Pancreatitis-induced inflammation contributes to pancreatic cancer by inhibiting oncogene-induced senescence. - Wikidata - wikimedia - TriplyDB

Pancreatitis-induced inflammation contributes to pancreatic cancer by inhibiting oncogene-induced senescence.

Pancreatitis-induced inflammation contributes to pancreatic cancer by inhibiting oncogene-induced senescence.

http://www.wikidata.org/entity/Q42573716

about

Targeting inflammation in pancreatic cancer: Clinical translation GEMMs as preclinical models for testing pancreatic cancer therapies Reserve stem cells: Differentiated cells reprogram to fuel repair, metaplasia, and neoplasia in the adult gastrointestinal tract Protein kinase D enzymes: novel kinase targets in pancreatic cancer Vaccines for pancreatic cancer Macroautophagy and the oncogene-induced senescence Genetically engineered mouse models of pancreatic adenocarcinoma Human correlates of provocative questions in pancreatic pathology Disruptive chemicals, senescence and immortality Live imaging and gene expression analysis in zebrafish identifies a link between neutrophils and epithelial to mesenchymal transition Silencing Mist1 Gene Expression Is Essential for Recovery from Acute Pancreatitis Caught in the cross fire: p53 in inflammation.Genetically engineered mouse models in oncology research and cancer medicine Utilizing past and present mouse systems to engineer more relevant pancreatic cancer models Conditional transgenic expression of PIM1 kinase in prostate induces inflammation-dependent neoplasia Interleukin-6 is required for pancreatic cancer progression by promoting MAPK signaling activation and oxidative stress resistance EGF receptor is required for KRAS-induced pancreatic tumorigenesis EMT and dissemination precede pancreatic tumor formation Analysis of mRNA profiles after MEK1/2 inhibition in human pancreatic cancer cell lines reveals pathways involved in drug sensitivity.Aberrant over-expression of TRPM7 ion channels in pancreatic cancer: required for cancer cell invasion and implicated in tumor growth and metastasis Senescent cells communicate via intercellular protein transfer.Reconstituting development of pancreatic intraepithelial neoplasia from primary human pancreas duct cells.MAPK signaling is required for dedifferentiation of acinar cells and development of pancreatic intraepithelial neoplasia in mice.Inflammation to cancer: The molecular biology in the pancreas (Review).The Presence of Interleukin-13 at Pancreatic ADM/PanIN Lesions Alters Macrophage Populations and Mediates Pancreatic Tumorigenesis Pancreatic cancer, inflammation, and microbiome.Cellular senescence and the senescent secretory phenotype: therapeutic opportunities.Pancreatic cancer and its stroma: a conspiracy theory Genetic inactivation of the pancreatitis-inducible gene Nupr1 impairs PanIN formation by modulating Kras(G12D)-induced senescence Depletion of carcinoma-associated fibroblasts and fibrosis induces immunosuppression and accelerates pancreas cancer with reduced survival The transcription factor GLI1 modulates the inflammatory response during pancreatic tissue remodeling Risk factors for pancreatic cancer: underlying mechanisms and potential targets.HPV associated tumor cells control tumor microenvironment and leukocytosis in experimental models Transcriptome analysis of pancreatic cancer reveals a tumor suppressor function for HNF1A.The tumor suppressor rpl36 restrains KRAS(G12V)-induced pancreatic cancer.PI3K regulation of RAC1 is required for KRAS-induced pancreatic tumorigenesis in mice.Discovering the route from inflammation to pancreatic cancer.Stromal disrupting effects of nab-paclitaxel in pancreatic cancer Kras as a key oncogene and therapeutic target in pancreatic cancer Epithelial Notch signaling is a limiting step for pancreatic carcinogenesis.

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Pancreatitis-induced inflammation contributes to pancreatic cancer by inhibiting oncogene-induced senescence.

http://www.wikidata.org/entity/Q42573716

description

2011 nî lūn-bûn

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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2011年论文

@zh

2011年论文

@zh-cn

name

Pancreatitis-induced inflammat ...... g oncogene-induced senescence.

@en

Pancreatitis-induced inflammat ...... g oncogene-induced senescence.

@nl

type

label

Pancreatitis-induced inflammat ...... g oncogene-induced senescence.

@en

Pancreatitis-induced inflammat ...... g oncogene-induced senescence.

@nl

prefLabel

Pancreatitis-induced inflammat ...... g oncogene-induced senescence.

@en

Pancreatitis-induced inflammat ...... g oncogene-induced senescence.

@nl

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J.CCR.2011.05.011

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Pancreatitis-induced inflammat ...... g oncogene-induced senescence.

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Carolina Navas

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Isabel Hernández-Porras

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Mariano Barbacid

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Marta Cañamero

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P2860

Core signaling pathways in human pancreatic cancers revealed by global genomic analyses

SOX9 is required for maintenance of the pancreatic progenitor cell pool

Pancreatic cancer

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.

Effect of daily aspirin on long-term risk of death due to cancer: analysis of individual patient data from randomised trials.

Non-steroidal anti-inflammatory drugs and pancreatic cancer risk: a nested case-control study.

Context-dependent transformation of adult pancreatic cells by oncogenic K-Ras.

Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma.

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