mTOR inhibitors alone and in combination with JAK2 inhibitors effectively inhibit cells of myeloproliferative neoplasms. - Wikidata - awgldk - TriplyDB

mTOR inhibitors alone and in combination with JAK2 inhibitors effectively inhibit cells of myeloproliferative neoplasms.

mTOR inhibitors alone and in combination with JAK2 inhibitors effectively inhibit cells of myeloproliferative neoplasms.

http://www.wikidata.org/entity/Q34575726

about

JAK kinase targeting in hematologic malignancies: a sinuous pathway from identification of genetic alterations towards clinical indications Genetics of myeloproliferative neoplasms Novel therapies for myelofibrosis Heterozygous and homozygous JAK2(V617F) states modeled by induced pluripotent stem cells from myeloproliferative neoplasm patients Microarray and Proteomic Analyses of Myeloproliferative Neoplasms with a Highlight on the mTOR Signaling Pathway A data-driven network model of primary myelofibrosis: transcriptional and post-transcriptional alterations in CD34+ cells.AKT is a therapeutic target in myeloproliferative neoplasms Autophagy is a survival mechanism of acute myelogenous leukemia precursors during dual mTORC2/mTORC1 targeting Co-targeting the PI3K/mTOR and JAK2 signalling pathways produces synergistic activity against myeloproliferative neoplasms Intersection of mTOR and STAT signaling in immunity Targeting phosphatidylinositol-3-kinase pathway for the treatment of Philadelphia-negative myeloproliferative neoplasms.The PIM inhibitor AZD1208 synergizes with ruxolitinib to induce apoptosis of ruxolitinib sensitive and resistant JAK2-V617F-driven cells and inhibit colony formation of primary MPN cells.Stathmin 1 inhibition amplifies ruxolitinib-induced apoptosis in JAK2V617F cells JAK2-V617F-induced MAPK activity is regulated by PI3K and acts synergistically with PI3K on the proliferation of JAK2-V617F-positive cells JAK2 mutants (e.g., JAK2V617F) and their importance as drug targets in myeloproliferative neoplasms Advances in myelofibrosis: a clinical case approach.Proliferation and survival signaling from both Jak2-V617F and Lyn involving GSK3 and mTOR/p70S6K/4EBP1 in PVTL-1 cell line newly established from acute myeloid leukemia transformed from polycythemia vera.Critical role of the mTOR pathway in development and function of myeloid-derived suppressor cells in lal-/- mice.Molecular classification of myeloproliferative neoplasms-pros and cons.Preclinical models for drug selection in myeloproliferative neoplasms.Targeting the PI3K/mTOR Pathway in Pediatric Hematologic Malignancies.Clinical end points for drug treatment trials in BCR-ABL1-negative classic myeloproliferative neoplasms: consensus statements from European LeukemiaNET (ELN) and Internation Working Group-Myeloproliferative Neoplasms Research and Treatment (IWG-MRT)Emerging drugs for the treatment of myelofibrosis.Setting Appropriate Goals for the Next Generation of Clinical Trials in Myelofibrosis.Targeting mTOR for the treatment of B cell malignancies.Combination of PIM and JAK2 inhibitors synergistically suppresses MPN cell proliferation and overcomes drug resistance.PI3K-Akt Signal Transduction Molecules Maybe Involved in Downregulation of Erythroblasts Apoptosis and Perifosine Increased Its Apoptosis in Chronic Mountain Sickness.Inhibitors of the PI3K/mTOR pathway prevent STAT5 phosphorylation in JAK2V617F mutated cells through PP2A/CIP2A axis.mTOR Cross-Talk in Cancer and Potential for Combination Therapy.Targeting few to help hundreds: JAK, MAPK and ROCK pathways as druggable targets in atypical chronic myeloid leukemia.Pharmacokinetics and Safety of Momelotinib in Subjects With Hepatic or Renal Impairment.Mechanisms for mTORC1 activation and synergistic induction of apoptosis by ruxolitinib and BH3 mimetics or autophagy inhibitors in JAK2-V617F-expressing leukemic cells including newly established PVTL-2.

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mTOR inhibitors alone and in combination with JAK2 inhibitors effectively inhibit cells of myeloproliferative neoplasms.

http://www.wikidata.org/entity/Q34575726

description

2013 nî lūn-bûn

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2013 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2013 թվականի հունվարին հրատարակված գիտական հոդված

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2013年の論文

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年學術文章

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name

mTOR inhibitors alone and in c ...... myeloproliferative neoplasms.

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mTOR inhibitors alone and in c ...... myeloproliferative neoplasms.

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mTOR inhibitors alone and in c ...... myeloproliferative neoplasms.

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type

label

mTOR inhibitors alone and in c ...... myeloproliferative neoplasms.

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mTOR inhibitors alone and in c ...... myeloproliferative neoplasms.

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mTOR inhibitors alone and in c ...... myeloproliferative neoplasms.

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prefLabel

mTOR inhibitors alone and in c ...... myeloproliferative neoplasms.

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mTOR inhibitors alone and in c ...... myeloproliferative neoplasms.

@en

mTOR inhibitors alone and in c ...... myeloproliferative neoplasms.

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mTOR inhibitors alone and in c ...... myeloproliferative neoplasms.

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Alessandro M Vannucchi

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Associazione Italiana per la R ...... no Malattie Mieloproliferative

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Costanza Bogani

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Serena Martinelli

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P2860

Active-site inhibitors of mTOR target rapamycin-resistant outputs of mTORC1 and mTORC2

mTOR interacts with raptor to form a nutrient-sensitive complex that signals to the cell growth machinery

JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis

Targeting the mTOR signaling network for cancer therapy

Abnormalities of GATA-1 in megakaryocytes from patients with idiopathic myelofibrosis

Erythropoietin stimulates phosphorylation and activation of GATA-1 via the PI3-kinase/AKT signaling pathway

GbetaL, a positive regulator of the rapamycin-sensitive pathway required for the nutrient-sensitive interaction between raptor and mTOR

A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera

The evolution of phosphatidylinositol 3-kinases as regulators of growth and metabolism

Drug combination studies and their synergy quantification using the Chou-Talalay method

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Paola Guglielmelli

Niccolò Bartalucci

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