Molecular mechanisms of hepatocarcinogenesis in transgenic mouse models of liver cancer. - Wikidata - wikimedia - TriplyDB

Molecular mechanisms of hepatocarcinogenesis in transgenic mouse models of liver cancer.

Molecular mechanisms of hepatocarcinogenesis in transgenic mouse models of liver cancer.

http://www.wikidata.org/entity/Q36086444

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Mouse models of liver cancer: Progress and recommendations MYC activation is a hallmark of cancer initiation and maintenance Global gene profiling of spontaneous hepatocellular carcinoma in B6C3F1 mice: similarities in the molecular landscape with human liver cancer The cell polarity protein Scrib functions as a tumor suppressor in liver cancer.Hepatocyte IKKbeta/NF-kappaB inhibits tumor promotion and progression by preventing oxidative stress-driven STAT3 activation Inactivation of MYC reverses tumorigenesis.Application of magnetic resonance imaging in transgenic and chemical mouse models of hepatocellular carcinoma.TGF-beta inactivation and TGF-alpha overexpression cooperate in an in vivo mouse model to induce hepatocellular carcinoma that recapitulates molecular features of human liver cancer miRNAs affect the development of hepatocellular carcinoma via dysregulation of their biogenesis and expression.Non-mammalian fat-1 gene prevents neoplasia when introduced to a mouse hepatocarcinogenesis model: Omega-3 fatty acids prevent liver neoplasia.Postnatal liver growth and regeneration are independent of c-myc in a mouse model of conditional hepatic c-myc deletion Gremlin in the pathogenesis of hepatocellular carcinoma complicating chronic hepatitis C: an immunohistochemical and PCR study of human liver biopsies.Loss of hepatic NF-kappa B activity enhances chemical hepatocarcinogenesis through sustained c-Jun N-terminal kinase 1 activation β-catenin accumulation in nuclei of hepatocellular carcinoma cells up-regulates glutathione-s-transferase M3 mRNA.Transgenic mouse model expressing P53(R172H), luciferase, EGFP, and KRAS(G12D) in a single open reading frame for live imaging of tumor.Minimal cooperation between mutant Hras and c-myc or TGFα in the regulation of mouse hepatocyte growth or transformation in vivo.A cell-penetrating ARF peptide inhibitor of FoxM1 in mouse hepatocellular carcinoma treatment.Molecular characterization of hepatocarcinogenesis using mouse models Gadoxetate acid-enhanced MRI of hepatocellular carcinoma in a c-myc/TGFα transgenic mouse model including signal intensity and fat content: initial experience.The PPAR alpha-humanized mouse: a model to investigate species differences in liver toxicity mediated by PPAR alpha.In vivo MRS assessment of altered fatty acyl unsaturation in liver tumor formation of a TGF alpha/c-myc transgenic mouse model.Queuosine modification of tRNA: its divergent role in cellular machinery.In vivo Reprogramming of Cancer Metabolism by MYC.Reviewing once more the c-myc and Ras collaboration: converging at the cyclin D1-CDK4 complex and challenging basic concepts of cancer biology.Hepatic overexpression of cAMP-responsive element modulator α induces a regulatory T-cell response in a murine model of chronic liver disease.Animal models of biliary injury and altered bile acid metabolism.Low-level shRNA cytotoxicity can contribute to MYC-induced hepatocellular carcinoma in adult mice.Aberrant iNOS signaling is under genetic control in rodent liver cancer and potentially prognostic for the human disease.Molecular Link between Liver Fibrosis and Hepatocellular Carcinoma.Induced differentiation of hepatocellular carcinoma by natural products.Epigenetic effects of ethanol on liver and gastrointestinal injury.Targeting mitogen-activated protein kinase kinase with the inhibitor PD0325901 decreases hepatocellular carcinoma growth in vitro and in mouse model systems.Dysregulation of the Hedgehog pathway in human hepatocarcinogenesis.Preventive Effects of Vitamin C on Diethylnitrosamine-induced Hepatotoxicity in Smp30 Knockout Mice.Molecular Mechanisms of Hepatocarcinogenesis Following Sustained Virological Response in Patients with Chronic Hepatitis C Virus Infection Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) is an important protumorigenic factor in hepatocellular carcinoma

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Molecular mechanisms of hepatocarcinogenesis in transgenic mouse models of liver cancer.

http://www.wikidata.org/entity/Q36086444

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Molecular mechanisms of hepatocarcinogenesis in transgenic mouse models of liver cancer.

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Molecular mechanisms of hepatocarcinogenesis in transgenic mouse models of liver cancer.

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Molecular mechanisms of hepatocarcinogenesis in transgenic mouse models of liver cancer.

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Molecular mechanisms of hepatocarcinogenesis in transgenic mouse models of liver cancer.

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Molecular mechanisms of hepatocarcinogenesis in transgenic mouse models of liver cancer.

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Toxicologic Pathology

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Molecular mechanisms of hepatocarcinogenesis in transgenic mouse models of liver cancer.

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Diego F Calvisi

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Snorri S Thorgeirsson

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P2860

Beta-catenin mutations are associated with a subset of low-stage hepatocellular carcinoma negative for hepatitis B virus and with favorable prognosis

Function and activation of NF-kappa B in the immune system

Somatic mutations of the beta-catenin gene are frequent in mouse and human hepatocellular carcinomas

Vitamin E reduces chromosomal damage and inhibits hepatic tumor formation in a transgenic mouse model

Nonrandom cytogenetic alterations in hepatocellular carcinoma from transgenic mice overexpressing c-Myc and transforming growth factor-alpha in the liver.

Acceleration of c-myc-induced hepatocarcinogenesis by Co-expression of transforming growth factor (TGF)-alpha in transgenic mice is associated with TGF-beta1 signaling disruption.

Transforming growth factor-beta: possible roles in carcinogenesis.

Genetic alterations associated with hepatocellular carcinomas define distinct pathways of hepatocarcinogenesis.

Disruption of beta-catenin pathway or genomic instability define two distinct categories of liver cancer in transgenic mice.

Disruption of redox homeostasis in the transforming growth factor-alpha/c-myc transgenic mouse model of accelerated hepatocarcinogenesis.

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