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About 50% of cancer patients receive radiation therapy. Herewe investigated the hypothesis that tumor response to radiationis determined not only by tumor cell phenotype but also by microvascularsensitivity. MCA/129 fibrosarcomas and B16F1 melanomas grownin apoptosis-resistant acid sphingomyelinase (asmase)–deficientor Bax-deficient mice displayed markedly reduced baseline microvascularendothelial apoptosis and grew 200 to 400% faster than tumorson wild-type microvasculature. Thus, endothelial apoptosis isa homeostatic factor regulating angiogenesis-dependent tumorgrowth. Moreover, these tumors exhibited reduced endothelialapoptosis upon irradiation and, unlike tumors in wild-type mice,they were resistant to single-dose radiation up to 20 grays(Gy). These studies indicate that microvascular damage regulatestumor cell response to radiation at the clinically relevantdose range.
1 Laboratory of Signal Transduction, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA. 2 Department of Pathology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA. 3 Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA. 4 Department of Radiation Oncology, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA. 5 Department of Hematology-Oncology, Cornell University Medical College, New York, NY 10021, USA.
* These authors contributed equally to this work.
To whom correspondence should be addressed. E-mail: r-kolesnick{at}ski.mskcc.org
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Translating angiogenesis research into the clinic: the challenges ahead.
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