Tgf-Beta superfamily receptors-targets for antiangiogenic therapy?

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Tgf-Beta superfamily receptors-targets for antiangiogenic therapy? / Wellbrock, Jasmin; Bokemeyer, Carsten; Fiedler, Walter.

in: J Oncol, Jahrgang 2010, 2010, S. 317068.

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@article{7622662ae6c14cb5ac7cdbdb2a3aa46b,
title = "Tgf-Beta superfamily receptors-targets for antiangiogenic therapy?",
abstract = "The TGF-beta pathway controls a broad range of cellular behavior including cell proliferation, differentiation, and apoptosis of various cell types including tumor cells, endothelial cells, immune cells, and fibroblasts. Besides TGF-beta's direct effects on tumor growth and its involvement in neoangiogenesis have received recent attention. Germline mutations in TGF-beta receptors or coreceptors causing Hereditary Hemorrhagic Teleangiectasia and the Loeys-Dietz syndrome underline the involvement of TGF-beta in vessel formation and maturation. Several therapeutic approaches are evaluated at present targeting the TGF-beta pathway including utilization of antisense oligonucleotides against TGF-beta itself or antibodies or small molecule inhibitors of TGF-beta receptors. Some of these therapeutic agents have already entered the clinical arena including an antibody against the endothelium specific TGF-beta class I receptor ALK-1 targeting tumor vasculature. In conclusion, therapeutic manipulation of the TGF-beta pathway opens great opportunities in future cancer therapy.",
author = "Jasmin Wellbrock and Carsten Bokemeyer and Walter Fiedler",
year = "2010",
doi = "10.1155/2010/317068",
language = "Deutsch",
volume = "2010",
pages = "317068",
journal = "J ONCOL",
issn = "1687-8450",
publisher = "Hindawi Publishing Corporation",

}

RIS

TY - JOUR

T1 - Tgf-Beta superfamily receptors-targets for antiangiogenic therapy?

AU - Wellbrock, Jasmin

AU - Bokemeyer, Carsten

AU - Fiedler, Walter

PY - 2010

Y1 - 2010

N2 - The TGF-beta pathway controls a broad range of cellular behavior including cell proliferation, differentiation, and apoptosis of various cell types including tumor cells, endothelial cells, immune cells, and fibroblasts. Besides TGF-beta's direct effects on tumor growth and its involvement in neoangiogenesis have received recent attention. Germline mutations in TGF-beta receptors or coreceptors causing Hereditary Hemorrhagic Teleangiectasia and the Loeys-Dietz syndrome underline the involvement of TGF-beta in vessel formation and maturation. Several therapeutic approaches are evaluated at present targeting the TGF-beta pathway including utilization of antisense oligonucleotides against TGF-beta itself or antibodies or small molecule inhibitors of TGF-beta receptors. Some of these therapeutic agents have already entered the clinical arena including an antibody against the endothelium specific TGF-beta class I receptor ALK-1 targeting tumor vasculature. In conclusion, therapeutic manipulation of the TGF-beta pathway opens great opportunities in future cancer therapy.

AB - The TGF-beta pathway controls a broad range of cellular behavior including cell proliferation, differentiation, and apoptosis of various cell types including tumor cells, endothelial cells, immune cells, and fibroblasts. Besides TGF-beta's direct effects on tumor growth and its involvement in neoangiogenesis have received recent attention. Germline mutations in TGF-beta receptors or coreceptors causing Hereditary Hemorrhagic Teleangiectasia and the Loeys-Dietz syndrome underline the involvement of TGF-beta in vessel formation and maturation. Several therapeutic approaches are evaluated at present targeting the TGF-beta pathway including utilization of antisense oligonucleotides against TGF-beta itself or antibodies or small molecule inhibitors of TGF-beta receptors. Some of these therapeutic agents have already entered the clinical arena including an antibody against the endothelium specific TGF-beta class I receptor ALK-1 targeting tumor vasculature. In conclusion, therapeutic manipulation of the TGF-beta pathway opens great opportunities in future cancer therapy.

U2 - 10.1155/2010/317068

DO - 10.1155/2010/317068

M3 - SCORING: Zeitschriftenaufsatz

VL - 2010

SP - 317068

JO - J ONCOL

JF - J ONCOL

SN - 1687-8450

ER -