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Related Concept Videos

The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
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...

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Related Experiment Video

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Isolation and Culture Expansion of Tumor-specific Endothelial Cells
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Isolation and Culture Expansion of Tumor-specific Endothelial Cells

Published on: October 14, 2015

Tumor endothelial cells.

Andrew C Dudley1

  • 1Department of Cellular and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA; Lineberger Comprehensive Cancer Center, Chapel Hill, North Carolina 27599, USA; and McAllister Heart Institute, Chapel Hill, North Carolina 27599, USA. acdudley@med.unc.edu

Cold Spring Harbor Perspectives in Medicine
|March 7, 2012
PubMed
Summary
This summary is machine-generated.

Tumor blood vessels exhibit dysfunction due to factors like hypoxia, leading to abnormal blood flow and contributing to tumor growth and metastasis. Understanding these endothelial abnormalities is key for developing effective anti-cancer therapies.

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Area of Science:

  • Oncology
  • Vascular Biology
  • Cellular Biology

Background:

  • The vascular endothelium is a vital cellular layer regulating nutrient and leukocyte transport.
  • Tumor microenvironments induce endothelial dysfunction, characterized by irregular, fragile, and leaky tumor blood vessels.
  • Abnormalities in tumor endothelium are implicated in tumor progression, growth, and metastasis.

Purpose of the Study:

  • To investigate the biological basis of tumor endothelial dysfunction.
  • To understand the role of endothelial abnormalities in tumor pathophysiology.
  • To inform the development of targeted antiangiogenic therapies.

Main Methods:

  • This study focuses on the biological mechanisms of tumor endothelial dysfunction.
  • Analysis of factors contributing to abnormal tumor vasculature.
  • Review of evidence linking tumor endothelium to cancer progression.

Main Results:

  • Tumor-associated factors such as hypoxia and growth factors cause endothelial dysfunction.
  • Tumor blood vessels display irregular diameters, fragility, leakiness, and abnormal blood flow.
  • These vascular abnormalities significantly contribute to tumor growth and metastasis.

Conclusions:

  • Endothelial dysfunction is a critical component of tumor pathophysiology.
  • Understanding tumor vasculature is essential for effective cancer treatment.
  • Targeting tumor angiogenesis holds promise for anti-cancer strategies.