Journal ArticleDOI
Involvement of vascular endothelial growth factor receptor-3 in maintenance of integrity of endothelial cell lining during tumor angiogenesis.
Hajime Kubo,Takashi Fujiwara,Takashi Fujiwara,Takashi Fujiwara,Lotta Jussila,Lotta Jussila,Lotta Jussila,Hiroyuki Hashi,Hiroyuki Hashi,Hiroyuki Hashi,Minetaro Ogawa,Minetaro Ogawa,Minetaro Ogawa,Kenji Shimizu,Kenji Shimizu,Kenji Shimizu,Masaaki Awane,Masaaki Awane,Masaaki Awane,Yoshiharu Sakai,Yoshiharu Sakai,Yoshiharu Sakai,Arimichi Takabayashi,Arimichi Takabayashi,Arimichi Takabayashi,Kari Alitalo,Kari Alitalo,Kari Alitalo,Yoshio Yamaoka,Yoshio Yamaoka,Yoshio Yamaoka,Shin-Ichi Nishikawa,Shin-Ichi Nishikawa,Shin-Ichi Nishikawa +33 more
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TLDR
It is demonstrated that the inactivation of VEGFR-3 by a novel blocking monoclonal antibody (mAb) suppresses tumor growth by inhibiting the neo-angiogenesis of tumor-bearing tissues and suggests that the VEGF-C/VEG FR-3 pathway may serve another candidate target for cancer therapy.About:
This article is published in Blood.The article was published on 2000-07-15. It has received 223 citations till now. The article focuses on the topics: Angiogenesis & Vascular endothelial growth factor B.read more
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Vascular endothelial growth factor C is required for sprouting of the first lymphatic vessels from embryonic veins.
Marika J. Karkkainen,Paula Haiko,Kirsi Sainio,Juha Partanen,Jussi Taipale,Tatiana V. Petrova,Michael Jeltsch,David A. Jackson,Marja Talikka,Heikki Rauvala,Christer Betsholtz,Kari Alitalo +11 more
TL;DR: The results indicate that VEGF-C is the paracrine factor essential for lymphangiogenesis, and show that both Vegfc alleles are required for normal lymphatic development.
Journal ArticleDOI
VEGF-D promotes the metastatic spread of tumor cells via the lymphatics.
Steven A. Stacker,Carol Caesar,Megan E. Baldwin,Gillian E. Thornton,Richard A. Williams,Remko Prevo,David A. Jackson,Shin-Ichi Nishikawa,Hajime Kubo,Hajime Kubo,Marc G. Achen +10 more
TL;DR: It is demonstrated that lymphatics can be established in solid tumors and implicates VEGF family members in determining the route of metastatic spread and could be blocked with an antibody specific for V EGF-D.
Journal ArticleDOI
Vascular endothelial growth factor‐C‐mediated lymphangiogenesis promotes tumour metastasis
Stefano J. Mandriota,Lotta Jussila,Michael Jeltsch,Amelia Compagni,Danielle Baetens,Remko Prevo,Suneale Banerji,Joachim Huarte,Roberto Montesano,David A. Jackson,Lelio Orci,Kari Alitalo,Gerhard Christofori,Michael S. Pepper +13 more
TL;DR: It is demonstrated that VEGF‐C‐induced lymphangiogenesis mediates tumour cell dissemination and the formation of lymph node metastases.
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Phase I Safety and Pharmacokinetic Study of Recombinant Human Anti-Vascular Endothelial Growth Factor in Patients With Advanced Cancer
Michael S. Gordon,Kim Margolin,M. Talpaz,George W. Sledge,E. Holmgren,R. Benjamin,Susan Stalter,S. Shak,Daniel C. Adelman +8 more
TL;DR: Multiple doses of rhuMAb VEGF were well tolerated, and pharmacokinetic studies indicate that doses of > or = 0.3 mg/kg have a half-life similar to that of other humanized antibodies.
Journal ArticleDOI
Inhibition of lymphangiogenesis with resulting lymphedema in transgenic mice expressing soluble VEGF receptor-3.
Taija Makinen,Lotta Jussila,Tanja Veikkola,Terhi Karpanen,Mikko I. Kettunen,Kalevi J. Pulkkanen,Risto A. Kauppinen,David A. Jackson,Hajime Kubo,Shin-Ichi Nishikawa,Seppo Ylä-Herttuala,Kari Alitalo +11 more
TL;DR: It is shown that a soluble form of VEGFR-3 is a potent inhibitor of Vascular endothelial growth factor (VEGF)-C and VEGF-D signaling, and when expressed in the skin of transgenic mice, it inhibits fetal lymphangiogenesis and induces a regression of already formed lymphatic vessels, though the blood vasculature remains normal.
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Patterns and Emerging Mechanisms of the Angiogenic Switch during Tumorigenesis
TL;DR: The work from the authors' laboratories reviewed herein was supported by grants from the National Cancer Institute.
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What is the evidence that tumors are angiogenesis dependent
TL;DR: Method of treating a wound or burn which comprises directly dressing its surface with non-woven fabric comprising staple fibers of spun, regenerated collagen substantially free of telopeptides is disclosed.
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Abnormal blood vessel development and lethality in embryos lacking a single VEGF allele
Peter Carmeliet,Valérie Ferreira,Georg Breier,Saskia Pollefeyt,Lena Kieckens,Marina Gertsenstein,Michaela Fahrig,Ann Vandenhoeck,Kendraprasad Harpal,Carmen Eberhardt,Cathérine Declercq,Judy Pawling,Lieve Moons,Desire Collen,Werner Risau,Andras Nagy,Andras Nagy +16 more
TL;DR: It is reported that formation of blood vessels was abnormal, but not abolished, in heterozygous VEGF-deficient (VEGF+/-) embryos, generated by aggregation of embryonic stem (ES) cells with tetraploid embryos (T-ES)16,17, and even more impaired in homozygous D1-VEGF- deficient (VDGF-/-) T-ES embryos, resulting in death at mid-gestation.
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Failure of blood-island formation and vasculogenesis in Flk-1-deficient mice.
Fouad Shalaby,Janet Rossant,Janet Rossant,Terry P. Yamaguchi,Terry P. Yamaguchi,Marina Gertsenstein,Xiang-Fu Wu,Xiang-Fu Wu,Martin L. Breitman,Martin L. Breitman,Andre C. Schuh +10 more
TL;DR: The generation of mice deficient in Flk-1 by disruption of the gene using homologous recombination in embryonic stem (ES) cells is reported, indicating that FlK-1 is essential for yolk-sac blood-island formation and vasculogenesis in the mouse embryo.
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Inhibition of vascular endothelial growth factor-induced angiogenesis suppresses tumour growth in vivo
TL;DR: It is demonstrated that inhibition of the action of an angiogenic factor spontaneously produced by tumour cells may suppress tumour growth in vivo.