Prof. Dr. Porta Chiara
Università del Piemonte Orientale
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Academic Career Length
21Years (2006-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications1 October 2008 in Seminars in Cancer Biology
Journal Article
ASAntonio Sica
Antonio SicaPLPaola Larghi
Paola LarghiAMAlessandra Mancino
Alessandra MancinoLRLuca Rubino
Luca Rubino
Porta Chiara
Alberto Mantovani +4
1 April 2008 in Critical Reviews in Oncology/Hematology
Journal Article
PAPaola Allavena
Paola AllavenaASAntonio Sica
Antonio Sica
GSGraziella Solinas
Graziella Solinas
Porta ChiaraAlberto Mantovani12 September 2006 in Cancer and Metastasis Reviews
Journal Article
Alberto MantovaniTSTiziana Schioppa
Tiziana SchioppaPorta ChiaraPAPaola Allavena
Paola AllavenaASAntonio Sica
Antonio Sica
Tumor-Associated Macrophages (TAM) represent the major inflammatory component of the stroma of many tumors, able to affect different aspects of the neoplastic tissue. Many observations indicate that TAM express several M2-associated protumoral functions, including promotion of angiogenesis, matrix remodelling and suppression of adaptive immunity. The protumoral role of TAM in cancer is further supported by clinical studies that found a correlation between the high macrophage content of tumors and poor patient prognosis and by evidence showing that long-term use of non-steroidal anti-inflammatory drugs reduces the risk of several cancers. Here, we discuss evidence supporting the view that TAM represent a unique and distinct M2-skewed myeloid population and a potential target of anti-cancer therapy.
26 July 2015 in Cellular and Molecular Life Sciences
Journal Article
ASAntonio Sica
Antonio SicaMEMarco Erreni
Marco ErreniPAPaola Allavena
Paola AllavenaPorta Chiara1 September 2009 in Proceedings of the National Academy of Sciences
Journal Article
Porta ChiaraMRMonica Rimoldi
Monica Rimoldi
GRGeert Raes
Geert RaesLBLea Brys
Lea Brys
PGPietro Ghezzi
Pietro GhezziASAntonio Sica
Antonio Sica +6
Cells of the monocyte–macrophage lineage play a central role in the orchestration and resolution of inflammation. Plasticity is a hallmark of mononuclear phagocytes, and in response to environmental signals these cells undergo different forms of polarized activation, the extremes of which are called classic or M1 and alternative or M2. NF-κB is a key regulator of inflammation and resolution, and its activation is subject to multiple levels of regulation, including inhibitory, which finely tune macrophage functions. Here we identify the p50 subunit of NF-κB as a key regulator of M2-driven inflammatory reactions in vitro and in vivo. p50 NF-κB inhibits NF-κB–driven, M1-polarizing, IFN-β production. Accordingly, p50-deficient mice show exacerbated M1-driven inflammation and defective capacity to mount allergy and helminth-driven M2-polarized inflammatory reactions. Thus, NF-κB p50 is a key component in the orchestration of M2-driven inflammatory reactions.
1 December 2006 in Cancer Research
Journal Article
ASAlessandra Saccani
Alessandra Saccani
TSTiziana Schioppa
Tiziana SchioppaPorta ChiaraSBSubhra K. Biswas
Subhra K. Biswas
MNManuela Nebuloni
Manuela NebuloniASAntonio Sica
Antonio Sica
+4
Tumor-associated macrophages (TAM) are a major inflammatory infiltrate in tumors and a major component of the protumor function of inflammation. TAM in established tumors generally have an M2 phenotype with defective production of interleukin-12 (IL-12) and high IL-10. Here, we report that defective responsiveness of TAM from a murine fibrosarcoma and human ovarian carcinoma to M1 activation signals was associated with a massive nuclear localization of the p50 nuclear factor-κB (NF-κB) inhibitory homodimer. p50 overexpression inhibited IL-12 expression in normal macrophages. TAM isolated from p50−/− mice showed normal production of M1 cytokines, associated with reduced growth of transplanted tumors. Bone marrow chimeras showed that p50 inactivation in hematopoietic cells was sufficient to result in reduced tumor growth. Thus, p50 NF-κB overexpression accounts for the inability of TAM to mount an effective M1 antitumor response capable of inhibiting tumor growth. (Cancer Res 2006; 66(23): 11432-40)
About Me
Dr. Porta graduated from the Biotechnology School, University of Milan, Italy in 2000 and subsequently obtained a PhD in Applied Medical Science Biotechnology at the University of Milan, Italy in 2003. Dr. Porta spent 18 months at the Institute André Lwoff, CNRS, Villejuif, France, studying interferon-dependent apoptotic signaling under the supervision of Dr Mounirà Chelbi-Alix. Since 2004, Dr. Porta's research activity has been mainly focused on the molecular mechanisms underlying macrophage-polarized activation in tumor and other inflammatory conditions in a group directed by Professor Sica, initially at “Istituto di Ricerche Farmacologiche Mario Negri”, Milan Italy, then at “Humanitas Clinical and Research Center”, Rozzano , Italy. Since 2011, Dr Porta has been working at the Department of Pharmaceutical Sciences at the University of Piemonte Orientale “A. Avogradro” as an assistant and then as an associate professor of pathology. Dr. Porta's current research focuses on macrophages in chronic inflammatory disorders (e.g. IBD) and in different types of cancer (colorectal cancer, malignant pleura mesothelioma).