Does an activated oncogene that initiates tumor growth need to remain activated to maintain the cancer phenotype? This question has been answered affirmatively by experiments in which doxycycline-regulated oncogene activation induces growth of large tumors that regress completely upon oncogene inactivation - a phenomenon called oncogene addiction. We assemble here the evidence that oncogene addiction is angiogenesis-dependent. Although activated oncogenes increase tumor cell proliferation and decrease their apoptosis, these activities are not sufficient to expand tumor mass beyond a microscopic size. Oncogenes must also induce tumor angiogenesis for expansion of tumor mass. We propose experiments to validate the "endothelial centric" hypothesis of oncogene addiction. © 2005 Cold Spring Harbor Laboratory Press.
CITATION STYLE
Folkman, J., & Ryeom, S. (2005). Is oncogene addiction angiogenesis-dependent? In Cold Spring Harbor Symposia on Quantitative Biology (Vol. 70, pp. 389–397). https://doi.org/10.1101/sqb.2005.70.042
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