Molecular pathways linking inflammation and cancer: from bench to bedside
Il 25/11/2016 ore 14.30 - 16.00
Sala Conferenze Cnr, Area delle Ricerca Na1
Via P. Castellino, 111 80131 Napoli
Il 25 Novembre 2016, presso la Sala conferenze Cnr, Area della Ricerca Na1 (Napoli), si terrà 'ImmuNapoli 2016'. L’evento, promosso dal gruppo di Immunologia dell’Istituto di biochimica delle proteine, sarà dedicato al ruolo dei macrofagi nell’infiammazione cronica associata all’instaurarsi delle neoplasie. Lo speaker principale sarà Alberto Mantovani (Humanitas clinical and research center, Humanitas University, Milano) che terrà una lectio magistralis dal titolo 'Molecular pathways linking inflammation and cancer: from bench to bedside'
Macrophages are key orchestrators of chronic inflammation. They respond to microenvironmental signals with polarized genetic and functional programmes. M1 macrophages which are classically activated by microbial products and interferon-γ, are potent effector cells which kill microorganisms and tumours. In contrast, M2 cells tune inflammation and adaptive immunity; promote cell proliferation by producing growth factors and products of the arginase pathway (ornithine and polyamines); scavenge debris by expressing scavenger receptors; promote angiogenesis, tissue remodeling and repair. M1 and M2 cells represent simplified extremes of a continuum of functional states. Available information suggests that some TAM are a prototypic M2 population. Polarization of phagocytes sets these cells in a tissue remodeling and repair mode and orchestrate the smouldering and polarized chronic inflammation associated to established neoplasia. Intrinsic metabolic features and orchestration of metabolism are key components of macrophage polarization and function. Recent studies have begun to address the central issue of the relationship between genetic events causing cancer and activation of protumour, smouldering, non-resolving tumour-promoting inflammation. New vistas have emerged on molecules associated with M2 or M2-like polarization and its orchestration in cancer. Recently, proof-of-principle has been obtained that targeting TAM can be beneficial in human cancer. Moreover, complement has emerged as a key component of tumor-promoting inflammation.
References
Bonavita E, Gentile S, Rubino M, et al. PTX3 is an extrinsic oncosuppressor regulating complement-dependent inflammation in cancer. Cell 160: 700-714, 2015.
Mantovani A, Allavena P. The interaction of anticancer therapies with tumor-associated macrophages. J Exp Med. 2015 Apr 6;212(4):435-445.
Sica A and Mantovani A. Macrophage plasticity and polarization: in vivo veritas. J. Clin. Invest. 2012: 122, 787-795.
Biswas S.K. and Mantovani A. Macrophage plasticity and interaction with lymphocyte subsets: cancer as paradigm. Nat Immunol 2010: 11, 889-896.
Mantovani A, Allavena P, Sica A, Balkwill F Cancer-Related Inflammation. Nature 454: 436-444, 2008.
Mantovani, A., Romero, P., Paluka, AK., Marincola, FM. Tumor immunity: effector response to tumor and the influence of the microenvironment. Lancet 371:771-783, 2008.
Balkwill F. and Mantovani A. Inflammation and cancer: back to Virchow? Lancet 357: 539-545, 2001.
Mantovani et al. Tumor-associated macrophages as treatment targets in oncology. Nature Rev, Clin. Oncol. (under revision).
Organizzato da:
Cnr - Ibp
Referente organizzativo:
Piergiuseppe De Berardinis
Cnr - Istituto di biochimica delle proteine
Via P. Castellino, 111 80131 Napoli
p.deberardinis@ibp.cnr.it
081/6132566
Modalità di accesso: ingresso libero
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