BRAF Inhibition Stimulates Melanoma-Associated Macrophages to Drive Tumor Growth
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The Complexity of the ERK/MAP-Kinase Pathway and the Treatment of Melanoma Skin CancerMetastatic colonization by circulating tumour cellsAvoiding Severe Toxicity From Combined BRAF Inhibitor and Radiation Treatment: Consensus Guidelines from the Eastern Cooperative Oncology Group (ECOG)Control of immune cell entry through the tumour vasculature: a missing link in optimising melanoma immunotherapy?Managing leptomeningeal melanoma metastases in the era of immune and targeted therapy.An adaptive signaling network in melanoma inflammatory niches confers tolerance to MAPK signaling inhibition.Fibroblast-derived neuregulin 1 promotes compensatory ErbB3 receptor signaling in mutant BRAF melanomaATR Mutations Promote the Growth of Melanoma Tumors by Modulating the Immune Microenvironment.Downregulation of sphingosine kinase-1 induces protective tumor immunity by promoting M1 macrophage response in melanoma.Propranolol induces a favourable shift of anti-tumor immunity in a murine spontaneous model of melanoma.Crosstalk signaling in targeted melanoma therapy.Influences of BRAF Inhibitors on the Immune Microenvironment and the Rationale for Combined Molecular and Immune Targeted Therapy.Primary Tr1 cells from metastatic melanoma eliminate tumor-promoting macrophages through granzyme B- and perforin-dependent mechanisms.Targeted agents and immunotherapies: optimizing outcomes in melanoma.The role of myeloid cells in cancer therapies.Molecular Pathways: Maintaining MAPK Inhibitor Sensitivity by Targeting Nonmutational Tolerance.Golgi-Related Proteins GOLPH2 (GP73/GOLM1) and GOLPH3 (GOPP1/MIDAS) in Cutaneous Melanoma: Patterns of Expression and Prognostic Significance.The macrophage: Switches from a passenger to a driver during anticancer therapy.Overcoming resistance to BRAF inhibitors.TAMeless traitors: macrophages in cancer progression and metastasis.The combination of checkpoint immunotherapy and targeted therapy in cancer.Intercellular Resistance to BRAF Inhibition Can Be Mediated by Extracellular Vesicle-Associated PDGFRβ.Novel combination strategies for enhancing efficacy of immune checkpoint inhibitors in the treatment of metastatic solid malignancies.Connexin 43 upregulation by dioscin inhibits melanoma progression via suppressing malignancy and inducing M1 polarization.Nuclear ERK5 inhibits progression of leukemic monocytes to macrophages by regulating the transcription factor PU.1 and heat shock protein HSP70.Blockade of MIF-CD74 Signalling on Macrophages and Dendritic Cells Restores the Antitumour Immune Response Against Metastatic Melanoma.Immune-checkpoint inhibitors in melanoma and kidney cancer: from sequencing to rational selection.Mechanisms of resistance to BRAF and MEK inhibitors and clinical update of US Food and Drug Administration-approved targeted therapy in advanced melanoma
P2860
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P2860
BRAF Inhibition Stimulates Melanoma-Associated Macrophages to Drive Tumor Growth
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2015 nî lūn-bûn
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2015 թուականի Յունուարին հրատարակուած գիտական յօդուած
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2015 թվականի հունվարին հրատարակված գիտական հոդված
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2015年の論文
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2015年学术文章
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2015年学术文章
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name
BRAF Inhibition Stimulates Melanoma-Associated Macrophages to Drive Tumor Growth
@ast
BRAF Inhibition Stimulates Melanoma-Associated Macrophages to Drive Tumor Growth
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type
label
BRAF Inhibition Stimulates Melanoma-Associated Macrophages to Drive Tumor Growth
@ast
BRAF Inhibition Stimulates Melanoma-Associated Macrophages to Drive Tumor Growth
@en
prefLabel
BRAF Inhibition Stimulates Melanoma-Associated Macrophages to Drive Tumor Growth
@ast
BRAF Inhibition Stimulates Melanoma-Associated Macrophages to Drive Tumor Growth
@en
P2093
P2860
P1476
BRAF Inhibition Stimulates Melanoma-Associated Macrophages to Drive Tumor Growth
@en
P2093
Alfonso Lopez-Coral
Eric Belser
Giorgos Karakousis
Lynn M Schuchter
Melissa Lieu
Molly B Halloran
P2860
P304
P356
10.1158/1078-0432.CCR-14-1554
P407
P577
2015-01-23T00:00:00Z