Overview of angiogenesis: Biologic implications for antiangiogenic therapy

Ellis, Lee M.; Liu, Wenbiao; Ahmad, Syed A.; Fan, Fan; Jung, Young Do; Shaheen, Raymond M.; Reinmuth, Niels

doi:10.1016/s0093-7754(01)90287-8

Cited by 115 publications

(38 citation statements)

References 51 publications

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“…One explanation for this lung-specific action might be that the lung EC, which are exposed to increased fluid shear stress because of chronic hypoxia and/or hypoxic vasoconstriction, are hyperproliferative because high fluid shear stress stimulates EC growth [51]. Therefore, VEGF is required for a vascular repair attempt in the pulmonary artery, but it is not required for merely maintaining mature vessels like systemic arteries [63], thus suggesting that they are particularly vulnerable to VEGFR-2 blockade. However, SU5416 could affect the normoxic pulmonary circulation because it increases pulmonary arterial pressure slightly but significantly under normoxic conditions [14].…”

Section: Discussionmentioning

confidence: 99%

The Effects of Antiangiogenic Compound SU5416 in a Rat Model of Pulmonary Arterial Hypertension

Sakao

2010

Respiration

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Several lines of evidence indicate that vascular endothelial growth factor (VEGF) plays a prosurvival and antiapoptotic role in endothelial cells. SU5416 is the first VEGF receptor 2 inhibitor to enter clinical development for cancer therapy. A phase I/II study of SU5416 has been completed, and the results show that SU5416 is well tolerated in patients with terminal cancers. It has been shown that VEGF receptor blockade using SU5416 combined with chronic hypoxia results in severe angioproliferative pulmonary hypertension (PAH) with neointimal changes in adult rats. Although classic animal models of pulmonary hypertension (that is, the monocrotaline and hypoxic models) do not form obstructive intimal lesions in the peripheral pulmonary arteries, the SU5416 model has shown pulmonary arterial changes resembling plexiform lesions. Therefore, the SU5416 model of PAH has been used for some time, and it has thus contributed to a better understanding of the pulmonary hypertensive process. However, the mechanism by which SU5416 combined with chronic hypoxia can result in PAH with plexiform-like lesions in adult rats is complex and still remains to be fully elucidated. The most likely explanation is that there is increased apoptosis of endothelial cells in response to the loss of the survival signaling, creating conditions favoring the emergence of apoptosis-resistant cells with increased growth potential, that is, the endothelial cell hyperproliferation that might characterize the plexiform lesions of human PAH. The aim of the present review is to provide information useful for understanding a potent inhibitor of VEGF receptor tyrosine kinase, SU5416, and to better understand its use for generating animal models of PAH.

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Section: Discussionmentioning

confidence: 99%

The Effects of Antiangiogenic Compound SU5416 in a Rat Model of Pulmonary Arterial Hypertension

Sakao

2010

Respiration

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“…Continued investigations have lead to the development and characterization of several other anti-angiogenic agents such as fragments of naturally occurring proteins, neutralizing antibodies to angiogenic factors, kinase inhibitors and antibiotic derivatives [17]. Investigations of anti-angiogenic agents have been conducted in preclinical and clinical trials [18]. Therapeutic approaches using such anti-angiogenic factors hold great potential in inhibiting the growth of primary and metastatic/secondary tumors.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of angiogenesis by vitamin D-binding protein: Characterization of anti-endothelial activity of DBP-maf

et al. 2006

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“…At the prevascular stage, the tumor is unable to grow to a size beyond 2-3 mm 3 and remains in its dormant state. However, once the angiogenic phenotype of tumor is switched on, tumor growth rate changes from linear to exponential [11] . Metastases are also dependent on angiogenesis at least two steps of metastatic events.…”

Section: Discussionmentioning

confidence: 99%

Growth inhibition of breast cancer in rat by AAV mediated angiostatin gene

Chen

Chang-shan

2007

Chin. J. Cancer Res.

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Objective:To observe growth inhibition effect of adeno-associated viral vectors (AAV) mediated angiostatin (ANG) gene on implanted breast cancer in rat and its mechanism. Methods: Gene transfer technique was used to transfer AAV-ANG to the tumor. Growth curves were drawn to observe the growth of breast cancer implanted in rat, and immunohistochemical method was used to detect the effects of angiostatin on microvesel density (MVD) of breast cancer implanted in rat. Results: Angiostatin inhibited the growth of breast cancer implanted in rat and decreased the microvessel density of tumor. Conclusion: Expression of an angiostatin transgene can suppress the growth of breast cancer implanted in rat through the inhibition of the growth of microvessels, surggesting that angiostatin gene transfer technique may be effective against breast cancer.

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Overview of angiogenesis: Biologic implications for antiangiogenic therapy

Cited by 115 publications

References 51 publications

The Effects of Antiangiogenic Compound SU5416 in a Rat Model of Pulmonary Arterial Hypertension

The Effects of Antiangiogenic Compound SU5416 in a Rat Model of Pulmonary Arterial Hypertension

Inhibition of angiogenesis by vitamin D-binding protein: Characterization of anti-endothelial activity of DBP-maf

Growth inhibition of breast cancer in rat by AAV mediated angiostatin gene

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