Leukemia regression by vascular disruption and antiangiogenic therapy. - sprookjes - yvandenbroek - TriplyDB

Leukemia regression by vascular disruption and antiangiogenic therapy.

Leukemia regression by vascular disruption and antiangiogenic therapy.

http://www.wikidata.org/entity/Q34124965

about

Functional and Biological Role of Endothelial Precursor Cells in Tumour Progression: A New Potential Therapeutic Target in Haematological Malignancies In vivo spectral and fluorescence microscopy comparison of microvascular function after treatment with OXi4503, Sunitinib and their combination in Caki-2 tumors.Molecular targets for selective killing of TRAIL-resistant leukemic cells.Functional integration of acute myeloid leukemia into the vascular niche.Support of a free radical mechanism for enhanced antitumor efficacy of the microtubule disruptor OXi4503.Activation of the vascular niche supports leukemic progression and resistance to chemotherapy Leukemia Mediated Endothelial Cell Activation Modulates Leukemia Cell Susceptibility to Chemotherapy through a Positive Feedback Loop Mechanism A perspective on vascular disrupting agents that interact with tubulin: preclinical tumor imaging and biological assessment Overexpression of GATA1 confers resistance to chemotherapy in acute megakaryocytic Leukemia.Gene expression profiles in BCL11B-siRNA treated malignant T cells.Angiogenesis in acute myeloid leukemia and opportunities for novel therapies.Angiogenic cytokines are antibody targets during graft-versus-leukemia reactions.Cardiovascular toxicity profiles of vascular-disrupting agents.Oncolytic virotherapy for hematological malignancies.Serial monitoring of human systemic and xenograft models of leukemia using a novel vascular disrupting agent.Preclinical Activity of the Vascular Disrupting Agent OXi4503 against Head and Neck Cancer Identification of leukemia stem cells in acute myeloid leukemia and their clinical relevance.Targeting the vascular endothelial growth factor in hematologic malignancies.Tubulin-interactive stilbene derivatives as anticancer agents.Synthesis and anti-cancer screening of novel heterocyclic-(2H)-1,2,3-triazoles as potential anti-cancer agents.Angiogenesis and proliferation index in patients with acute leukemia: a prospective study In vitro and in vivo effects of an anti-mouse endoglin (CD105)-immunotoxin on the early stages of mouse B16MEL4A5 melanoma tumours.A VEGFR-3 antagonist increases IFN-γ expression on low functioning NK cells in acute myeloid leukemia.Realizing the Potential of Vascular Targeted Therapy: The Rationale for Combining Vascular Disrupting Agents and Anti-Angiogenic Agents to Treat Cancer.Cross-talk between leukemic and endothelial cells promotes angiogenesis by VEGF activation of the Notch/Dll4 pathway.Therapeutic Antibodies for Myeloid Neoplasms-Current Developments and Future Directions.Acute Myeloid Leukemia and the Bone Marrow Niche-Take a Closer Look

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P2860

Leukemia regression by vascular disruption and antiangiogenic therapy.

http://www.wikidata.org/entity/Q34124965

description

2010 nî lūn-bûn

@nan

2010 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2010 թվականի մայիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

Leukemia regression by vascular disruption and antiangiogenic therapy.

@ast

Leukemia regression by vascular disruption and antiangiogenic therapy.

@en

Leukemia regression by vascular disruption and antiangiogenic therapy.

@nl

type

label

Leukemia regression by vascular disruption and antiangiogenic therapy.

@ast

Leukemia regression by vascular disruption and antiangiogenic therapy.

@en

Leukemia regression by vascular disruption and antiangiogenic therapy.

@nl

prefLabel

Leukemia regression by vascular disruption and antiangiogenic therapy.

@ast

Leukemia regression by vascular disruption and antiangiogenic therapy.

@en

Leukemia regression by vascular disruption and antiangiogenic therapy.

@nl

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Leukemia regression by vascular disruption and antiangiogenic therapy.

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Amy M Meacham

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Christopher R Cogle

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Dietmar W Siemann

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Edward W Scott

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Gerard J Madlambayan

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Koji Hosaka

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Marda Jorgensen

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Saad Mir

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P2860

Vascular endothelial growth factor (VEGF)-C signaling through FLT-4 (VEGFR-3) mediates leukemic cell proliferation, survival, and resistance to chemotherapy

In vivo and in vitro evaluation of combretastatin A-4 and its sodium phosphate prodrug

Inhibition of vascular endothelial growth factor-induced angiogenesis suppresses tumour growth in vivo

Vascular endothelial growth factor induced by hypoxia may mediate hypoxia-initiated angiogenesis

Regulation of angiogenesis by hypoxia: role of the HIF system

Oxi4503, a novel vascular targeting agent: effects on blood flow and antitumor activity in comparison to combretastatin A-4 phosphate.

Effect of the second-generation vascular disrupting agent OXi4503 on tumor vascularity.

Inhibition of both paracrine and autocrine VEGF/ VEGFR-2 signaling pathways is essential to induce long-term remission of xenotransplanted human leukemias

The presence of a FLT3 internal tandem duplication in patients with acute myeloid leukemia (AML) adds important prognostic information to cytogenetic risk group and response to the first cycle of chemotherapy: analysis of 854 patients from the Unite

Analysis of FLT3 length mutations in 1003 patients with acute myeloid leukemia: correlation to cytogenetics, FAB subtype, and prognosis in the AMLCG study and usefulness as a marker for the detection of minimal residual disease.

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1539-1547

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