Inhibition of KRAS-driven tumorigenicity by interruption of an autocrine cytokine circuit.
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Targeting TBK1 inhibits migration and resistance to MEK inhibitors in mutant NRAS melanoma.Genomic profiling toward precision medicine in non-small cell lung cancer: getting beyond EGFRTargeting pathways downstream of KRAS in lung adenocarcinoma.Transforming Big Data into Cancer-Relevant Insight: An Initial, Multi-Tier Approach to Assess Reproducibility and Relevance.Molecular pathways and therapeutic targets in lung cancerCcl5 establishes an autocrine high-grade glioma growth regulatory circuit critical for mesenchymal glioblastoma survival.Ras oncogene-independent activation of RALB signaling is a targetable mechanism of escape from NRAS(V12) oncogene addiction in acute myeloid leukemia.CHZ868, a Type II JAK2 Inhibitor, Reverses Type I JAK Inhibitor Persistence and Demonstrates Efficacy in Myeloproliferative Neoplasms.Oncogene mimicry as a mechanism of primary resistance to BRAF inhibitorsTargeting an IKBKE cytokine network impairs triple-negative breast cancer growth.Drugging the undruggable RAS: Mission possible?The broad-spectrum receptor tyrosine kinase inhibitor dovitinib suppresses growth of BRAF-mutant melanoma cells in combination with other signaling pathway inhibitors.NF2 blocks Snail-mediated p53 suppression in mesothelioma.RAS signaling and anti-RAS therapy: lessons learned from genetically engineered mouse models, human cancer cells, and patient-related studies.An Arntl2-Driven Secretome Enables Lung Adenocarcinoma Metastatic Self-SufficiencyIL6 Blockade Reprograms the Lung Tumor Microenvironment to Limit the Development and Progression of K-ras-Mutant Lung Cancer.Oncogenic Ras modulates p38 MAPK-mediated inflammatory cytokine production in glioblastoma cells.Therapeutic Approaches to RAS Mutation.Challenges in Drug Discovery for Neurofibromatosis Type 1-Associated Low-Grade GliomaA module of inflammatory cytokines defines resistance of colorectal cancer to EGFR inhibitors.TBK1 inhibitors: a review of patent literature (2011 - 2014).Overview of KRAS-Driven Genetically Engineered Mouse Models of Non-Small Cell Lung Cancer.Decomposing Oncogenic Transcriptional Signatures to Generate Maps of Divergent Cellular States.Modeling K-Ras-driven lung adenocarcinoma in mice: preclinical validation of therapeutic targets.JAK1/STAT3 activation through a proinflammatory cytokine pathway leads to resistance to molecularly targeted therapy in non-small cell lung cancer.TBK1 Provides Context-Selective Support of the Activated AKT/mTOR Pathway in Lung Cancer.The RB-IL-6 axis controls self-renewal and endocrine therapy resistance by fine-tuning mitochondrial activity.IKBKE Is Required during KRAS-Induced Pancreatic Tumorigenesis.STK11/LKB1 Deficiency Promotes Neutrophil Recruitment and Proinflammatory Cytokine Production to Suppress T-cell Activity in the Lung Tumor Microenvironment.MEK and TAK1 Regulate Apoptosis in Colon Cancer Cells with KRAS-Dependent Activation of Proinflammatory Signaling.GSK-3β Governs Inflammation-Induced NFATc2 Signaling Hubs to Promote Pancreatic Cancer Progression.Mutational landscape of metastatic cancer revealed from prospective clinical sequencing of 10,000 patients.Inflammation as a driver and vulnerability of KRAS mediated oncogenesisLong-term Benefit of PD-L1 Blockade in Lung Cancer Associated with JAK3 Activation.Intracellular and intercellular signaling networks in cancer initiation, development and precision anti-cancer therapy: RAS acts as contextual signaling hub.CCR5 in recruitment and activation of myeloid-derived suppressor cells in melanoma.The intersection of RB tumor suppressor function, stem cells, metabolism and inflammation.Effectors and potential targets selectively upregulated in human KRAS-mutant lung adenocarcinomas.Autophagy Inhibition Dysregulates TBK1 Signaling and Promotes Pancreatic Inflammation.Workshop on challenges, insights, and future directions for mouse and humanized models in cancer immunology and immunotherapy: a report from the associated programs of the 2016 annual meeting for the Society for Immunotherapy of cancer.
P2860
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P2860
Inhibition of KRAS-driven tumorigenicity by interruption of an autocrine cytokine circuit.
description
2014 nî lūn-bûn
@nan
2014年の論文
@ja
2014年学术文章
@wuu
2014年学术文章
@zh-cn
2014年学术文章
@zh-hans
2014年学术文章
@zh-my
2014年学术文章
@zh-sg
2014年學術文章
@yue
2014年學術文章
@zh
2014年學術文章
@zh-hant
name
Inhibition of KRAS-driven tumo ...... an autocrine cytokine circuit.
@en
type
label
Inhibition of KRAS-driven tumo ...... an autocrine cytokine circuit.
@en
altLabel
Inhibition of KRAS-driven tumorigenicity by interruption of an autocrine cytokine circuit
@en
prefLabel
Inhibition of KRAS-driven tumo ...... an autocrine cytokine circuit.
@en
P2093
P2860
P50
P1433
P1476
Inhibition of KRAS-driven tumorigenicity by interruption of an autocrine cytokine circuit
@en
P2093
Amir R Aref
Anna C Schinzel
Asher N Page
David A Barbie
Jacob B Reibel
Jason T Godfrey
Jeffrey A Engelman
Jill P Mesirov
Lior Rozhansky
Mary T Labowsky
P2860
P304
P356
10.1158/2159-8290.CD-13-0646
P407
P577
2014-01-20T00:00:00Z