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Loss or inhibition of stromal-derived PlGF prolongs survival of mice with imatinib-resistant Bcr-Abl1(+) leukemia.

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Loss or inhibition of stromal-derived PlGF prolongs survival of mice with imatinib-resistant Bcr-Abl1(+) leukemia. / Schmidt, Thomas; Behzad, Kharabi Masouleh; Loges, Sonja; Cauwenberghs, Sandra; Fraisl, Peter; Maes, Christa; Jonckx, Bart; Kim, De Keersmaecker; Kleppe, Maria; Tjwa, Marc; Schenk, Thomas; Vinckier, Stefan; Fragoso, Rita; Maria, De Mol; Beel, Karolien; Dias, Sérgio; Verfaillie, Catherine; Clark, Richard E; Brümmendorf, Tim H; Vandenberghe, Peter; Rafii, Shahin; Holyoake, Tessa; Hochhaus, Andreas; Cools, Jan; Karin, Michael; Carmeliet, Geert; Dewerchin, Mieke; Carmeliet, Peter.

in: CANCER CELL, Jahrgang 19, Nr. 6, 6, 2011, S. 740-753.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Schmidt, T, Behzad, KM, Loges, S, Cauwenberghs, S, Fraisl, P, Maes, C, Jonckx, B, Kim, DK, Kleppe, M, Tjwa, M, Schenk, T, Vinckier, S, Fragoso, R, Maria, DM, Beel, K, Dias, S, Verfaillie, C, Clark, RE, Brümmendorf, TH, Vandenberghe, P, Rafii, S, Holyoake, T, Hochhaus, A, Cools, J, Karin, M, Carmeliet, G, Dewerchin, M & Carmeliet, P 2011, 'Loss or inhibition of stromal-derived PlGF prolongs survival of mice with imatinib-resistant Bcr-Abl1(+) leukemia.', CANCER CELL, Jg. 19, Nr. 6, 6, S. 740-753. <http://www.ncbi.nlm.nih.gov/pubmed/21665148?dopt=Citation>

APA

Schmidt, T., Behzad, K. M., Loges, S., Cauwenberghs, S., Fraisl, P., Maes, C., Jonckx, B., Kim, D. K., Kleppe, M., Tjwa, M., Schenk, T., Vinckier, S., Fragoso, R., Maria, D. M., Beel, K., Dias, S., Verfaillie, C., Clark, R. E., Brümmendorf, T. H., ... Carmeliet, P. (2011). Loss or inhibition of stromal-derived PlGF prolongs survival of mice with imatinib-resistant Bcr-Abl1(+) leukemia. CANCER CELL, 19(6), 740-753. [6]. http://www.ncbi.nlm.nih.gov/pubmed/21665148?dopt=Citation

Vancouver

Schmidt T, Behzad KM, Loges S, Cauwenberghs S, Fraisl P, Maes C et al. Loss or inhibition of stromal-derived PlGF prolongs survival of mice with imatinib-resistant Bcr-Abl1(+) leukemia. CANCER CELL. 2011;19(6):740-753. 6.

Bibtex

@article{7dc75fec7dbc48db96d6c72937d9ee3a,
title = "Loss or inhibition of stromal-derived PlGF prolongs survival of mice with imatinib-resistant Bcr-Abl1(+) leukemia.",
abstract = "Imatinib has revolutionized the treatment of Bcr-Abl1(+) chronic myeloid leukemia (CML), but, in most patients, some leukemia cells persist despite continued therapy, while others become resistant. Here, we report that PlGF levels are elevated in CML and that PlGF produced by bone marrow stromal cells (BMSCs) aggravates disease severity. CML cells foster a soil for their own growth by inducing BMSCs to upregulate PlGF, which not only stimulates BM angiogenesis, but also promotes CML proliferation and metabolism, in part independently of Bcr-Abl1 signaling. Anti-PlGF treatment prolongs survival of imatinib-sensitive and -resistant CML mice and adds to the anti-CML activity of imatinib. These results may warrant further investigation of the therapeutic potential of PlGF inhibition for (imatinib-resistant) CML.",
keywords = "Animals, Humans, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Cell Line, Tumor, Bone Marrow Cells/metabolism, Drug Resistance, Neoplasm, Fusion Proteins, bcr-abl/*physiology, Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug therapy/etiology/metabolism/mortality, NF-kappa B/physiology, Osteolysis/prevention & control, Piperazines/*therapeutic use, Pregnancy Proteins/antagonists & inhibitors/blood/*physiology, Pyrimidines/*therapeutic use, Animals, Humans, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Cell Line, Tumor, Bone Marrow Cells/metabolism, Drug Resistance, Neoplasm, Fusion Proteins, bcr-abl/*physiology, Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug therapy/etiology/metabolism/mortality, NF-kappa B/physiology, Osteolysis/prevention & control, Piperazines/*therapeutic use, Pregnancy Proteins/antagonists & inhibitors/blood/*physiology, Pyrimidines/*therapeutic use",
author = "Thomas Schmidt and Behzad, {Kharabi Masouleh} and Sonja Loges and Sandra Cauwenberghs and Peter Fraisl and Christa Maes and Bart Jonckx and Kim, {De Keersmaecker} and Maria Kleppe and Marc Tjwa and Thomas Schenk and Stefan Vinckier and Rita Fragoso and Maria, {De Mol} and Karolien Beel and S{\'e}rgio Dias and Catherine Verfaillie and Clark, {Richard E} and Br{\"u}mmendorf, {Tim H} and Peter Vandenberghe and Shahin Rafii and Tessa Holyoake and Andreas Hochhaus and Jan Cools and Michael Karin and Geert Carmeliet and Mieke Dewerchin and Peter Carmeliet",
year = "2011",
language = "English",
volume = "19",
pages = "740--753",
journal = "CANCER CELL",
issn = "1535-6108",
publisher = "Cell Press",
number = "6",

}

RIS

TY - JOUR

T1 - Loss or inhibition of stromal-derived PlGF prolongs survival of mice with imatinib-resistant Bcr-Abl1(+) leukemia.

AU - Schmidt, Thomas

AU - Behzad, Kharabi Masouleh

AU - Loges, Sonja

AU - Cauwenberghs, Sandra

AU - Fraisl, Peter

AU - Maes, Christa

AU - Jonckx, Bart

AU - Kim, De Keersmaecker

AU - Kleppe, Maria

AU - Tjwa, Marc

AU - Schenk, Thomas

AU - Vinckier, Stefan

AU - Fragoso, Rita

AU - Maria, De Mol

AU - Beel, Karolien

AU - Dias, Sérgio

AU - Verfaillie, Catherine

AU - Clark, Richard E

AU - Brümmendorf, Tim H

AU - Vandenberghe, Peter

AU - Rafii, Shahin

AU - Holyoake, Tessa

AU - Hochhaus, Andreas

AU - Cools, Jan

AU - Karin, Michael

AU - Carmeliet, Geert

AU - Dewerchin, Mieke

AU - Carmeliet, Peter

PY - 2011

Y1 - 2011

N2 - Imatinib has revolutionized the treatment of Bcr-Abl1(+) chronic myeloid leukemia (CML), but, in most patients, some leukemia cells persist despite continued therapy, while others become resistant. Here, we report that PlGF levels are elevated in CML and that PlGF produced by bone marrow stromal cells (BMSCs) aggravates disease severity. CML cells foster a soil for their own growth by inducing BMSCs to upregulate PlGF, which not only stimulates BM angiogenesis, but also promotes CML proliferation and metabolism, in part independently of Bcr-Abl1 signaling. Anti-PlGF treatment prolongs survival of imatinib-sensitive and -resistant CML mice and adds to the anti-CML activity of imatinib. These results may warrant further investigation of the therapeutic potential of PlGF inhibition for (imatinib-resistant) CML.

AB - Imatinib has revolutionized the treatment of Bcr-Abl1(+) chronic myeloid leukemia (CML), but, in most patients, some leukemia cells persist despite continued therapy, while others become resistant. Here, we report that PlGF levels are elevated in CML and that PlGF produced by bone marrow stromal cells (BMSCs) aggravates disease severity. CML cells foster a soil for their own growth by inducing BMSCs to upregulate PlGF, which not only stimulates BM angiogenesis, but also promotes CML proliferation and metabolism, in part independently of Bcr-Abl1 signaling. Anti-PlGF treatment prolongs survival of imatinib-sensitive and -resistant CML mice and adds to the anti-CML activity of imatinib. These results may warrant further investigation of the therapeutic potential of PlGF inhibition for (imatinib-resistant) CML.

KW - Animals

KW - Humans

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Inbred C57BL

KW - Cell Line, Tumor

KW - Bone Marrow Cells/metabolism

KW - Drug Resistance, Neoplasm

KW - Fusion Proteins, bcr-abl/physiology

KW - Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy/etiology/metabolism/mortality

KW - NF-kappa B/physiology

KW - Osteolysis/prevention & control

KW - Piperazines/therapeutic use

KW - Pregnancy Proteins/antagonists & inhibitors/blood/physiology

KW - Pyrimidines/therapeutic use

KW - Animals

KW - Humans

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Inbred C57BL

KW - Cell Line, Tumor

KW - Bone Marrow Cells/metabolism

KW - Drug Resistance, Neoplasm

KW - Fusion Proteins, bcr-abl/physiology

KW - Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy/etiology/metabolism/mortality

KW - NF-kappa B/physiology

KW - Osteolysis/prevention & control

KW - Piperazines/therapeutic use

KW - Pregnancy Proteins/antagonists & inhibitors/blood/physiology

KW - Pyrimidines/therapeutic use

M3 - SCORING: Journal article

VL - 19

SP - 740

EP - 753

JO - CANCER CELL

JF - CANCER CELL

SN - 1535-6108

IS - 6

M1 - 6

ER -