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Reduced proliferation of CD34(+) cells from patients with acute myeloid leukemia after gene transfer of INPP5D.

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Reduced proliferation of CD34(+) cells from patients with acute myeloid leukemia after gene transfer of INPP5D. / Metzner, A; Precht, Clarissa; Fehse, Boris; Fiedler, Walter; Stocking, C; Günther, A; Mayr, Georg W.; Jücker, Manfred.

in: GENE THER, Jahrgang 16, Nr. 4, 4, 2009, S. 570-573.

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

Harvard

Metzner, A, Precht, C, Fehse, B, Fiedler, W, Stocking, C, Günther, A, Mayr, GW & Jücker, M 2009, 'Reduced proliferation of CD34(+) cells from patients with acute myeloid leukemia after gene transfer of INPP5D.', GENE THER, Jg. 16, Nr. 4, 4, S. 570-573. <http://www.ncbi.nlm.nih.gov/pubmed/19148132?dopt=Citation>

APA

Metzner, A., Precht, C., Fehse, B., Fiedler, W., Stocking, C., Günther, A., Mayr, G. W., & Jücker, M. (2009). Reduced proliferation of CD34(+) cells from patients with acute myeloid leukemia after gene transfer of INPP5D. GENE THER, 16(4), 570-573. [4]. http://www.ncbi.nlm.nih.gov/pubmed/19148132?dopt=Citation

Vancouver

Metzner A, Precht C, Fehse B, Fiedler W, Stocking C, Günther A et al. Reduced proliferation of CD34(+) cells from patients with acute myeloid leukemia after gene transfer of INPP5D. GENE THER. 2009;16(4):570-573. 4.

Bibtex

@article{85306d0ff41241bba803abcb178f6ac7,
title = "Reduced proliferation of CD34(+) cells from patients with acute myeloid leukemia after gene transfer of INPP5D.",
abstract = "Acute myeloid leukemia (AML) is a malignant disease characterized by deregulated proliferation of immature myeloid cells. Constitutive activation of the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway is frequently detected in approximately 50-70% of AML patients. The gene INPP5D encodes the SH2-containing inositol 5-phosphatase 1 (SHIP1), which is a negative regulator of PI3K/AKT signaling. After lentiviral-mediated gene transfer of INPP5D into CD34(+) cells derived from AML patients (n=12) the granulocyte macrophage-colony stimulating factor (GM-CSF)-dependent proliferation was reduced in all samples analyzed (average 86%; range 72-93%). An enzymatically inactive form of SHIP1 (D672A) had no effect. In addition, SHIP1 reduced the autonomous proliferation of CD34(+) cells from a patient with a secondary AML who had a very high peripheral blast count (300 x 10(9) l(-1)). These data show that SHIP1 can effectively block GM-CSF-dependent and autonomous proliferation of AML cells.",
author = "A Metzner and Clarissa Precht and Boris Fehse and Walter Fiedler and C Stocking and A G{\"u}nther and Mayr, {Georg W.} and Manfred J{\"u}cker",
year = "2009",
language = "Deutsch",
volume = "16",
pages = "570--573",
journal = "GENE THER",
issn = "0969-7128",
publisher = "NATURE PUBLISHING GROUP",
number = "4",

}

RIS

TY - JOUR

T1 - Reduced proliferation of CD34(+) cells from patients with acute myeloid leukemia after gene transfer of INPP5D.

AU - Metzner, A

AU - Precht, Clarissa

AU - Fehse, Boris

AU - Fiedler, Walter

AU - Stocking, C

AU - Günther, A

AU - Mayr, Georg W.

AU - Jücker, Manfred

PY - 2009

Y1 - 2009

N2 - Acute myeloid leukemia (AML) is a malignant disease characterized by deregulated proliferation of immature myeloid cells. Constitutive activation of the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway is frequently detected in approximately 50-70% of AML patients. The gene INPP5D encodes the SH2-containing inositol 5-phosphatase 1 (SHIP1), which is a negative regulator of PI3K/AKT signaling. After lentiviral-mediated gene transfer of INPP5D into CD34(+) cells derived from AML patients (n=12) the granulocyte macrophage-colony stimulating factor (GM-CSF)-dependent proliferation was reduced in all samples analyzed (average 86%; range 72-93%). An enzymatically inactive form of SHIP1 (D672A) had no effect. In addition, SHIP1 reduced the autonomous proliferation of CD34(+) cells from a patient with a secondary AML who had a very high peripheral blast count (300 x 10(9) l(-1)). These data show that SHIP1 can effectively block GM-CSF-dependent and autonomous proliferation of AML cells.

AB - Acute myeloid leukemia (AML) is a malignant disease characterized by deregulated proliferation of immature myeloid cells. Constitutive activation of the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway is frequently detected in approximately 50-70% of AML patients. The gene INPP5D encodes the SH2-containing inositol 5-phosphatase 1 (SHIP1), which is a negative regulator of PI3K/AKT signaling. After lentiviral-mediated gene transfer of INPP5D into CD34(+) cells derived from AML patients (n=12) the granulocyte macrophage-colony stimulating factor (GM-CSF)-dependent proliferation was reduced in all samples analyzed (average 86%; range 72-93%). An enzymatically inactive form of SHIP1 (D672A) had no effect. In addition, SHIP1 reduced the autonomous proliferation of CD34(+) cells from a patient with a secondary AML who had a very high peripheral blast count (300 x 10(9) l(-1)). These data show that SHIP1 can effectively block GM-CSF-dependent and autonomous proliferation of AML cells.

M3 - SCORING: Zeitschriftenaufsatz

VL - 16

SP - 570

EP - 573

JO - GENE THER

JF - GENE THER

SN - 0969-7128

IS - 4

M1 - 4

ER -