Regulation of Angiogenesis and Tumorigenesis by Signal Transduction Cascades: Lessons from Benign and Malignant Endothelial Tumors  Robert Klafter, Jack L. Arbiser  Journal of Investigative Dermatology Symposium Proceedings  Volume 5, Issue 1, Pages 79-82 (December 2000) DOI: 10.1046/j.1087-0024.2000.00007.x Copyright © 2000 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 1 Dual regulation of MAP kinase and PI-3-K in normal cells by growth factors and oncogenes. Journal of Investigative Dermatology Symposium Proceedings 2000 5, 79-82DOI: (10.1046/j.1087-0024.2000.00007.x) Copyright © 2000 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 2 Regulation of the PI-3-K pathway by growth factors and oncogenes in p53 deficient cells. Journal of Investigative Dermatology Symposium Proceedings 2000 5, 79-82DOI: (10.1046/j.1087-0024.2000.00007.x) Copyright © 2000 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 3 Regulation of the MAP kinase pathway by growth factors and oncogenes in p16 deficient cells. Journal of Investigative Dermatology Symposium Proceedings 2000 5, 79-82DOI: (10.1046/j.1087-0024.2000.00007.x) Copyright © 2000 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 4 Two-hit hypothesis with reference to tumor angiogenesis. In neurofibromas, the first genetic hit is increased ras activation, so the benign tumors are already angiogenic. The second hit is loss of p53, which may result in only a slight increase in angiogenesis. In contrast, in melanoma progression, the first hit is loss of p16, which may not result in increased angiogenesis, but ras activation as a second hit will result in upregulation of angiogenesis. Journal of Investigative Dermatology Symposium Proceedings 2000 5, 79-82DOI: (10.1046/j.1087-0024.2000.00007.x) Copyright © 2000 The Society for Investigative Dermatology, Inc Terms and Conditions