pphmtoolong,
Well, there's some new stuff, to me, included in those lectures, (see below). Whether or not it's trumpeted by PPHM, we'll see...
Localized/targeted interferon therapy could be quite an improvement.
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2:15 PM
Targeting Inside-Out Phosphatidylserine (PS) on Tumor Vascular Endothelium
Vascular targeting agents (VTAs) for the treatment of cancer are designed to selectively destroy the existing blood vessels of tumors, cause tumor cell death from ischemia and extensive hemorrhagic necrosis, unlike antiangiogenic drugs that inhibit the formation of new vessels. We have recently developed a novel vascular targeting antibody, 3G4, which binds to phosphatidylserine, a newly discovered tumor vascular target. 3G4 can specifically localize to and destroy tumor vasculature, markedly suppress tumor growth in multiple tumor models. Our preclinical studies have shown 3G4 can significantly enhance the therapeutic efficacy of conventional chemotherapeutic agents, radiation against both primary and metastatic tumors in multiple tumor models, including drug-resistant tumors. Currently a chimeric version of 3G4 is being tested in the clinic by Peregrine Pharmaceuticals, Inc. under the name Bavituximab. Initial data indicates that Bavituximab is well tolerated in patients. Despite promising therapeutic potential in pre-clinical studies, the anti-tumor efficacy of type I interferons in clinical trials has been limited by the very short half life and significant systemic toxicity at high doses. To overcome these obstacles, we engineered fusion proteins between 3G4 and murine type I interferons. The resulting fusion proteins demonstrated both antigen binding and cytokine activities in vitro. The fusion protein was capable of targeting tumor blood vessels and displayed potent anticancer effects in various murine tumor models in vivo without causing any observable toxicity. These studies demonstrate that 3G4 immunocytokines could have great potential for targeted immunotherapy of solid tumors.
9:30 AM
2C3, a Monoclonal Anti-VEGF Antibody that Selectively Inhibits VEGF Receptor 2 Activity Blocks Macrophage Infiltration into Tumors and Reduces Metastasis in a Preclinical Orthotopic Model of Pancreatic Cancer
VEGF is a primary stimulant of the development and maintenance of vascular networks in tumors. VEGF receptor 1 (VEGFR1) and 2 (VEGFR2) are tyrosine kinase cell surface receptors for VEGF. 2C3 is a mouse monoclonal antibody that selectively inhibits VEGF from binding and activating VEGFR2 but not VEGFR1. We have found that 2C3 augments the anti-tumor activity of chemotherapy and alone can reduce significantly metastatic spread of tumor cells. Furthermore, 2C3 reduces the infiltration of macrophages into the tumor mass, demonstrating that VEGFR2 functions as an important mediator of VEGF-induced chemotaxis of macrophages.
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