Cancer neoantigens targeted by adoptive T cell transfer: private no more
Enrico Lugli,1,2 Pia Kvistborg,3 and Giovanni Galletti1
1Laboratory of Translational Immunology and
2Flow Cytometry Core, Humanitas Clinical and Research Center, Rozzano, Milan, Italy.
3Division of Molecular Oncology and Immunology, The Netherlands Cancer Institute, Amsterdam, Netherlands.
Address correspondence to: Enrico Lugli, Laboratory of Translational Immunology, Humanitas Clinical and Research Center, Via Alessandro Manzoni 113, Rozzano, Milan, Italy. Phone: 39.02.8224.5143; Email: enrico.lugli@humanitasresearch.it.
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1Laboratory of Translational Immunology and
2Flow Cytometry Core, Humanitas Clinical and Research Center, Rozzano, Milan, Italy.
3Division of Molecular Oncology and Immunology, The Netherlands Cancer Institute, Amsterdam, Netherlands.
Address correspondence to: Enrico Lugli, Laboratory of Translational Immunology, Humanitas Clinical and Research Center, Via Alessandro Manzoni 113, Rozzano, Milan, Italy. Phone: 39.02.8224.5143; Email: enrico.lugli@humanitasresearch.it.
Find articles by Kvistborg, P. in: JCI | PubMed | Google Scholar
1Laboratory of Translational Immunology and
2Flow Cytometry Core, Humanitas Clinical and Research Center, Rozzano, Milan, Italy.
3Division of Molecular Oncology and Immunology, The Netherlands Cancer Institute, Amsterdam, Netherlands.
Address correspondence to: Enrico Lugli, Laboratory of Translational Immunology, Humanitas Clinical and Research Center, Via Alessandro Manzoni 113, Rozzano, Milan, Italy. Phone: 39.02.8224.5143; Email: enrico.lugli@humanitasresearch.it.
Find articles by Galletti, G. in: JCI | PubMed | Google Scholar
First published February 4, 2019 - More info
J Clin Invest. 2019;129(3):949–951. https://doi.org/10.1172/JCI126295.
Copyright © 2019, American Society for Clinical Investigation
Effector T cell responses directed toward cancer neoantigens mediate tumor regression following checkpoint blockade or adoptive T cell immunotherapy, but are generally “private”, thus requiring considerable effort for their identification. In this issue of the JCI, Malekzadeh et al. show that a fraction of patients with epithelial cancers mount antigen-specific T cell responses to “hot spot” p53 mutations that in some cases are shared among patients. This work suggests that other genes frequently mutated in human cancer can be immunogenic, thus offering a rapid way to screen for cancer neoantigens that can be targeted by subsequent T cell–based therapies.
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