Colombo, M.P. (Mario P.)

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    Seventh annual meeting of the Italian Network for Tumor Biotherapy (NIBIT), Siena, 1-3 October 2009
    (Springer Verlag, 2010) Moschella, F. (F.); Protti, M.P. (M.P.); Monsurro, V. (V); Queirolo, P. (Paola); Hwu, P. (Patrick); Camerini, R. (Roberto); Calabro, L. (L); Colombo, M.P. (Mario P.); Giovannoni, L. (L.); Russo, V. (Vicenzo); Fonsati, E. (Ester); Di-Giacomo, A.M. (A.M.); Camisaschi, C. (C); Nicolay, H.J.M. (Hugues J.M.); Maio, M. (Michele); Puccetti, P. (P); Maccalli, C. (Cristina); Bronstein, J. (Judith); Lehmann, F. (F.); Sangiolo, D. (D.); Anichini, A. (A); Allavena, P. (P); Bellone, M. (M); Shuler, G. (G); Melero, I. (Ignacio); Ferlazzo, G. (G.); Danova, M. (M); Parmiani, G. (Giorgio); Di-Nicola, M. (Massimo); Ponzoni, M. (M); Montagna, D. (D.); Castelli, C. (Chiara); Ascierto, P.A. (Paolo Antonio); Belardelli, F. (Filipppo); Ridolfi, R. (Ruggero)
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    Low surface expression of B7-1 (CD80) is an immunoescape mechanism of colon carcinoma
    (American Association for Cancer Research, 2006) Berraondo, P. (Pedro); Berasain, C. (Carmen); Colombo, M.P. (Mario P.); Murillo, O. (Oihana); Gonzalez-Hernandez, A. (Alvaro); Zaratiegui, M. (Mikel); Melero, I. (Ignacio); Prieto, J. (Jesús); Huarte, E. (Eduardo); Tirapu, I. (Íñigo); Fortes, P. (Puri); Guiducci, C. (Cristiana); Chen, L. (Lieping); Arina, A. (Ainhoa)
    Artificially enforced expression of CD80 (B7-1) and CD86 (B7-2) on tumor cells renders them more immunogenic by triggering the CD28 receptor on T cells. The enigma is that such B7s interact with much higher affinity with CTLA-4 (CD152), an inhibitory receptor expressed by activated T cells. We show that unmutated CD80 is spontaneously expressed at low levels by mouse colon carcinoma cell lines and other transplantable tumor cell lines of various tissue origins. Silencing of CD80 by interfering RNA led to loss of tumorigenicity of CT26 colon carcinoma in immunocompetent mice, but not in immunodeficient Rag-/- mice. CT26 tumor cells bind CTLA-4Ig, but much more faintly with a similar CD28Ig chimeric protein, thus providing an explanation for the dominant inhibitory effects on tumor immunity displayed by CD80 at that expression level. Interestingly, CD80-negative tumor cell lines such as MC38 colon carcinoma and B16 melanoma express CD80 at dim levels during in vivo growth in syngeneic mice. Therefore, low CD80 surface expression seems to give an advantage to cancer cells against the immune system. Our findings are similar with the inhibitory role described for the dim CD80 expression on immature dendritic cells, providing an explanation for the low levels of CD80 expression described in various human malignancies.
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    Feeding dendritic cells with tumor antigens: self-service buffet or à la carte?
    (Nature Publishing Group, 2000) Vile, R.G. (Richard G.); Colombo, M.P. (Mario P.); Melero, I. (Ignacio)
    Adoptive transfer of autologous dendritic cells (DC) presenting tumor-associated antigens initiate and sustain an immune response which eradicate murine malignancies. Based on these observations, several clinical trials are in progress testing safety and efficacy with encouraging preliminary reports. In these approaches, ex vivo incubation of DC with a source of tumor antigens is required to load the relevant antigenic epitopes on the adequate antigen presenting molecules. Recent data show that in some instances exogenous DC artificially injected into malignant tissue or endogenous DC attracted to the tumor nodule by means of gene transfer of GM-CSF and CD40L into malignant cells result in efficacious antitumor immunity. In the case of intratumoral injection of DC the procedure is curative only if DC had been genetically engineered to produce IL-12, IL-6 or to express CD40L. Evidence has been obtained showing that intratumoral DC can capture and process tumor antigens to be presented to T-lymphocytes. Although the exact mechanisms of tumor antigen acquisition by DC are still unclear, available data suggest a role for heat shock proteins released from dying malignant cells and for the internalization of tumor-derived apoptotic bodies. Roles for tumor necrosis versus apoptosis are discussed in light of the 'danger theory'.
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    Classification of current anticancer immunotherapies
    (Impact Journals, 2014) Bracci, L. (Laura); Silva-Santos, B. (Bruno); Mach, J.P. (Jean-Pierre); Hoos, A. (Axel); Abastado, J.P. (Jean-Pierre); Ayyoub, M. (Maha); Whiteside, T.L. (Theresa L.); Vile, R.G. (Richard G.); Rizvi, N. (Naiyer); Galon, J. (Jerome); Odunsi, A. (Adekunke); Kirkwood, J.M. (John M.); Galluzzi, L. (Lorenzo); Ghiringhelli, F. (François); Cerundolo, V. (Vincenzo); Gabrilovich, D.I. (Dmitry I.); Melief, C.J. (Cornelis J.); Speiser, D.E. (Daniel E.); Castoldi, F. (Francesca); Kalinski, P. (Pawel); Senovilla, L. (Laura); Tartour, E. (Eric); Colombo, M.P. (Mario P.); Schreiber, H. (Hans); Jäger, D. (Dirk); Mavilio, D. (Domenico); Kroemer, G. (Guido); Apte, R.N. (Ron N.); Porgador A. (Ángel); Blay, J.Y. (Jean-Yves); Fucíková, J. (Jitka); Rabinovich, G.A. (Gabriel A.); Sautès-Fridman, C. (Catherine); Lugli, E. (Enrico); Fridman, W.H. (Wolf H.); Baracco, E.E. (Elisa Elena); Van-Der-Burg, S.H. (Sjoerd H.); Klein, E. (Eva); Srivastava, P.K. (Pramod K.); Kärre, K. (Klas); Gnjatic,S. (Sacha); Agostinis, P. (Patrizia); Aranda, F. (Fernando); Lewis, C.E. (Claire E.); Bloy, N. (Norma); Vacchelli, E. (Erika); Caignard, A. (Anne); Melero, I. (Ignacio); Kiessling, R. (Rolf); Restifo, N.P. (Nicholas P.); Smyth, M.J. (Mark J.); Zitvogel, L. (Laurence); Fearon, D.T. (Douglas T.); Seliger, B. (Barbara); Prendergast, G.C. (George C.); Pienta, K.J. (Kenneth J.); Wolchok, J.D. (Jedd D.); Clayton, A. (Aled); Cavallo, F. (Federica); Hosmalin, A. (Anne); Knuth, A. (Alexander); Lotze, M.T. (Michael T.); Coussens, L. (Lisa); Beckhove, P. (Philipp); Gilboa, E. (Eli); Mittendorf, E.A. (Elizabeth A.); Palucka, A.K. (Anna Karolina); Weber, J.S. (Jeffrey S.); Talmadge, J.E. (James E.); Celis, E. (Esteban); Castelli, C. (Chiara); Spisek, R. (Radek); Zou, W. (Weiping); Eggermont, A.M. (Alexander M.); Garg, A. (Abhishek); Okada, H. (Hideho); Buque, A. (Aitziber); Mattei, F. (Fabrizio); Bravo-San-Pedro, J.M. (José-Manuel); Moretta, L. (Lorenzo); Dhodapkar, M.V. (Madhav V.); Van-Den-Eynde, B.J. (Benoît J.); Peter, M.E. (Marcus E.); Shiku, H. (Hiroshi); Liblau, R. (Roland); Giaccone, G. (Giuseppe); Kepp, O. (Oliver); Wagner, H. (Hermann)
    During the past decades, anticancer immunotherapy has evolved from a promising therapeutic option to a robust clinical reality. Many immunotherapeutic regimens are now approved by the US Food and Drug Administration and the European Medicines Agency for use in cancer patients, and many others are being investigated as standalone therapeutic interventions or combined with conventional treatments in clinical studies. Immunotherapies may be subdivided into “passive” and “active” based on their ability to engage the host immune system against cancer. Since the anticancer activity of most passive immunotherapeutics (including tumor-targeting monoclonal antibodies) also relies on the host immune system, this classification does not properly reflect the complexity of the drug-host-tumor interaction. Alternatively, anticancer immunotherapeutics can be classified according to their antigen specificity. While some immunotherapies specifically target one (or a few) defined tumor-associated antigen(s), others operate in a relatively non-specific manner and boost natural or therapy-elicited anticancer immune responses of unknown and often broad specificity. Here, we propose a critical, integrated classification of anticancer immunotherapies and discuss the clinical relevance of these approaches.