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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...
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,...
Selectins01:25

Selectins

Cell adhesion is  an essential aspect of multicellularity. While stable cell interactions usually occur between cells of the same type, transient cell interactions occur between cells of different tissue types, such as between neutrophils and endothelial cells. Selectins are one class of cell adhesion molecules (CAMs) that bind carbohydrate ligands to form transient cell adhesion. They are rod-like proteins with a long extracellular part of variable length ending with the lectin domain, which...

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Updated: Jun 21, 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 endothelial cells join the resistance.

Andrew C Dudley1, Michael Klagsbrun

  • 1Vascular Biology Program, Departments of Surgery and Pathology, Harvard Medical School, Boston, MA 02115, USA. andrew.dudley@childrens.harvard.edu

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|July 30, 2009
PubMed
Summary

Tumor blood vessels are surprisingly complex. Tumor-specific endothelial cells show reduced sensitivity to anti-cancer drugs compared to normal cells, impacting antiangiogenesis therapy effectiveness.

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Area of Science:

  • Oncology
  • Vascular Biology
  • Cancer Therapeutics

Background:

  • Antiangiogenesis research aims to inhibit tumor blood vessel formation.
  • Tumor vasculature is unexpectedly complex and dynamic.
  • Previous assumptions about tumor blood vessels require revision.

Purpose of the Study:

  • To investigate the sensitivity of tumor-specific endothelial cells to cytotoxic and antiangiogenic drugs.
  • To understand the implications of endothelial cell heterogeneity in cancer treatment.

Main Methods:

  • Comparative drug sensitivity assays.
  • Analysis of endothelial cell responses to various therapeutic agents.
  • Utilizing models to study tumor-specific endothelial cell behavior.

Main Results:

  • Tumor-specific endothelial cells exhibit significantly lower sensitivity to cytotoxic drugs.
  • These specialized cells are also less responsive to antiangiogenic agents.
  • This differential sensitivity challenges existing therapeutic strategies.

Conclusions:

  • Endothelial cell differences between tumors and normal tissues are critical.
  • The reduced drug sensitivity of tumor endothelial cells may limit the efficacy of antiangiogenesis therapies.
  • Further research is needed to develop strategies overcoming this resistance.