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Related Concept Videos

Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
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...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Related Experiment Video

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Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells
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Published on: November 23, 2014

Response to anti-angiogenesis: an ever changing feature.

Francesco Bertolini1

  • 1Laboratory of Hematology-Oncology, Department of Pathology, European Institute of Oncology, 20141 Milan, Italy. francesco.bertolini@ieo.it

Breast (Edinburgh, Scotland)
|October 22, 2011
PubMed
Summary

New anti-angiogenic drugs show promise for cancer therapy, but clinical benefits are limited. Future research should explore resistance mechanisms and identify new vascular targets beyond VEGF.

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Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Anti-angiogenic drugs are approved for various advanced cancers, including breast, lung, colorectal, kidney, and CNS cancers.
  • Despite approvals, the clinical benefit of current anti-angiogenic therapies remains limited.

Purpose of the Study:

  • To review and discuss rational developments for a new generation of anti-angiogenic drugs.
  • To explore strategies for improving the efficacy of anti-angiogenic cancer therapies.

Main Methods:

  • Literature review focusing on current anti-angiogenic drug mechanisms and clinical outcomes.
  • Analysis of resistance and escape mechanisms associated with anti-VEGF therapies.
  • Identification of potential complementary vascular targets for novel anti-angiogenic drug development.

Main Results:

  • Current anti-angiogenic drugs primarily target Vascular Endothelial Growth Factor (VEGF) and its pathways.
  • Understanding resistance to anti-VEGF therapy is crucial for advancing treatment.
  • Identifying novel vascular targets is essential for developing next-generation anti-angiogenic drugs.

Conclusions:

  • Further research is needed to overcome limitations of current anti-angiogenic therapies.
  • Elucidating resistance mechanisms to anti-VEGF agents is a key area for investigation.
  • Discovering and validating complementary vascular targets will enable the development of more effective anti-angiogenic drugs.