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Luigi Naldini

Researcher at Vita-Salute San Raffaele University

Publications -  370
Citations -  59320

Luigi Naldini is an academic researcher from Vita-Salute San Raffaele University. The author has contributed to research in topics: Genetic enhancement & Viral vector. The author has an hindex of 108, co-authored 345 publications receiving 55080 citations. Previous affiliations of Luigi Naldini include Università telematica San Raffaele & Sangamo BioSciences.

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Tumor-Targeted Interferon-α Delivery by Tie2-Expressing Monocytes Inhibits Tumor Growth and Metastasis

TL;DR: This work exploited the tumor-homing ability of proangiogenic Tie2-expressing monocytes (TEMs) to deliver IFN-alpha to tumors and obtained significant antitumor responses and near complete abrogation of metastasis.
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Lentiviral vectors containing the human immunodeficiency virus type-1 central polypurine tract can efficiently transduce nondividing hepatocytes and antigen-presenting cells in vivo

TL;DR: Potential uses of improved lentiviral vectors for gene therapy of genetic blood disorders resulting from serum protein deficiencies, such as hemophilia, and hepatic disease are suggested and the use of liver-specific promoters may be warranted to circumvent inadvertent transgene expression in APCs.
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Efficient gene delivery and targeted expression to hepatocytes in vivo by improved lentiviral vectors.

TL;DR: It is shown that rat hepatocytes were transduced ex vivo to high frequency without requirement for proliferation, indicating the potential efficacy of improved lentiviral vectors for the gene therapy of hemophilias and other diseases.
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Biological activation of pro-HGF (hepatocyte growth factor) by urokinase is controlled by a stoichiometric reaction.

TL;DR: The stoichiometry of the activation reaction suggests that the biological effects of HGF can be titrated in vivo by the level of uPA activity, which would condition the tissue microenvironment by rendering HGF bioavailable to its target cells.
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The MET oncogene drives a genetic programme linking cancer to haemostasis.

TL;DR: In vivo analysis showed that both proteins support the thrombohaemorrhagic phenotype, thus providing direct genetic evidence for the long-sought-after link between oncogene activation and haemostasis.