Generation of Multiple Angiogenesis Inhibitors by Human Pancreatic Cancer1
[CANCER RESEARCH 61, 7298–7304, October 1, 2001] Generation of Multiple Angiogenesis Inhibitors by Human Pancreatic Cancer1 Oliver Kisker, Shinya Onizuka, Jacqueline Banyard, Tomoko Komiyama, Christian M. Becker, Eike Gert Achilles, Carmen M. Barnes, Michael S. O’Reilly, Judah Folkman,2 and Steven R. Pirie-Shepherd Laboratory of Surgical Research, Children’s Hospital, Boston, Massachusetts 02115 [O. K., S. O., J. B., C. M. Be., E. G. A., C. M. Ba., J. F., S. R. P-S.]; University Hospital Marburg, Department of General Surgery, Philipps University, Marburg, Germany [O. K.]; Department of Surgery II, Nagasaki University, Nagasaki Japan [S. O.]; Department of Biological Chemistry, University Michigan Medical School, Ann Arbor, Michigan 48109 [T. K.]; University Hospital Benjamin Franklin, Department of Gynecology and Obstetrics, Free University Berlin, Berlin, Germany [C. M. Be.]; University Hospital Hamburg, Department of Hepato-Biliary Surgery, University of Hamburg, Hamburg, Germany [E. G. A.]; Department of Radiation Oncology, University of Texas, MD Anderson Cancer Center, Houston, Texas 77030 [M. S. O.]; Departments of Surgery and Cell Biology, Harvard Medical School, Boston, Massachusetts 02115 [J. F.]; and Attenuon LLC, San Diego, California 92121 [S. R. P-S.] ABSTRACT Such inhibition of angiogenesis is thought to be achieved via the generation of circulating endothelial cell-specific inhibitors by the A primary inoculum of human pancreatic cancer cells (BxPC-3) has the primary tumor mass (10). Consequently, removal of certain primary ability to inhibit the growth of a secondary tumor in an in vivo animal tumors can often result in rapid growth of metastases undetected model. Such ability suggests that the primary tumor is producing inhib- itors that act at the site of the secondary tumor.
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