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Related Concept Videos

Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
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Regulation of Angiogenesis and Blood Supply

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Related Experiment Video

Updated: Jul 11, 2026

Modeling Spontaneous Metastatic Renal Cell Carcinoma (mRCC) in Mice Following Nephrectomy
11:27

Modeling Spontaneous Metastatic Renal Cell Carcinoma (mRCC) in Mice Following Nephrectomy

Published on: April 29, 2014

[Angiogenesis and renal cell carcinoma].

Bertrand Billemont1, Jean-Baptiste Méric, Hassan Izzedine

  • 1Hôpital Pitié-Salpêtrière, Service d'oncologie médicale, 47, boulevard de l'Hôpital, 75013 Paris.

Bulletin Du Cancer
|September 13, 2007
PubMed
Summary

Targeting angiogenesis with targeted therapies like sunitinib and sorafenib has shown significant improvements in treating metastatic renal cell carcinoma (RCC). These novel treatments offer better response rates and progression-free survival compared to traditional therapies.

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Modeling Spontaneous Metastatic Renal Cell Carcinoma (mRCC) in Mice Following Nephrectomy
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Comparing Metastatic Clear Cell Renal Cell Carcinoma Model Established in Mouse Kidney and on Chicken Chorioallantoic Membrane

Published on: February 8, 2020

Area of Science:

  • Molecular biology of renal cell carcinoma (RCC)
  • Oncology
  • Pharmacology

Background:

  • Angiogenesis is crucial in renal cell carcinoma (RCC) pathophysiology.
  • Key mediators include Von Hippel-Lindau (VHL) alterations, HIFalpha accumulation, and VEGF overexpression.
  • Targeting angiogenesis is a key strategy for metastatic RCC treatment.

Purpose of the Study:

  • To review developments in the molecular biology of RCC over the past 20 years.
  • To discuss anti-angiogenic strategies for metastatic RCC treatment.
  • To present clinical data on targeted therapies such as sunitinib and sorafenib.

Main Methods:

  • Review of molecular biology knowledge in RCC.
  • Analysis of anti-angiogenic therapeutic strategies.
  • Presentation of data from phase III clinical trials (sunitinib vs. interferon-alpha, sorafenib vs. placebo).

Main Results:

  • Sunitinib demonstrated superior response rates (31% vs. 6%) and progression-free survival (11 vs. 5 months) compared to interferon-alpha in metastatic RCC.
  • Sorafenib showed a significantly longer time to progression (24 vs. 12 weeks) compared to placebo in a phase III study.
  • Other targeted agents like axitinib, pazopanib, and bevacizumab are also under investigation.

Conclusions:

  • Targeted therapies inhibiting angiogenesis, such as sunitinib and sorafenib, represent significant advancements in metastatic RCC treatment.
  • These agents offer improved efficacy over traditional therapies.
  • Ongoing research continues to explore novel anti-angiogenic molecules for RCC.