Targeted Anticancer Therapies: Mouse Models Help Uncover the Mechanisms of Tumor Escape

Abstract

(Cancer Cell 13, 5–7; January 2008) We erroneously reported that the studies by Williams et al., 2006Williams R.T. Roussel M.F. Sherr C.J. Arf gene loss enhances oncogenicity and limits imatinib response in mouse models of Bcr-Abl-induced acute lymphoblastic leukemia.Proc. Natl. Acad. Sci. USA. 2006; 103: 6688-6693Crossref PubMed Scopus (161) Google Scholar, Williams et al., 2007Williams R.T. den Besten W. Sherr C.J. Cytokine-dependent imatinib resistance in mouse BCR-ABL+, Arf-null lymphoblastic leukemia.Genes Dev. 2007; 21: 2283-2287Crossref PubMed Scopus (143) Google Scholar were performed in a mouse model for CML, which shows a favorable clinical response to imatinib treatment. In fact, their studies addressed the role of the p19ARF locus in BCR/ABL-driven ALL, which shows a poor response to treatment with imatinib. We sincerely apologize for this inaccuracy but feel compelled to inform the reader of our mistake. Targeted Anticancer Therapies: Mouse Models Help Uncover the Mechanisms of Tumor Escapevan Amerongen et al.Cancer CellJanuary 08, 2008In BriefIn contrast to conventional chemotherapeutic agents, modern anticancer therapies are aimed at attacking specific targets in a tumor. While these therapies show promising clinical effects, their success is limited by the development of resistance to the antitumor agent, a phenomenon that is well known in regular cancer therapies. As illustrated in a novel study by Debies and colleagues in The Journal of Clinical Investigation, mouse models for cancer serve as promising tools for advancing our understanding of the tumor response to targeted therapy. Full-Text PDF Open Archive