Antimyeloangiogenic therapy for cancer by inhibiting PlGF.
Standard
Antimyeloangiogenic therapy for cancer by inhibiting PlGF. / Loges, Sonja; Schmidt, Thomas; Carmeliet, Peter.
in: CLIN CANCER RES, Jahrgang 15, Nr. 11, 11, 2009, S. 3648-3653.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
Harvard
APA
Vancouver
Bibtex
}
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 -