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Pier Giuseppe Pelicci

  • Research activities

    One of the challenges for the next decade is to understand how distinct, simple molecular functions may be part of complex pathways and systems, how multiple systems may come together to control complicated cellular behaviors and how alteration of this composite molecular machinery may ultimately lead to cancer. Our group is trying to investigate these molecular mechanisms/interactions with research that extends from the regulation of cell division and proliferation to the control of DNA transcription and replication, to the role of tumor-associated oncogenes and suppressors in tumor development and progression, and to the links between cancer and metabolism and cancer and aging. Accumulating evidence suggests that only rare cancer cells [which possess characteristics associated with normal stem cells (SCs) and are thus called cancer stem cells (CSCs)] have the capacity to maintain tumor growth, so a considerable part of our research efforts is specifically devoted to the characterization of normal and cancer SCs, and to study whether common mechanisms are controlling the growth and maintenance of both these types of cells across different normal and cancer tissues. To this end, we generate accurate models of carcinogenesis in mammals, creating, in these model systems, mutations that mimic those that occur spontaneously in human cancers (especially leukemia and breast). We use these model systems in combination with primary patient derived samples to identify biological markers of disease and to develop innovative strategies to target CSCs in a clinical setting.

  • Publications

    • Insinga A, Cicalese A, Faretta M, Gallo B, Albano L, Ronzoni S, Furia L, Viale A, Pelicci PG. DNA damage in stem cells activates p21, inhibits p53, and induces symmetric self-renewing divisions. Proc Natl Acad Sci U S A 110(10):3931-6, 2013.
    • Dellino GI, Cittaro D, Piccioni R, Luzi L, Banfi S, Segalla S, Cesaroni M, Mendoza-Maldonado R, Giacca M, Pelicci PG. Genome-wide mapping of human DNA-replication origins: Levels of transcription at ORC1 sites regulate origin selection and replication timing. Genome Res 23(1):1-11, 2013.
    • Gambino V, De Michele G, Venezia O, Migliaccio P, Dall'olio V, Bernard L, Minardi SP, Fazia MA, Bartoli D, Servillo G, Alcalay M, Luzi L, Giorgio M, Scrable H, Pelicci PG, Migliaccio E. Oxidative stress activates a specific p53 transcriptional-response that regulates cellular senescence and aging. Aging Cell 12(3):435-45, 2013.
    • Viale A, De Franco F, Orleth A, Cambiaghi V, Giuliani V, Bossi D, Ronchini C, Ronzoni S, Muradore I, Monestiroli S, Gobbi A, Alcalay M, Minucci S, Pelicci PG. Cell-cycle restriction limits DNA damage and maintains self-renewal of leukaemia stem cells. Nature 457(7225):51-6, 2009.
    • Cicalese A, Bonizzi G, Pasi CE, Faretta M, Ronzoni S, Giulini B, Brisken C, Minucci S, Di Fiore PP, Pelicci PG. The tumor suppressor p53 regulates polarity of self-renewing divisions in mammary stem cells. Cell 138:1083-95, 2009.

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PARTNERSHIP

Università degli Studi di Milano Ecancer Medical Science IFOM-IEO Campus

CREDITS

Ministero della Salute Joint Commission International Breastcertification bollinirosa

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