Introduction: Although anti-angiogenic inhibition (AI) therapy has demonstrable efficacy in mouse models of cancer and in certain types of human cancer, responses are typically transitory, followed by resumption of malignant progression that limits survival benefit. Unconventional modes of evasive/adaptive resistance underlay the eventual failures of anti-angiogenic therapy. Functionally established resistance mechanisms include revascularization mediated by alternative pro-angiogenic signals, protection by peri-vascular macrophages and monocytes to induce an immunosuppressive microenvironment, and normal vessel cooption via heightened local invasion and distant metastasis. All three mechanisms have been documented in the prototypical RIP-Tag2 mouse model of multistep tumorigenesis, in which the angiogenic switch is a discrete step in the pathway to invasive pancreatic neuroendocrine cancer.
Aim(s): Study evasion from AI.
Materials and methods: Preclinical studies
Conference: 14th Annual ENETS conference (2017)
Category: Medical treatment - Targeted therapies
Presenting Author: PhD Elizabeth Allen
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