Constitutive expression of c-FLIP in Hodgkin and Reed-Sternberg cells. - Wikidata - awgldk - TriplyDB

Constitutive expression of c-FLIP in Hodgkin and Reed-Sternberg cells.

Constitutive expression of c-FLIP in Hodgkin and Reed-Sternberg cells.

http://www.wikidata.org/entity/Q35788898

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Critical role for Fas-associated death domain-like interleukin-1-converting enzyme-like inhibitory protein in anoikis resistance and distant tumor formation Expression of the cellular FLICE-inhibitory protein (c-FLIP) protects Hodgkin's lymphoma cells from autonomous Fas-mediated death Predictive value of Sp1/Sp3/FLIP signature for prostate cancer recurrence.The role of cellular FLICE inhibitory protein (c-FLIP) in the pathogenesis and treatment of cancer.Expression of cellular FLICE-inhibitory protein and its association with p53 mutation in colon cancer.Cellular FLICE-inhibitory protein: an attractive therapeutic target?c-FLIP mediates resistance of Hodgkin/Reed-Sternberg cells to death receptor-induced apoptosis.Targeting cellular FLICE-like inhibitory protein as a novel approach to the treatment of Hodgkin's lymphoma.Recent insights into the biology of Hodgkin lymphoma: unraveling the mysteries of the Reed-Sternberg cell.Contribution of the Epstein Barr virus to the molecular pathogenesis of Hodgkin lymphoma.FLIP as an anti-cancer therapeutic target.Expression and biological significance of c-FLIP in human hepatocellular carcinomas Treatment of Hodgkin lymphoma: the past, present, and future.Biologic features of Hodgkin lymphoma and the development of biologic prognostic factors in Hodgkin lymphoma: tumor and microenvironment.Direct repression of FLIP expression by c-myc is a major determinant of TRAIL sensitivity.Non-Hodgkin's B-cell lymphoma: advances in molecular strategies targeting drug resistance.Mutations of NFKBIA, encoding IkappaB alpha, are a recurrent finding in classical Hodgkin lymphoma but are not a unifying feature of non-EBV-associated cases.The side population, as a precursor of Hodgkin and Reed-Sternberg cells and a target for nuclear factor-κB inhibitors in Hodgkin's lymphoma.Caspase-8 and its inhibitors in RCCs in vivo: the prominent role of ARC.Curcumin induces cell-arrest and apoptosis in association with the inhibition of constitutively active NF-kappaB and STAT3 pathways in Hodgkin's lymphoma cells.IkappaBalpha independent induction of NF-kappaB and its inhibition by DHMEQ in Hodgkin/Reed-Sternberg cells.cIAP2 is highly expressed in Hodgkin-Reed-Sternberg cells and inhibits apoptosis by interfering with constitutively active caspase-3.Rapid turnover of c-FLIPshort is determined by its unique C-terminal tail.FLIP is frequently expressed in endometrial carcinoma and has a role in resistance to TRAIL-induced apoptosis.FLIP overexpression inhibits death receptor-induced apoptosis in malignant mesothelial cells.Heat stress downregulates FLIP and sensitizes cells to Fas receptor-mediated apoptosis.C/EBPalpha or C/EBPalpha oncoproteins regulate the intrinsic and extrinsic apoptotic pathways by direct interaction with NF-kappaB p50 bound to the bcl-2 and FLIP gene promoters.Low frequency of FAS mutations in Reed-Sternberg cells of Hodgkin's lymphoma Involvement of FLIP in 2-methoxyestradiol-induced tumor regression in transgenic adenocarcinoma of mouse prostate model.The Epstein-Barr virus oncoprotein, latent membrane protein-1, reprograms germinal centre B cells towards a Hodgkin's Reed-Sternberg-like phenotype.STAT3 is essential for Hodgkin lymphoma cell proliferation and is a target of tyrphostin AG17 which confers sensitization for apoptosis.Resistance to Fas-mediated apoptosis is restored by cycloheximide through the downregulation of cellular FLIPL in NK/T-cell lymphoma.c-FLIP expression in colorectal carcinomas: association with Fas/FasL expression and prognostic implications.Increased expression of FLIP, an inhibitor of Fas-mediated apoptosis, in stomach cancer.Apoptosis-resistant phenotype of classical Hodgkin's lymphoma is not mediated by somatic mutations within genes encoding members of the death-inducing signaling complex (DISC).Troglitazone sensitizes tumor cells to TRAIL-induced apoptosis via down-regulation of FLIP and Survivin.cFLIP expression correlates with tumour progression and patient outcome in non-Hodgkin lymphomas of low grade of malignancy Analysis of NF-κB Pathway Proteins in Pediatric Hodgkin Lymphoma: Correlations with EBV Status and Clinical Outcome—A Children's Oncology Group Study

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Constitutive expression of c-FLIP in Hodgkin and Reed-Sternberg cells.

http://www.wikidata.org/entity/Q35788898

description

2002 nî lūn-bûn

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年论文

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2002年论文

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2002年论文

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name

Constitutive expression of c-FLIP in Hodgkin and Reed-Sternberg cells.

@ast

Constitutive expression of c-FLIP in Hodgkin and Reed-Sternberg cells.

@en

type

label

Constitutive expression of c-FLIP in Hodgkin and Reed-Sternberg cells.

@ast

Constitutive expression of c-FLIP in Hodgkin and Reed-Sternberg cells.

@en

prefLabel

Constitutive expression of c-FLIP in Hodgkin and Reed-Sternberg cells.

@ast

Constitutive expression of c-FLIP in Hodgkin and Reed-Sternberg cells.

@en

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S0002-9440(10)62578-3

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The American Journal of Pathology

P1476

Constitutive expression of c-FLIP in Hodgkin and Reed-Sternberg cells.

@en

P2093

Andreas Draube

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Anne Kallenborn

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Claudia Wickenhauser

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Daniel Re

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Jürgen Wolf

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Martina Vockerodt

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Roman Kurt Thomas

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Volker Diehl

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P2860

Inhibition of death receptor signals by cellular FLIP

FLICE is activated by association with the CD95 death-inducing signaling complex (DISC).

FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death--inducing signaling complex

The role of c-FLIP in modulation of CD95-induced apoptosis

The Fas death factor

Fas gene mutations in the Canale-Smith syndrome, an inherited lymphoproliferative disorder associated with autoimmunity.

Autoimmunity as a consequence of retrovirus-mediated expression of C-FLIP in lymphocytes.

Activation of NF-kappaB by FADD, Casper, and caspase-8.

Overexpression of I kappa B alpha without inhibition of NF-kappaB activity and mutations in the I kappa B alpha gene in Reed-Sternberg cells.

Hodgkin and Reed-Sternberg cells in Hodgkin's disease represent the outgrowth of a dominant tumor clone derived from (crippled) germinal center B cells.

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1521-1528

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4

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160

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Joachim Schultze

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2002-04-01T00:00:00Z

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11943736

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1867202

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