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Gene transfer of SHIP-1 inhibits proliferation of juvenile myelomonocytic leukemia cells carrying KRAS2 or PTPN11 mutations.

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Gene transfer of SHIP-1 inhibits proliferation of juvenile myelomonocytic leukemia cells carrying KRAS2 or PTPN11 mutations. / Metzner, A; Horstmann, Martin; Fehse, Boris; Ortmeyer, Gerhard; Niemeyer, C M; Stocking, C; Mayr, Georg W.; Jücker, Manfred.

in: GENE THER, Jahrgang 14, Nr. 8, 8, 2007, S. 699-703.

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

Harvard

Metzner, A, Horstmann, M, Fehse, B, Ortmeyer, G, Niemeyer, CM, Stocking, C, Mayr, GW & Jücker, M 2007, 'Gene transfer of SHIP-1 inhibits proliferation of juvenile myelomonocytic leukemia cells carrying KRAS2 or PTPN11 mutations.', GENE THER, Jg. 14, Nr. 8, 8, S. 699-703. <http://www.ncbi.nlm.nih.gov/pubmed/17268534?dopt=Citation>

APA

Metzner, A., Horstmann, M., Fehse, B., Ortmeyer, G., Niemeyer, C. M., Stocking, C., Mayr, G. W., & Jücker, M. (2007). Gene transfer of SHIP-1 inhibits proliferation of juvenile myelomonocytic leukemia cells carrying KRAS2 or PTPN11 mutations. GENE THER, 14(8), 699-703. [8]. http://www.ncbi.nlm.nih.gov/pubmed/17268534?dopt=Citation

Vancouver

Metzner A, Horstmann M, Fehse B, Ortmeyer G, Niemeyer CM, Stocking C et al. Gene transfer of SHIP-1 inhibits proliferation of juvenile myelomonocytic leukemia cells carrying KRAS2 or PTPN11 mutations. GENE THER. 2007;14(8):699-703. 8.

Bibtex

@article{154667950df8437fa75a8e919437e0c1,
title = "Gene transfer of SHIP-1 inhibits proliferation of juvenile myelomonocytic leukemia cells carrying KRAS2 or PTPN11 mutations.",
abstract = "Juvenile myelomonocytic leukemia (JMML) is a malignant disease of early childhood characterized by a hypersensitivity to granulocyte/macrophage colony-stimulating factor (GM-CSF). Mutations in RAS or PTPN11 are frequently detected in JMML patients. The SH2-containing inositol 5-phosphatase 1 (SHIP-1) is a negative regulator of GM-CSF signaling, and inactivation of SHIP-1 in mice results in a myeloproliferative disease. Here, we report the effects of SHIP-1 expression on GM-CSF-dependent proliferation and colony formation of human hematopoietic cells. After retroviral-mediated transduction of SHIP-1 into CD34+ cells from cord blood of healthy newborns or peripheral blood of JMML patients carrying mutations in KRAS2 or PTPN11, we observed a reduction in GM-CSF-dependent proliferation and colony formation. An enzymatically inactive form of SHIP-1 (D672A) had no effect. These data indicate that SHIP-1 can effectively block GM-CSF hypersensitivity in JMML progenitor cells with mutations in KRAS2 or PTPN11 and may be a useful approach for the treatment of JMML patients.",
author = "A Metzner and Martin Horstmann and Boris Fehse and Gerhard Ortmeyer and Niemeyer, {C M} and C Stocking and Mayr, {Georg W.} and Manfred J{\"u}cker",
year = "2007",
language = "Deutsch",
volume = "14",
pages = "699--703",
journal = "GENE THER",
issn = "0969-7128",
publisher = "NATURE PUBLISHING GROUP",
number = "8",

}

RIS

TY - JOUR

T1 - Gene transfer of SHIP-1 inhibits proliferation of juvenile myelomonocytic leukemia cells carrying KRAS2 or PTPN11 mutations.

AU - Metzner, A

AU - Horstmann, Martin

AU - Fehse, Boris

AU - Ortmeyer, Gerhard

AU - Niemeyer, C M

AU - Stocking, C

AU - Mayr, Georg W.

AU - Jücker, Manfred

PY - 2007

Y1 - 2007

N2 - Juvenile myelomonocytic leukemia (JMML) is a malignant disease of early childhood characterized by a hypersensitivity to granulocyte/macrophage colony-stimulating factor (GM-CSF). Mutations in RAS or PTPN11 are frequently detected in JMML patients. The SH2-containing inositol 5-phosphatase 1 (SHIP-1) is a negative regulator of GM-CSF signaling, and inactivation of SHIP-1 in mice results in a myeloproliferative disease. Here, we report the effects of SHIP-1 expression on GM-CSF-dependent proliferation and colony formation of human hematopoietic cells. After retroviral-mediated transduction of SHIP-1 into CD34+ cells from cord blood of healthy newborns or peripheral blood of JMML patients carrying mutations in KRAS2 or PTPN11, we observed a reduction in GM-CSF-dependent proliferation and colony formation. An enzymatically inactive form of SHIP-1 (D672A) had no effect. These data indicate that SHIP-1 can effectively block GM-CSF hypersensitivity in JMML progenitor cells with mutations in KRAS2 or PTPN11 and may be a useful approach for the treatment of JMML patients.

AB - Juvenile myelomonocytic leukemia (JMML) is a malignant disease of early childhood characterized by a hypersensitivity to granulocyte/macrophage colony-stimulating factor (GM-CSF). Mutations in RAS or PTPN11 are frequently detected in JMML patients. The SH2-containing inositol 5-phosphatase 1 (SHIP-1) is a negative regulator of GM-CSF signaling, and inactivation of SHIP-1 in mice results in a myeloproliferative disease. Here, we report the effects of SHIP-1 expression on GM-CSF-dependent proliferation and colony formation of human hematopoietic cells. After retroviral-mediated transduction of SHIP-1 into CD34+ cells from cord blood of healthy newborns or peripheral blood of JMML patients carrying mutations in KRAS2 or PTPN11, we observed a reduction in GM-CSF-dependent proliferation and colony formation. An enzymatically inactive form of SHIP-1 (D672A) had no effect. These data indicate that SHIP-1 can effectively block GM-CSF hypersensitivity in JMML progenitor cells with mutations in KRAS2 or PTPN11 and may be a useful approach for the treatment of JMML patients.

M3 - SCORING: Zeitschriftenaufsatz

VL - 14

SP - 699

EP - 703

JO - GENE THER

JF - GENE THER

SN - 0969-7128

IS - 8

M1 - 8

ER -