Stefano Casola, 2006

  • Latest publications

    Mihailovich M, Bremang M, Spadotto V, Musiani D, Vitale E, Varano G, Zambelli F, Mancuso FM, Cairns DA, Pavesi G, Casola S, Bonaldi T. miR-17-92 fine-tunes MYC expression and function to ensure optimal B cell lymphoma growth. Nat Commun. 2015 Nov 10;6:8725. doi: 10.1038/ncomms9725. PubMed PMID: 26555894.

    Kumar R, Bach MP, Mainoldi F, Maruya M, Kishigami S, Jumaa H, Wakayama T, Kanagawa O, Fagarasan S, Casola S. Antibody repertoire diversification through VH gene replacement in mice cloned from an IgA plasma cell. Proc Natl Acad Sci U S A. 2015 Feb 3;112(5):E450-7. doi: 10.1073/pnas.1417988112. Epub 2015 Jan 21. PubMed PMID: 25609671.

    Alberghini F, Petrocelli V, Rahmat M, Casola S. An epigenetic view of B-cell disorders. Immunol Cell Biol. 2015 Mar;93(3):253-60. doi: 10.1038/icb.2014.116. Epub 2015 Jan 20. Review. PubMed PMID: 25601271.

    Piunti A, Rossi A, Cerutti A, Albert M, Jammula S, Scelfo A, Cedrone L, Fragola G, Olsson L, Koseki H, Testa G, Casola S, Helin K, d’Adda di Fagagna F, Pasini D. Polycomb proteins control proliferation and transformation independently of cell cycle checkpoints by regulating DNA replication. Nat Commun. 2014 Apr 14;5:3649. doi: 10.1038/ncomms4649. PubMed PMID: 24728135.

    Caganova M, Carrisi C, Varano G, Mainoldi F, Zanardi F, Germain PL, George L, Alberghini F, Ferrarini L, Talukder AK, Ponzoni M, Testa G, Nojima T, Doglioni C, Kitamura D, Toellner KM, Su IH, Casola S. Germinal center dysregulation by histone methyltransferase EZH2 promotes lymphomagenesis. J Clin Invest. 2013 Dec;123(12):5009-22. doi: 10.1172/JCI70626. Epub 2013 Nov 8. Erratum in: J Clin Invest. 2014 Apr 1;124(4):1869. PubMed PMID: 24200695.

  • Prizes and awards

    Cariplo Foundation Grant, 2016; 2010; 2009

    European Research Council (ERC) Starting Grant (sponsored by the FIRB-IDEAS program), 2009

    Italian Association for Cancer Research (AIRC) Grant, 2014; 2011; 2010; 2007; 2006 (New Unit Start-up grant award)

    Telethon Foundation Investigator Grant, 2014

    Lombardia Region Grant, 2011

    International Collaborative Research Award (RCAI),RIKEN Research Center for Allergy and Immunology Japan, 2009

    Italian Ministry of Health Grant, 2009; 2008

    Italian Ministry of Research Grant, 2009

    Career Development Award, Armenise-Harvard Foundation, 2006

Career Development Award Project Title

“The role of the B cell antigen receptor in the pathogenesis of B cell lymphomas. Lessons from mouse models”, 2006

Who he is 

Stefano Casola is a molecular oncologist specialized in the study of the processes controlling B lymphocyte differentiation and malignant B cell transformation.

After receiving his MD and PhD degrees from the University Federico II of Naples, he joined the Institute of Genetics at the University of Cologne in Germany as post-doctoral fellow, working in the group of immunologist K. Rajewsky. Here he began to study the function of genes controlling normal B cells development and their involvement in the occurrence of malignant lymphomas, blood tumors that affect lymphocytes.

After his postdoc experience, Casola moved on to the Harvard Medical School in Boston becoming Junior Investigator at the CBR Institute for Biomedical Research and Instructor in the Department of Pathology, Harvard Medical School. In 2006, he returned to Italy thanks to the Armenise-Harvard Career Development Award and to the Italian Foundation for Cancer Research, to lead his own laboratory at the FIRC Institute of Molecular Oncology (IFOM) in Milan.

There he set up the research program on Genetics of B cells and lymphomas, dedicated to the study of immune cells and their malignant cancerous counterparts.

What he does

His lab studies B cell immunity and lymphomas, common forms of blood cancers, often resulting from an aberrant response of the immune system. When B cells recognize a pathogen, such as a virus or bacteria, they produce antibodies to fight it. This process relies on the massive expansion of pathogen-specific B cells, which is accompanied by genetic rearrangements that ensure lymphocytes to produce antibodies with greater neutralizing activity. Alterations in this highly coordinated process lead to the development of malignant B cell lymphomas.

Casola’s research team is also interested in understanding the physiological process controlling B-cell dependent immune responses.

News from the Lab

Using pre-clinical models and the most advanced technologies for genomic analysis, Casola’s team has recently identified about a hundred novel candidate genes implicated in the development of lymphomas.

Such findings, combined with ongoing investigations on the role of the immunoglobulin receptor in cancerous B cells, are expected to improve diagnostics and prognostics of human B cell malignancies. They are also intended to accelerate the development of patient-tailored therapies to overcome treatment failures that still occur in about a third of the patients diagnosed with aggressive forms of lymphomas.