Antiangiogenic treatment with endostatin inhibits progression of AML in vivo.
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Antiangiogenic treatment with endostatin inhibits progression of AML in vivo. / Schuch, G; Oliveira-Ferrer, Leticia; Loges, Sonja; Laack, E; Bokemeyer, C; Hossfeld, D K; Fiedler, W; Ergun, S.
in: LEUKEMIA, Jahrgang 19, Nr. 8, 8, 2005, S. 1312-1317.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Antiangiogenic treatment with endostatin inhibits progression of AML in vivo.
AU - Schuch, G
AU - Oliveira-Ferrer, Leticia
AU - Loges, Sonja
AU - Laack, E
AU - Bokemeyer, C
AU - Hossfeld, D K
AU - Fiedler, W
AU - Ergun, S
PY - 2005
Y1 - 2005
N2 - Increased vessel density in the bone marrow of patients with acute myeloid leukemia as well as elevated expression of proangiogenic factors by leukemic cells implies a central role of angiogenesis in hematological malignancies. Endostatin (ES), a fragment of collagen XVIII, is an endogenous inhibitor of angiogenesis that has shown therapeutic activity in solid tumors in various preclinical models. Using microencapsulation technology, we studied the therapeutic effect of ES in AML. While ES had no effect on proliferation of M1 murine leukemic cells in vitro, ES producing microbeads significantly inhibited growth of subcutaneous chloromas in SCID mice as compared to controls. In a leukemia model using M1 cells the concomitant treatment of mice with ES microbeads prolonged median survival significantly. Histological analysis revealed a decreased microvessel density and a reduced number of CD31-positive single cells, putatively endothelial progenitor cells, in the bone marrow of treated animals. Taken together, ES has inhibitory effects on neo-angiogenesis in the bone marrow and on progression of leukemia in vivo. These experiments suggest a possible therapeutic role of antiangiogenic gene therapy with ES in AML.
AB - Increased vessel density in the bone marrow of patients with acute myeloid leukemia as well as elevated expression of proangiogenic factors by leukemic cells implies a central role of angiogenesis in hematological malignancies. Endostatin (ES), a fragment of collagen XVIII, is an endogenous inhibitor of angiogenesis that has shown therapeutic activity in solid tumors in various preclinical models. Using microencapsulation technology, we studied the therapeutic effect of ES in AML. While ES had no effect on proliferation of M1 murine leukemic cells in vitro, ES producing microbeads significantly inhibited growth of subcutaneous chloromas in SCID mice as compared to controls. In a leukemia model using M1 cells the concomitant treatment of mice with ES microbeads prolonged median survival significantly. Histological analysis revealed a decreased microvessel density and a reduced number of CD31-positive single cells, putatively endothelial progenitor cells, in the bone marrow of treated animals. Taken together, ES has inhibitory effects on neo-angiogenesis in the bone marrow and on progression of leukemia in vivo. These experiments suggest a possible therapeutic role of antiangiogenic gene therapy with ES in AML.
M3 - SCORING: Zeitschriftenaufsatz
VL - 19
SP - 1312
EP - 1317
JO - LEUKEMIA
JF - LEUKEMIA
SN - 0887-6924
IS - 8
M1 - 8
ER -