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 Blood, 7 May 2009, Vol. 113, No. 19, pp. 4525-4533.
Prepublished online as a Blood First Edition Paper on February 4, 2009; DOI 10.1182/blood-2008-09-180307.

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GENE THERAPY

Antineoplastic activity of lentiviral vectors expressing interferon-{alpha} in a preclinical model of primary effusion lymphoma

Maria Luisa Calabrò1, Paola Gasperini2,*, Iole Maria Di Gangi1,*, Stefano Indraccolo1, Massimo Barbierato2, Alberto Amadori1,2, and Luigi Chieco-Bianchi2

1 Immunology and Diagnostic Molecular Oncology, Istituto Oncologico Veneto, Istituto di Ricovero e Cura a Carattere Scientifico, Padova; and 2 Department of Oncology and Surgical Sciences, Oncology Section, University of Padova, Padova, Italy

The peculiar site of development of primary effusion lymphoma (PEL) highlights a specific role of body cavities in the pathogenesis of this neoplasia. We used a xenograft murine model of PEL to characterize the contribution of the host microenvironment to PEL growth. The activity of a murine (ie, host-specific) interferon-{alpha}1 (IFN-{alpha}1)–expressing lentiviral vector (mIFN-{alpha}1-LV) was compared with that of a human (h) IFN-{alpha}2b-LV. LVs efficiently delivered the transgene to PEL cells and conferred long-term transgene expression in vitro and in vivo. Treatment of PEL-injected severe combined immunodeficiency mice with hIFN-{alpha}2b-LV significantly prolonged mice survival and reduced ascites development. Interestingly, mIFN-{alpha}1-LV showed an antineoplastic activity comparable with that observed with hIFN-{alpha}2b-LV. As mIFN-{alpha}1 retained species-restricted activity in vitro, it probably acted in vivo on the intracavitary murine milieu. mIFN-{alpha}1–treated murine mesothelial cells were found to express tumor necrosis factor–related apoptosis-inducing ligand and to significantly trigger apoptosis of cocultured PEL cells in a tumor necrosis factor–related apoptosis-inducing ligand-dependent manner. These data suggest that the interaction between lymphomatous and mesothelial cells lining the body cavities may play a key role in PEL growth control and also indicate that the specific targeting of microenvironment may impair PEL development.


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