High-throughput mutation profiling of CTCL samples reveals KRAS and NRAS mutations sensitizing tumors toward inhibition of the RAS/RAF/MEK signaling cascade.
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Cutaneous T-cell lymphoma: 2014 update on diagnosis, risk-stratification, and managementCombined targeting of MEK and PI3K/mTOR effector pathways is necessary to effectively inhibit NRAS mutant melanoma in vitro and in vivo.Mutant HRAS as novel target for MEK and mTOR inhibitorsTargeting the mTOR Complex by Everolimus in NRAS Mutant Neuroblastoma.Genome-wide profiling identified a set of miRNAs that are differentially expressed in glioblastoma stem cells and normal neural stem cells.High-throughput mutation profiling of primary and metastatic endometrial cancers identifies KRAS, FGFR2 and PIK3CA to be frequently mutatedImpaired proteasome function activates GATA3 in T cells and upregulates CTLA-4: relevance for Sézary syndromeIdentification of p38β as a therapeutic target for the treatment of Sézary syndrome.Suppression of Ras/Mapk pathway signaling inhibits Myc-induced lymphomagenesis.Thyroid carcinoma-associated genetic mutations also occur in thyroid lymphomasCutaneous T-cell lymphoma: 2016 update on diagnosis, risk-stratification, and management.Simultaneous inhibition of pan-phosphatidylinositol-3-kinases and MEK as a potential therapeutic strategy in peripheral T-cell lymphomas.Involvement of KRAS G12A mutation in the IL-2-independent growth of a human T-LGL leukemia cell line, PLT-2.MEK inhibitors selectively suppress alloreactivity and graft-versus-host disease in a memory stage-dependent manner.Altered expression of Bcl-2, c-Myc, H-Ras, K-Ras, and N-Ras does not influence the course of mycosis fungoidesCutaneous T-cell lymphoma: 2011 update on diagnosis, risk-stratification, and management.Novel therapies for cutaneous T-cell lymphoma: what does the future hold?Prognostic factors, prognostic indices and staging in mycosis fungoides and Sézary syndrome: where are we now?Sézary syndrome: old enigmas, new targets.Sézary Syndrome: Clinical and Biological Aspects.Genomic analysis of mycosis fungoides and Sézary syndrome identifies recurrent alterations in TNFR2.Genotype-selective combination therapies for melanoma identified by high-throughput drug screening.Genomic analyses reveal recurrent mutations in epigenetic modifiers and the JAK-STAT pathway in Sézary syndromeNRAS mutations in cutaneous T cell lymphoma (CTCL) sensitize tumors towards treatment with the multikinase inhibitor Sorafenib.Mutation of NRAS but not KRAS significantly reduces myeloma sensitivity to single-agent bortezomib therapy.Mutated JAK kinases and deregulated STAT activity are potential therapeutic targets in cutaneous T-cell lymphoma.T-cell prolymphocytic leukemia in Japan: is it a variant?p-MAPK1 expression associated with poor prognosis in angioimmunoblastic T-cell lymphoma patients.
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High-throughput mutation profiling of CTCL samples reveals KRAS and NRAS mutations sensitizing tumors toward inhibition of the RAS/RAF/MEK signaling cascade.
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 05 January 2011
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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
High-throughput mutation profi ...... RAS/RAF/MEK signaling cascade.
@en
High-throughput mutation profi ...... RAS/RAF/MEK signaling cascade.
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type
label
High-throughput mutation profi ...... RAS/RAF/MEK signaling cascade.
@en
High-throughput mutation profi ...... RAS/RAF/MEK signaling cascade.
@nl
prefLabel
High-throughput mutation profi ...... RAS/RAF/MEK signaling cascade.
@en
High-throughput mutation profi ...... RAS/RAF/MEK signaling cascade.
@nl
P2093
P2860
P1433
P1476
High-throughput mutation profi ...... RAS/RAF/MEK signaling cascade
@en
P2093
Chandrani Mondal
Charlie Hatton
Claus-Detlev Klemke
Dorothee Süss
Gernot Polier
Karsten Gülow
Laura E Macconaill
Maria B Karpova
Marie C Zipser
Michael Girardi
P2860
P304
P356
10.1182/BLOOD-2010-09-305128
P407
P577
2011-01-05T00:00:00Z