pancreatic tumorigenesis in mice

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Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia

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Canonical wnt signaling is required for pancreatic carcinogenesis

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STAT3 plays a critical role in KRAS-induced pancreatic tumorigenesis.

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Membrane-bound heparin-binding epidermal growth factor like growth factor regulates E-cadherin expression in pancreatic carcinoma cells

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Luteolin sensitizes tumor necrosis factor-alpha-induced apoptosis in human tumor cells.

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Identification of Sox9-dependent acinar-to-ductal reprogramming as the principal mechanism for initiation of pancreatic ductal adenocarcinoma

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Luteolin decreases invasiveness, deactivates STAT3 signaling, and reverses interleukin-6 induced epithelial-mesenchymal transition and matrix metalloproteinase secretion of pancreatic cancer cells

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The ZEB1/miR-200 feedback loop controls Notch signalling in cancer cells.

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Differential effects of caspase-1/interleukin-1beta-converting enzyme on acinar cell necrosis and apoptosis in severe acute experimental pancreatitis

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Luteolin inhibits vascular endothelial growth factor-induced angiogenesis; inhibition of endothelial cell survival and proliferation by targeting phosphatidylinositol 3'-kinase activity.

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Pancreatitis and the risk of pancreatic cancer.

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Pancreatic Cancer

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