MyD88 inhibition amplifies dendritic cell capacity to promote pancreatic carcinogenesis via Th2 cells. - Wikidata - awgldk - TriplyDB

MyD88 inhibition amplifies dendritic cell capacity to promote pancreatic carcinogenesis via Th2 cells.

MyD88 inhibition amplifies dendritic cell capacity to promote pancreatic carcinogenesis via Th2 cells.

http://www.wikidata.org/entity/Q36193536

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Targeting inflammation in pancreatic cancer: Clinical translation Genetics and biology of pancreatic ductal adenocarcinoma Roles of Commensal Microbiota in Pancreas Homeostasis and Pancreatic Pathologies Pattern Recognition Receptors in Cancer Progression and Metastasis Role of bacterial infections in pancreatic cancer The Yin and Yang of Toll-like receptors in cancer Exploiting inflammation for therapeutic gain in pancreatic cancer Environmental risk factors for pancreatic cancer: an update.The intestinal microbiome and surgical disease.Inhibition of Myeloid Differentiation Factor 88 Reduces Human and Mouse T-Cell Interleukin-17 and IFNγ Production and Ameliorates Experimental Autoimmune Encephalomyelitis Induced in Mice Immunotherapy in pancreatic cancer: Unleash its potential through novel combinations.Pancreatic cancer, inflammation, and microbiome.Microbiota, oral microbiome, and pancreatic cancer.Discovering the route from inflammation to pancreatic cancer.The microbiome and cancer.Macrophage polarization in pancreatic carcinoma: role of heparanase enzyme.Innate sensing of microbial products promotes wound-induced skin cancer Ginseng Berry Extract Promotes Maturation of Mouse Dendritic Cells.TGF-β Blockade Reduces Mortality and Metabolic Changes in a Validated Murine Model of Pancreatic Cancer Cachexia Increased expression of the interleukin-1 receptor-associated kinase (IRAK)-1 is associated with adipose tissue inflammatory state in obesity Biological Mechanisms for the Effect of Obesity on Cancer Risk: Experimental Evidence.Effect of myeloid differentiation primary response gene 88 on expression profiles of genes during the development and progression of Helicobacter-induced gastric cancer TLR9 ligation in pancreatic stellate cells promotes tumorigenesis Dectin-1 Regulates Hepatic Fibrosis and Hepatocarcinogenesis by Suppressing TLR4 Signaling Pathways EBV-encoded RNA via TLR3 induces inflammation in nasopharyngeal carcinoma.Combination OX40 agonism/CTLA-4 blockade with HER2 vaccination reverses T-cell anergy and promotes survival in tumor-bearing mice.Activation of TLR4 is required for the synergistic induction of dual oxidase 2 and dual oxidase A2 by IFN-γ and lipopolysaccharide in human pancreatic cancer cell lines.Expanding roles for CD4 T cells and their subpopulations in tumor immunity and therapy.The necrosome promotes pancreatic oncogenesis via CXCL1 and Mincle-induced immune suppression.Role of immune cells and immune-based therapies in pancreatitis and pancreatic ductal adenocarcinoma.Radiation Therapy Induces Macrophages to Suppress T-Cell Responses Against Pancreatic Tumors in Mice Diet- and Genetically-induced Obesity Produces Alterations in the Microbiome, Inflammation and Wnt Pathway in the Intestine of Apc+/1638N Mice: Comparisons and Contrasts.MyD88 and its divergent toll in carcinogenesis.Deficiency of the myeloid differentiation primary response molecule MyD88 leads to an early and rapid development of Helicobacter-induced gastric malignancy.Dysregulation of signaling pathways associated with innate antibacterial immunity in patients with pancreatic cancer.The immune network in pancreatic cancer development and progression.Immune cells and immune-based therapy in pancreatitis.Intervention on toll-like receptors in pancreatic cancer.Strategies to relieve immunosuppression in pancreatic cancer.Stromal biology and therapy in pancreatic cancer: a changing paradigm.

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P2860

MyD88 inhibition amplifies dendritic cell capacity to promote pancreatic carcinogenesis via Th2 cells.

http://www.wikidata.org/entity/Q36193536

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name

MyD88 inhibition amplifies den ...... carcinogenesis via Th2 cells.

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MyD88 inhibition amplifies den ...... carcinogenesis via Th2 cells.

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MyD88 inhibition amplifies den ...... carcinogenesis via Th2 cells.

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MyD88 inhibition amplifies den ...... carcinogenesis via Th2 cells.

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MyD88 inhibition amplifies den ...... carcinogenesis via Th2 cells.

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MyD88 inhibition amplifies den ...... carcinogenesis via Th2 cells.

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Journal of Experimental Medicine

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Adeel Rehman

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Andrea S Bedrosian

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Andrew H Nguyen

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Cristina H Hajdu

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Dafna Bar-Sagi

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George Miller

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Harry M Mushlin

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Nina C Fallon

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Saman Zarbakhsh

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Sana Badar

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P2860

Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability

The pancreatic stellate cell: a star on the rise in pancreatic diseases

Regulation of spontaneous intestinal tumorigenesis through the adaptor protein MyD88

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

Toll-like receptors activate innate and adaptive immunity by using dendritic cell-intrinsic and -extrinsic mechanisms

Distinct populations of metastases-enabling myeloid cells expand in the liver of mice harboring invasive and preinvasive intra-abdominal tumor.

Functional linkage of cirrhosis-predictive single nucleotide polymorphisms of Toll-like receptor 4 to hepatic stellate cell responses.

Acute pancreatitis markedly accelerates pancreatic cancer progression in mice expressing oncogenic Kras.

Dual function of MyD88 in RAS signaling and inflammation, leading to mouse and human cell transformation

An illustrated consensus on the classification of pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasms.

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1671-1687

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10.1084/JEM.20111706

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9

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209

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Constantinos P Zambirinis

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2012-08-20T00:00:00Z

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230712414

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22908323

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3428946

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