A novel HIV-based lentiviral vector can introduce a gene to pancreatic tumor cells that makes them more sensitive to the chemotherapeutic drug gemcitabine, without integrating into cellular DNA. This integrase-defective lentiviral delivery system greatly reduces the risk of insertional mutagenesis and replication-competent lentivirus production, as described in a new study published in Human Gene Therapy, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The full article is available free to read on the Human Gene Therapy website until March 31, 2016. The article, titled "Initial Characterization of Integrase-Defective Lentiviral Vectors for Pancreatic Cancer Gene Therapy," (http://online.liebertpub.com/doi/full/10.1089/hum.2015.151) is part of a special issue of Human Gene Therapy focusing on advances in gene and cell therapy research in France. The issue has been coordinated by guest editors Nathalie Cartier, M.D., Director of Research, INSERM, Paris, and President, European Society of Gene and Cell Therapy (ESGCT), and Pierre Cordelier, Ph.D., Senior Researcher, INSERM, Toulouse, France, and President, French Society of Cell and Gene Therapy (SFTCG). The special issue will be distributed at the SFTCG meeting, March 9-11, in Marseilles, France. In the referenced article, Naima Hanoun, Marion Gayral, Adeline Pointreau, Louis Buscail, and Pierre Cordelier, of INSERM (Toulouse), Université Toulouse III-Paul Sabatier, and CHU Toulouse-Rangueil, present work demonstrating that an integrase-deficient lentiviral vector can deliver the gene that codes for the DCK protein to pancreatic adenocarcinoma-derived cells in the laboratory with high efficacy. These cells are typically very resistant to gene transfer. Deficiency of DCK protein is commonly associated with resistance to anti-cancer chemotherapy.
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