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Tumor response to radiotherapy regulated by endothelial cell apoptosis

Monica Garcia-Barros1, Francois Paris, Carlos Cordon-Cardo

  • 1Laboratory of Signal Transduction, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA.

Science (New York, N.Y.)
|May 17, 2003
PubMed

Insights

Tumor response to radiation therapy depends on both cancer cell type and blood vessel sensitivity. Impaired endothelial apoptosis in tumor vasculature leads to radiation resistance, highlighting microvascular damage as a key factor in cancer treatment outcomes.

Area of Science:

  • Oncology
  • Cancer Biology
  • Radiation Oncology

Background:

  • Radiation therapy is a common cancer treatment, affecting approximately 50% of patients.
  • Tumor response to radiation is influenced by tumor cell characteristics and the tumor microenvironment.
  • The role of microvascular sensitivity in radiation response requires further investigation.

Purpose of the Study:

  • To investigate the hypothesis that tumor response to radiation therapy is determined by microvascular sensitivity.
  • To explore the impact of endothelial apoptosis on tumor growth and radiation resistance.
  • To determine if microvascular damage influences tumor cell response to clinically relevant radiation doses.

Main Methods:

  • Utilized MCA/129 fibrosarcomas and B16F1 melanomas in genetically modified mice.
  • Compared tumor growth and microvascular endothelial apoptosis in apoptosis-resistant (acid sphingomyelinase-deficient or Bax-deficient) mice versus wild-type mice.
  • Assessed tumor response to single-dose radiation up to 20 grays (Gy).

Main Results:

  • Tumors grown in apoptosis-resistant mice showed significantly reduced baseline microvascular endothelial apoptosis.
  • These tumors exhibited 200-400% faster growth compared to tumors in wild-type mice.
  • Tumors in apoptosis-resistant mice demonstrated reduced endothelial apoptosis upon irradiation and were resistant to radiation doses up to 20 Gy.
  • Tumors in wild-type mice showed sensitivity to radiation.

Conclusions:

  • Endothelial apoptosis acts as a homeostatic factor regulating angiogenesis-dependent tumor growth.
  • Microvascular sensitivity, specifically endothelial apoptosis, is a critical determinant of tumor response to radiation therapy.
  • Targeting microvascular damage could be a strategy to enhance radiation therapy efficacy in cancer treatment.

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