Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction. - Wikidata - awgldk - TriplyDB

Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction.

Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction.

http://www.wikidata.org/entity/Q35409292

about

MYC activation is a hallmark of cancer initiation and maintenance Inactivation of MYC reverses tumorigenesis.Addiction to multiple oncogenes can be exploited to prevent the emergence of therapeutic resistance.MYC through miR-17-92 suppresses specific target genes to maintain survival, autonomous proliferation, and a neoplastic state.NCI's provocative questions on cancer: some answers to ignite discussion.Concurrent expression of MYC and BCL2 in diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone.Cancer prevention as biomodulation: targeting the initiating stimulus and secondary adaptations Noncanonical roles of the immune system in eliciting oncogene addiction BIM mediates oncogene inactivation-induced apoptosis in multiple transgenic mouse models of acute lymphoblastic leukemia.Real-time nanoscale proteomic analysis of the novel multi-kinase pathway inhibitor rigosertib to measure the response to treatment of cancer.Downregulation of Critical Oncogenes by the Selective SK2 Inhibitor ABC294640 Hinders Prostate Cancer Progression.In vivo imaging-based mathematical modeling techniques that enhance the understanding of oncogene addiction in relation to tumor growth.p19ARF is a critical mediator of both cellular senescence and an innate immune response associated with MYC inactivation in mouse model of acute leukemia.A tumor-immune mathematical model of CD4+ T helper cell dependent tumor regression by oncogene inactivation.The mitochondrial translation machinery as a therapeutic target in Myc-driven lymphomas Just like the rest of evolution in Mother Nature, the evolution of cancers may be driven by natural selection, and not by haphazard mutations DNA-binding of the Tet-transactivator curtails antigen-induced lymphocyte activation in mice.Oncogene addiction to c-MYC in myeloma cells.Tumor dormancy, oncogene addiction, cellular senescence, and self-renewal programs.

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P2860

Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction.

http://www.wikidata.org/entity/Q35409292

description

2011 nî lūn-bûn

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2011 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction.

@ast

Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction.

@en

type

label

Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction.

@ast

Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction.

@en

prefLabel

Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction.

@ast

Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction.

@en

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PNAS.1107303108

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction.

@en

P2093

Andrew J Gentles

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

Dean W Felsher

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Kavya Rakhra

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Pavan Bachireddy

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Peter S Choi

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Stacey J Adam

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Sylvia K Plevritis

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P2860

Identification of c-MYC as a target of the APC pathway

The ornithine decarboxylase gene is a transcriptional target of c-Myc

Tight control of gene expression in mammalian cells by tetracycline-responsive promoters

Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation

Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain

MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.

The Myc/Max/Mad network and the transcriptional control of cell behavior

Erlotinib in previously treated non-small-cell lung cancer

Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia

Cancer. Addiction to oncogenes--the Achilles heal of cancer

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42

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108

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Jan van Riggelen

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2011-10-03T00:00:00Z

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3198348

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