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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...
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.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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.
The mTOR pathway or the...

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Updated: Jul 4, 2026

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 microenvironment and angiogenesis.

Pia Nyberg1, Tuula Salo, Raghu Kalluri

  • 1Department of Diagnostics and Oral Medicine, Institute of Dentistry, University of Oulu, Finland. pia.nyberg@oulu.fi

Frontiers in Bioscience : a Journal and Virtual Library
|May 30, 2008
PubMed
Summary

The tumor microenvironment, a complex mix of cells and matrix, significantly influences pathological angiogenesis. It contains both inhibitors and promoters of blood vessel growth, crucial for tumor expansion and metastasis.

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Isolation and Culture Expansion of Tumor-specific Endothelial Cells
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Assessing Tumor Microenvironment of Metastasis Doorway-Mediated Vascular Permeability Associated with Cancer Cell Dissemination using Intravital Imaging and Fixed Tissue Analysis
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Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells

Published on: November 23, 2014

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • The tumor microenvironment (TME) comprises extracellular matrix, tumor cells, endothelial cells, fibroblasts, and immune cells.
  • Tumor growth and metastasis depend on angiogenesis, the formation of new blood vessels.
  • The TME plays a critical role in regulating this pathological angiogenic process.

Purpose of the Study:

  • To elucidate the multifaceted role of the tumor microenvironment in regulating pathological angiogenesis.
  • To understand how various components within the TME, including extracellular matrix and stromal cells, influence blood vessel formation.

Main Methods:

  • This study is a review and synthesis of existing research on the tumor microenvironment and angiogenesis.
  • Analysis of literature focusing on the composition and function of the TME.
  • Examination of the interactions between TME components and angiogenic processes.

Main Results:

  • The TME contains both angiogenesis inhibitors (e.g., endostatin) and promoters derived from extracellular matrix molecules.
  • Carcinoma-associated fibroblasts, a major stromal cell type, exhibit a distinct phenotype and contribute to angiogenesis by secreting growth factors.
  • Immune cells like macrophages and neutrophils are significant sources of chemokines and growth factors that regulate angiogenesis.

Conclusions:

  • The tumor microenvironment is a complex, disorganized tissue that actively regulates the angiogenic switch.
  • Understanding the intricate interactions within the TME is crucial for developing targeted anti-angiogenic therapies.
  • The diverse cellular and matrix components of the TME collectively orchestrate pathological angiogenesis, impacting tumor progression.