Sorafenib and vorinostat kill colon cancer cells by CD95-dependent and -independent mechanisms. - Wikidata - awgldk - TriplyDB

Sorafenib and vorinostat kill colon cancer cells by CD95-dependent and -independent mechanisms.

Sorafenib and vorinostat kill colon cancer cells by CD95-dependent and -independent mechanisms.

http://www.wikidata.org/entity/Q37268127

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Ceramide synthases at the centre of sphingolipid metabolism and biology Mammalian ceramide synthases A critical role for ceramide synthase 2 in liver homeostasis: II. insights into molecular changes leading to hepatopathy Modulation of Autophagy by Sorafenib: Effects on Treatment Response c-FLIP, a master anti-apoptotic regulator Sorafenib inhibits epithelial-mesenchymal transition through an epigenetic-based mechanism in human lung epithelial cells Sorafenib and HDAC inhibitors synergize with TRAIL to kill tumor cells.Autophagy and cancer therapy.The pleiotropic roles of sphingolipid signaling in autophagy Autophagic Mechanism in Anti-Cancer Immunity: Its Pros and Cons for Cancer Therapy.A natural BH3 mimetic induces autophagy in apoptosis-resistant prostate cancer via modulating Bcl-2-Beclin1 interaction at endoplasmic reticulum.Interdiction of sphingolipid metabolism to improve standard cancer therapies.Histone Deacetylase Inhibitors: Advancing Therapeutic Strategies in Hematological and Solid Malignancies.Bcl2L13 is a ceramide synthase inhibitor in glioblastoma.Sorafenib enhances pemetrexed cytotoxicity through an autophagy-dependent mechanism in cancer cells.PHY906(KD018), an adjuvant based on a 1800-year-old Chinese medicine, enhanced the anti-tumor activity of Sorafenib by changing the tumor microenvironment.Targeting the Anti-Apoptotic Protein c-FLIP for Cancer Therapy.Expression of Ceramide Synthase 6 Transcriptionally Activates Acid Ceramidase in a c-Jun N-terminal Kinase (JNK)-dependent Manner Combination of the deacetylase inhibitor panobinostat and the multi-kinase inhibitor sorafenib for the treatment of metastatic hepatocellular carcinoma - review of the underlying molecular mechanisms and first case report.Identification of initial leads directed at the calmodulin-binding region on the Src-SH2 domain that exhibit anti-proliferation activity against pancreatic cancer Endogenous modulators and pharmacological inhibitors of histone deacetylases in cancer therapy.By activating Fas/ceramide synthase 6/p38 kinase in lipid rafts, stichoposide D inhibits growth of leukemia xenografts.Sorafenib and pemetrexed toxicity in cancer cells is mediated via SRC-ERK signaling Synergistic antitumour activity of sorafenib in combination with tetrandrine is mediated by reactive oxygen species (ROS)/Akt signaling.Phase I study of pemetrexed with sorafenib in advanced solid tumors.Recently identified and potential targets for colon cancer treatment.Autophagy and tumorigenesis.The neoadjuvant therapy of colorectal hepatic metastases and the role of biologic sensitizing and resistance factors.Targeting the growth factors and angiogenesis pathways: small molecules in solid tumors.Regulation of autophagy by kinases.PDE5 inhibitors enhance the lethality of [pemetrexed + sorafenib].Sorafenib reverses resistance of gastric cancer to treatment by cisplatin through down-regulating MDR1 expression.Combination of Vorinostat and caspase-8 inhibition exhibits high anti-tumoral activity on endometrial cancer cells.Natural Bcl-2 inhibitor (-)- gossypol induces protective autophagy via reactive oxygen species-high mobility group box 1 pathway in Burkitt lymphoma.Perifosine and sorafenib combination induces mitochondrial cell death and antitumor effects in NOD/SCID mice with Hodgkin lymphoma cell line xenografts.Therapeutic implications of bioactive sphingolipids: A focus on colorectal cancer.Calmodulin mediates Fas-induced FADD-independent survival signaling in pancreatic cancer cells via activation of Src-extracellular signal-regulated kinase (ERK).Vorinostat and sorafenib increase CD95 activation in gastrointestinal tumor cells through a Ca(2+)-de novo ceramide-PP2A-reactive oxygen species-dependent signaling pathway.OSU-03012 enhances Ad.7-induced GBM cell killing via ER stress and autophagy and by decreasing expression of mitochondrial protective proteins.Evaluation of metastatic and angiogenic potentials of human colon carcinoma cells in chick embryo model systems.

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Sorafenib and vorinostat kill colon cancer cells by CD95-dependent and -independent mechanisms.

http://www.wikidata.org/entity/Q37268127

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 29 May 2009

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Sorafenib and vorinostat kill ...... t and -independent mechanisms.

@en

Sorafenib and vorinostat kill ...... t and -independent mechanisms.

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type

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Sorafenib and vorinostat kill ...... t and -independent mechanisms.

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Sorafenib and vorinostat kill ...... t and -independent mechanisms.

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prefLabel

Sorafenib and vorinostat kill ...... t and -independent mechanisms.

@en

Sorafenib and vorinostat kill ...... t and -independent mechanisms.

@nl

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Molecular Pharmacology

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Sorafenib and vorinostat kill ...... t and -independent mechanisms.

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Adly Yacoub

http://www.w3.org/2001/XMLSchema#string

Christina Voelkel-Johnson

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Clint Mitchell

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Margaret A Park

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Martin Graf

http://www.w3.org/2001/XMLSchema#string

Mohamed Rahmani

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Peter J Houghton

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Steven Grant

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Teneille Walker

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P2860

Global cancer statistics, 2002

JNK1-mediated phosphorylation of Bcl-2 regulates starvation-induced autophagy

Bile acid regulation of C/EBPbeta, CREB, and c-Jun function, via the extracellular signal-regulated kinase and c-Jun NH2-terminal kinase pathways, modulates the apoptotic response of hepatocytes.

Differences in the migration capacity of primary human colon carcinoma cells (SW480) and their lymph node metastatic derivatives (SW620).

Deoxycholic acid (DCA) causes ligand-independent activation of epidermal growth factor receptor (EGFR) and FAS receptor in primary hepatocytes: inhibition of EGFR/mitogen-activated protein kinase-signaling module enhances DCA-induced apoptosis.

Histone acetylation and chromatin remodeling.

The histone deacetylase inhibitor valproic acid selectively induces proteasomal degradation of HDAC2

Histone deacetylases.

MAPK pathways in radiation responses.

Radiation and ceramide-induced apoptosis.

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342-355

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scholarly article

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10.1124/MOL.109.056523

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2

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76

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2009-05-29T00:00:00Z

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26254011

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19483104

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2713126

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