Summary Studies in mice suggest that antiangiogenesis therapies could lead to tumor metastasis and should be modified to prevent this effect. In a mouse model of pancreatic neuroendocrine cancer, an anti-VEGFR2 antibody lowered tumor vasculature and volume compared with what was seen in untreated mice, but it caused increased tumor invasiveness following one week of treatment. In the mouse model, antiangiogenesis treatment also enlarged lymph nodes, caused increased liver metastasis and caused hypoxic cancer conditions. Similar results were seen in a model of glioblastoma multiforme (GBM) treated with the VEGFR-selective kinase inhibitor SU10944 and the multitargeted VEGFR kinase inhibitor Sutent sunitinib, both from Pfizer Inc. Additional studies are under way in different cancer types to identify the pathways responsible for the compounds' malignant effects so that they could be targeted by future therapeutics. Pfizer markets Sutent to treat renal and gastrointestinal cancers. ... Reference 1. Paez-Ribes, M. et al. Cell; published online March 2, 2009; doi:10.1016/j.ccr.2009.01.027 | Article | Contact: Oriol Casanovas, Catalan Institute of Oncology, L'Hospitalet de Llobregat, Spain e-mail: ocasanovas@iconcologia.net Contact: Douglas Hanahan, University of California, San Francisco, Calif. e-mail: dh@ucsf.edu