Research ExplorerPublicationsAntimyeloangiogenic therapy for cancer by inhibiting PlGF.

Antimyeloangiogenic therapy for cancer by inhibiting PlGF.

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Antimyeloangiogenic therapy for cancer by inhibiting PlGF. / Loges, Sonja; Schmidt, Thomas; Carmeliet, Peter.

In: CLIN CANCER RES, Vol. 15, No. 11, 11, 2009, p. 3648-3653.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Loges, S, Schmidt, T & Carmeliet, P 2009, 'Antimyeloangiogenic therapy for cancer by inhibiting PlGF.', CLIN CANCER RES, vol. 15, no. 11, 11, pp. 3648-3653. <http://www.ncbi.nlm.nih.gov/pubmed/19470735?dopt=Citation>

APA

Loges, S., Schmidt, T., & Carmeliet, P. (2009). Antimyeloangiogenic therapy for cancer by inhibiting PlGF. CLIN CANCER RES, 15(11), 3648-3653. [11]. http://www.ncbi.nlm.nih.gov/pubmed/19470735?dopt=Citation

Vancouver

Loges S, Schmidt T, Carmeliet P. Antimyeloangiogenic therapy for cancer by inhibiting PlGF. CLIN CANCER RES. 2009;15(11):3648-3653. 11.

Bibtex

@article{7a0acdd0de264cc280984dbaca66af1d,
title = "Antimyeloangiogenic therapy for cancer by inhibiting PlGF.",
abstract = "Inhibition of tumor angiogenesis emerged as valuable strategy to treat cancer and has revolutionized the face of clinical oncology by prolonging the life of numerous cancer patients. However, the duration of this response is rather short and tumors rapidly evade treatment, leaving antiangiogenic treatment thus far unable to cure cancer. Hence, novel targets are needed to diversify antiangiogenic treatments and to overcome resistance. Recent data support the concept that tumor infiltration by bone marrow-derived myeloid cells confers resistance to current antiangiogenic drugs targeting primarily vascular endothelial growth factor (VEGF). In this review, we will summarize (pre)clinical data on the role of PlGF and its receptor VEGFR-1 in promoting angiogenesis and inflammation, and the {"}antimyeloangiogenic{"} activity of an antibody against PlGF (alphaPlGF), which may help to overcome resistance against VEGF(R)Is. Because of these promising results, a humanized alphaPlGF antibody (TB403) is currently evaluated in different phase I clinical trials in cancer patients.",
author = "Sonja Loges and Thomas Schmidt and Peter Carmeliet",
year = "2009",
language = "Deutsch",
volume = "15",
pages = "3648--3653",
journal = "CLIN CANCER RES",
issn = "1078-0432",
publisher = "American Association for Cancer Research Inc.",
number = "11",

}

RIS

TY - JOUR

T1 - Antimyeloangiogenic therapy for cancer by inhibiting PlGF.

AU - Loges, Sonja

AU - Schmidt, Thomas

AU - Carmeliet, Peter

PY - 2009

Y1 - 2009

N2 - Inhibition of tumor angiogenesis emerged as valuable strategy to treat cancer and has revolutionized the face of clinical oncology by prolonging the life of numerous cancer patients. However, the duration of this response is rather short and tumors rapidly evade treatment, leaving antiangiogenic treatment thus far unable to cure cancer. Hence, novel targets are needed to diversify antiangiogenic treatments and to overcome resistance. Recent data support the concept that tumor infiltration by bone marrow-derived myeloid cells confers resistance to current antiangiogenic drugs targeting primarily vascular endothelial growth factor (VEGF). In this review, we will summarize (pre)clinical data on the role of PlGF and its receptor VEGFR-1 in promoting angiogenesis and inflammation, and the "antimyeloangiogenic" activity of an antibody against PlGF (alphaPlGF), which may help to overcome resistance against VEGF(R)Is. Because of these promising results, a humanized alphaPlGF antibody (TB403) is currently evaluated in different phase I clinical trials in cancer patients.

AB - Inhibition of tumor angiogenesis emerged as valuable strategy to treat cancer and has revolutionized the face of clinical oncology by prolonging the life of numerous cancer patients. However, the duration of this response is rather short and tumors rapidly evade treatment, leaving antiangiogenic treatment thus far unable to cure cancer. Hence, novel targets are needed to diversify antiangiogenic treatments and to overcome resistance. Recent data support the concept that tumor infiltration by bone marrow-derived myeloid cells confers resistance to current antiangiogenic drugs targeting primarily vascular endothelial growth factor (VEGF). In this review, we will summarize (pre)clinical data on the role of PlGF and its receptor VEGFR-1 in promoting angiogenesis and inflammation, and the "antimyeloangiogenic" activity of an antibody against PlGF (alphaPlGF), which may help to overcome resistance against VEGF(R)Is. Because of these promising results, a humanized alphaPlGF antibody (TB403) is currently evaluated in different phase I clinical trials in cancer patients.

M3 - SCORING: Zeitschriftenaufsatz

VL - 15

SP - 3648

EP - 3653

JO - CLIN CANCER RES

JF - CLIN CANCER RES

SN - 1078-0432

IS - 11

M1 - 11

ER -