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3. Data from Context-Dependent Role of Angiopoietin-1 Inhibition in the Suppression of Angiogenesis and Tumor Growth: Implications for AMG 386, an Angiopoietin-1/2–Neutralizing Peptibody

Author

Coxon, Angela, primary, Bready, James, primary, Min, Hosung, primary, Kaufman, Stephen, primary, Leal, Juan, primary, Yu, Dongyin, primary, Lee, Tani Ann, primary, Sun, Ji-Rong, primary, Estrada, Juan, primary, Bolon, Brad, primary, McCabe, James, primary, Wang, Ling, primary, Rex, Karen, primary, Caenepeel, Sean, primary, Hughes, Paul, primary, Cordover, David, primary, Kim, Haejin, primary, Han, Seog Joon, primary, Michaels, Mark L., primary, Hsu, Eric, primary, Shimamoto, Grant, primary, Cattley, Russell, primary, Hurh, Eunju, primary, Nguyen, Linh, primary, Wang, Shao Xiong, primary, Ndifor, Anthony, primary, Hayward, Isaac J., primary, Falcón, Beverly L., primary, McDonald, Donald M., primary, Li, Luke, primary, Boone, Tom, primary, Kendall, Richard, primary, Radinsky, Robert, primary, and Oliner, Jonathan D., primary

Published
2023
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4. Supplementary Figure 1 from Context-Dependent Role of Angiopoietin-1 Inhibition in the Suppression of Angiogenesis and Tumor Growth: Implications for AMG 386, an Angiopoietin-1/2–Neutralizing Peptibody

Author

Coxon, Angela, primary, Bready, James, primary, Min, Hosung, primary, Kaufman, Stephen, primary, Leal, Juan, primary, Yu, Dongyin, primary, Lee, Tani Ann, primary, Sun, Ji-Rong, primary, Estrada, Juan, primary, Bolon, Brad, primary, McCabe, James, primary, Wang, Ling, primary, Rex, Karen, primary, Caenepeel, Sean, primary, Hughes, Paul, primary, Cordover, David, primary, Kim, Haejin, primary, Han, Seog Joon, primary, Michaels, Mark L., primary, Hsu, Eric, primary, Shimamoto, Grant, primary, Cattley, Russell, primary, Hurh, Eunju, primary, Nguyen, Linh, primary, Wang, Shao Xiong, primary, Ndifor, Anthony, primary, Hayward, Isaac J., primary, Falcón, Beverly L., primary, McDonald, Donald M., primary, Li, Luke, primary, Boone, Tom, primary, Kendall, Richard, primary, Radinsky, Robert, primary, and Oliner, Jonathan D., primary

Published
2023
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5. Supplementary Methods, Figure Legends, and References from Context-Dependent Role of Angiopoietin-1 Inhibition in the Suppression of Angiogenesis and Tumor Growth: Implications for AMG 386, an Angiopoietin-1/2–Neutralizing Peptibody

Author

Coxon, Angela, primary, Bready, James, primary, Min, Hosung, primary, Kaufman, Stephen, primary, Leal, Juan, primary, Yu, Dongyin, primary, Lee, Tani Ann, primary, Sun, Ji-Rong, primary, Estrada, Juan, primary, Bolon, Brad, primary, McCabe, James, primary, Wang, Ling, primary, Rex, Karen, primary, Caenepeel, Sean, primary, Hughes, Paul, primary, Cordover, David, primary, Kim, Haejin, primary, Han, Seog Joon, primary, Michaels, Mark L., primary, Hsu, Eric, primary, Shimamoto, Grant, primary, Cattley, Russell, primary, Hurh, Eunju, primary, Nguyen, Linh, primary, Wang, Shao Xiong, primary, Ndifor, Anthony, primary, Hayward, Isaac J., primary, Falcón, Beverly L., primary, McDonald, Donald M., primary, Li, Luke, primary, Boone, Tom, primary, Kendall, Richard, primary, Radinsky, Robert, primary, and Oliner, Jonathan D., primary

Published
2023
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6. Supplementary Figure 4 from Context-Dependent Role of Angiopoietin-1 Inhibition in the Suppression of Angiogenesis and Tumor Growth: Implications for AMG 386, an Angiopoietin-1/2–Neutralizing Peptibody

Author

Coxon, Angela, primary, Bready, James, primary, Min, Hosung, primary, Kaufman, Stephen, primary, Leal, Juan, primary, Yu, Dongyin, primary, Lee, Tani Ann, primary, Sun, Ji-Rong, primary, Estrada, Juan, primary, Bolon, Brad, primary, McCabe, James, primary, Wang, Ling, primary, Rex, Karen, primary, Caenepeel, Sean, primary, Hughes, Paul, primary, Cordover, David, primary, Kim, Haejin, primary, Han, Seog Joon, primary, Michaels, Mark L., primary, Hsu, Eric, primary, Shimamoto, Grant, primary, Cattley, Russell, primary, Hurh, Eunju, primary, Nguyen, Linh, primary, Wang, Shao Xiong, primary, Ndifor, Anthony, primary, Hayward, Isaac J., primary, Falcón, Beverly L., primary, McDonald, Donald M., primary, Li, Luke, primary, Boone, Tom, primary, Kendall, Richard, primary, Radinsky, Robert, primary, and Oliner, Jonathan D., primary

Published
2023
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7. Supplementary Figure 2 from Context-Dependent Role of Angiopoietin-1 Inhibition in the Suppression of Angiogenesis and Tumor Growth: Implications for AMG 386, an Angiopoietin-1/2–Neutralizing Peptibody

Author

Coxon, Angela, primary, Bready, James, primary, Min, Hosung, primary, Kaufman, Stephen, primary, Leal, Juan, primary, Yu, Dongyin, primary, Lee, Tani Ann, primary, Sun, Ji-Rong, primary, Estrada, Juan, primary, Bolon, Brad, primary, McCabe, James, primary, Wang, Ling, primary, Rex, Karen, primary, Caenepeel, Sean, primary, Hughes, Paul, primary, Cordover, David, primary, Kim, Haejin, primary, Han, Seog Joon, primary, Michaels, Mark L., primary, Hsu, Eric, primary, Shimamoto, Grant, primary, Cattley, Russell, primary, Hurh, Eunju, primary, Nguyen, Linh, primary, Wang, Shao Xiong, primary, Ndifor, Anthony, primary, Hayward, Isaac J., primary, Falcón, Beverly L., primary, McDonald, Donald M., primary, Li, Luke, primary, Boone, Tom, primary, Kendall, Richard, primary, Radinsky, Robert, primary, and Oliner, Jonathan D., primary

Published
2023
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8. Supplementary Figure 3 from Context-Dependent Role of Angiopoietin-1 Inhibition in the Suppression of Angiogenesis and Tumor Growth: Implications for AMG 386, an Angiopoietin-1/2–Neutralizing Peptibody

Author

Coxon, Angela, primary, Bready, James, primary, Min, Hosung, primary, Kaufman, Stephen, primary, Leal, Juan, primary, Yu, Dongyin, primary, Lee, Tani Ann, primary, Sun, Ji-Rong, primary, Estrada, Juan, primary, Bolon, Brad, primary, McCabe, James, primary, Wang, Ling, primary, Rex, Karen, primary, Caenepeel, Sean, primary, Hughes, Paul, primary, Cordover, David, primary, Kim, Haejin, primary, Han, Seog Joon, primary, Michaels, Mark L., primary, Hsu, Eric, primary, Shimamoto, Grant, primary, Cattley, Russell, primary, Hurh, Eunju, primary, Nguyen, Linh, primary, Wang, Shao Xiong, primary, Ndifor, Anthony, primary, Hayward, Isaac J., primary, Falcón, Beverly L., primary, McDonald, Donald M., primary, Li, Luke, primary, Boone, Tom, primary, Kendall, Richard, primary, Radinsky, Robert, primary, and Oliner, Jonathan D., primary

Published
2023
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32. Context-Dependent Role of Angiopoietin-1 Inhibition in the Suppression of Angiogenesis and Tumor Growth: Implications for AMG 386, an Angiopoietin-1/2–Neutralizing Peptibody

Author

Coxon, Angela, primary, Bready, James, additional, Min, Hosung, additional, Kaufman, Stephen, additional, Leal, Juan, additional, Yu, Dongyin, additional, Lee, Tani Ann, additional, Sun, Ji-Rong, additional, Estrada, Juan, additional, Bolon, Brad, additional, McCabe, James, additional, Wang, Ling, additional, Rex, Karen, additional, Caenepeel, Sean, additional, Hughes, Paul, additional, Cordover, David, additional, Kim, Haejin, additional, Han, Seog Joon, additional, Michaels, Mark L., additional, Hsu, Eric, additional, Shimamoto, Grant, additional, Cattley, Russell, additional, Hurh, Eunju, additional, Nguyen, Linh, additional, Wang, Shao Xiong, additional, Ndifor, Anthony, additional, Hayward, Isaac J., additional, Falcón, Beverly L., additional, McDonald, Donald M., additional, Li, Luke, additional, Boone, Tom, additional, Kendall, Richard, additional, Radinsky, Robert, additional, and Oliner, Jonathan D., additional

Published
2010
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37. Cellular Actions of Angiogenesis Inhibitors on Blood Vessels.

Author

Marmé, Dieter, Fusenig, Norbert, Baluk, Peter, Falcón, Beverly L., Hashizume, Hiroya, Sennino, Barbara, and McDonald, Donald M.

Abstract

Blood vessels of tumors have multiple cellular abnormalities that impair blood flow and drug delivery but provide targets for novel therapeutics. These abnormalities involve all components of the vessel wall, including endothelial cells, pericytes, and vascular basement membrane. Endothelial cells of tumor vessels have abnormal gene expression, are dynamic, and undergo sprouting, proliferation, and regression. The endothelial cells have a defective barrier function, are leaky, and may depend on vascular endothelial growth factor (VEGF) for survival. Pericytes of tumor vessels lack the normally intimate association with endothelial cells, and the surrounding basement membrane has redundant loose layers that reflect continual remodeling of the vasculature. Studies of the cellular actions of VEGF inhibitors on mouse models of spontaneous and implanted tumors have shown rapid, robust changes in tumor vessels. Strikingly, in some tumors, within 24 h, endothelial fenestrations disappear, vascular sprouting is suppressed, blood flow ceases, and patency is lost in many vessels. As many as 80% of tumor vessels may regress within 7 days. Similarly, normal blood vessels with abundant endothelial fenestrations, as in the gastrointestinal tract, kidney, and endocrine organs, may be sensitive to VEGF inhibitors. Surviving tumor vessels acquire more normal features, including uniform caliber, diminished branching, reduced VEGFR-2 expression, and tighter pericyte coverage. Empty sleeves ofvascularbasementmembrane, leftbehind after endothelial cells degenerate, provide a record of pretreatment vessel number and a scaffold for vascular regrowth after cessation of therapy. Normalization of surviving tumor vessels may improve local hemodynamics and perivascular delivery of oxygen, nutrients, and therapeutics, despite reduced angiogenesis and tumor vascularity. [ABSTRACT FROM AUTHOR]

Published
2008
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38. VEGF and c-Met Blockade Amplify Angiogenesis Inhibition in Pancreatic Islet Cancer.

Author

Weon-Kyoo You, Sennino, Barbara, Williamson, Casey W., Falcón, Beverly, Hashizume, Hiroya, Li-Chin Yao, Aftab, Dana T., and McDonald, Donald M.

Subjects
*NEOVASCULARIZATION, *CANCER invasiveness, *METASTASIS, *ISLANDS of Langerhans, *PANCREATIC cancer, *PROTEIN-tyrosine kinases, *CANCER
Abstract

Angiogenesis inhibitors that block VEGF receptor (VEGFR) signaling slow the growth of many types of tumors, but eventually the disease progresses. Multiple strategies are being explored to improve efficacy by concurrent inhibition of other functionally relevant receptor tyrosine kinases (RTK). XL880 (foretinib, GSK1363089) and XL184 (cabozantinib) are small-molecule inhibitors that potently block multiple RTKs, including VEGFR and the receptor of hepatocyte growth factor c-Met, which can drive tumor invasion and metastasis. This study compared the cellular effects of XL880 and XL184 with those of an RTK inhibitor (XL999) that blocks VEGFR but not c-Met. Treatment of RIP-Tag2 mice with XL999 resulted in 43% reduction in vascularity of spontaneous pancreatic islet tumors over 7 days, but treatment with XL880 or XL184 eliminated approximately 80% of the tumor vasculature, reduced pericytes and empty basement membrane sleeves, caused widespread intratumoral hypoxia and tumor cell apoptosis, and slowed regrowth of the tumor vasculature after drug withdrawal. Importantly, XL880 and XL184 also decreased invasiveness of primary tumors and reduced metastasis. Overall, these findings indicate that inhibition of c-Met and functionally related kinases amplifies the effects of VEGFR blockade and leads to rapid, robust, and progressive regression of tumor vasculature, increased intratumoral hypoxia and apoptosis, and reduced tumor invasiveness and metastasis. Cancer Res; 71(14); 4758-68. © 2011 AACR. [ABSTRACT FROM AUTHOR]

Published
2011
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