The sensitivity of the Ewing's sarcoma family of tumours to fenretinide-induced cell death is increased by EWS-Fli1-dependent modulation of p38(MAPK) activity (Q28240934)

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scientific article (publication date: 7 February 2008)

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English	The sensitivity of the Ewing's sarcoma family of tumours to fenretinide-induced cell death is increased by EWS-Fli1-dependent modulation of p38(MAPK) activity	scientific article (publication date: 7 February 2008)

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The sensitivity of the Ewing's sarcoma family of tumours to fenretinide-induced cell death is increased by EWS-Fli1-dependent modulation of p38(MAPK) activity (English)

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S S Myatt

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S A Burchill

2

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publication date

7 February 2008

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27

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7

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985-96

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p38MAPK-Dependent sensitivity of Ewing's sarcoma family of tumors to fenretinide-induced cell death

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Expression profiling of EWS/FLI identifies NKX2.2 as a critical target gene in Ewing's sarcoma

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HIV-1 can escape from RNA interference by evolving an alternative structure in its RNA genome

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Inhibition of apoptosis by normal and aberrant Fli-1 and erg proteins involved in human solid tumors and leukemias

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Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases

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Implication of mitochondria-derived ROS and cardiolipin peroxidation in N-(4-hydroxyphenyl)retinamide-induced apoptosis

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Enhanced ROS production in oncogenically transformed cells potentiates c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation and sensitization to genotoxic stress

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The chemopreventive agent N-(4-hydroxyphenyl)retinamide induces apoptosis through a mitochondrial pathway regulated by proteins from the Bcl-2 family

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Ewing's sarcoma: diagnostic, prognostic, and therapeutic implications of molecular abnormalities

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Expression of the EWS/FLI-1 oncogene in murine primary bone-derived cells Results in EWS/FLI-1-dependent, ewing sarcoma-like tumors

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Targeting of EWS/FLI-1 by RNA interference attenuates the tumor phenotype of Ewing's sarcoma cells in vitro

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Randomized trial of fenretinide (4-HPR) to prevent recurrences, new localizations and carcinomas in patients operated on for oral leukoplakia: long-term results.

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Fenretinide: a p53-independent way to kill cancer cells

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Small interfering RNAs expressed from a Pol III promoter suppress the EWS/Fli-1 transcript in an Ewing sarcoma cell line

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Kinase signaling cascades in the mitochondrion: a matter of life or death.

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Inhibition of mammalian target of rapamycin activates apoptosis signal-regulating kinase 1 signaling by suppressing protein phosphatase 5 activity

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Sequence-specific knockdown of EWS-FLI1 by targeted, nonviral delivery of small interfering RNA inhibits tumor growth in a murine model of metastatic Ewing's sarcoma

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EWS-FLI1 fusion protein up-regulates critical genes in neural crest development and is responsible for the observed phenotype of Ewing's family of tumors

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N-(4-hydroxyphenyl)retinamide-induced apoptosis triggered by reactive oxygen species is mediated by activation of MAPKs in head and neck squamous carcinoma cells

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Fenretinide: a prototype cancer prevention drug

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The possible role of EWS-Fli1 in evasion of senescence in Ewing family tumors.

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Ewing sarcoma 11;22 translocation produces a chimeric transcription factor that requires the DNA-binding domain encoded by FLI1 for transformation.

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Improving the efficiency of RNA interference in mammals

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N-(4-hydroxyphenyl)retinamide increases ceramide and is cytotoxic to acute lymphoblastic leukemia cell lines, but not to non-malignant lymphocytes.

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Fenretinide induces sustained-activation of JNK/p38 MAPK and apoptosis in a reactive oxygen species-dependent manner in neuroblastoma cells

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Phase II chemoprevention trial of oral fenretinide in patients at risk for adenocarcinoma of the prostate.

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EWS/FLI-1 silencing and gene profiling of Ewing cells reveal downstream oncogenic pathways and a crucial role for repression of insulin-like growth factor binding protein 3.

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N-(4-Hydroxyphenyl)retinamide is more potent than other phenylretinamides in inhibiting the growth of BRCA1-mutated breast cancer cells

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Roles of MAPKKK ASK1 in stress-induced cell death.

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Divergent Ewing's sarcoma EWS/ETS fusions confer a common tumorigenic phenotype on NIH3T3 cells

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ASK1 is required for sustained activations of JNK/p38 MAP kinases and apoptosis

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Redox control of cell death

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Phase I trial of oral fenretinide in children with high-risk solid tumors: a report from the Children's Oncology Group (CCG 09709).

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Basic fibroblast growth factor-induced cell death is effected through sustained activation of p38MAPK and up-regulation of the death receptor p75NTR.

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Sphingolipid signaling and redox regulation

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Clinical trials with retinoids for breast cancer chemoprevention

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The Ewing Family of Tumors -- A Subgroup of Small-Round-Cell Tumors Defined by Specific Chimeric Transcripts

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Neuroblastoma cell detection by reverse transcriptase-polymerase chain reaction (RT-PCR) for tyrosine hydroxylase mRNA

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Five-year administration of fenretinide: pharmacokinetics and effects on plasma retinol concentrations

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Mechanism of fenretinide (4-HPR)-induced cell death

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10.1038/SJ.ONC.1210705

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10.1038/sj.onc.1210705

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