Search

Your search keyword '"Piovan, Claudia"' showing total 110 results
Start Over Author "Piovan, Claudia"
110 results on '"Piovan, Claudia"'

1. Supplementary Figure S1 from miR-9 and miR-200 Regulate PDGFRβ-Mediated Endothelial Differentiation of Tumor Cells in Triple-Negative Breast Cancer

Author

D'Ippolito, Elvira, primary, Plantamura, Ilaria, primary, Bongiovanni, Lucia, primary, Casalini, Patrizia, primary, Baroni, Sara, primary, Piovan, Claudia, primary, Orlandi, Rosaria, primary, Gualeni, Ambra V., primary, Gloghini, Annunziata, primary, Rossini, Anna, primary, Cresta, Sara, primary, Tessari, Anna, primary, De Braud, Filippo, primary, Di Leva, Gianpiero, primary, Tripodo, Claudio, primary, and Iorio, Marilena V., primary

Published
2023
Full Text
View/download PDF

2. Supplementary Tables 1 through 4 from miR-9 and miR-200 Regulate PDGFRβ-Mediated Endothelial Differentiation of Tumor Cells in Triple-Negative Breast Cancer

Author

D'Ippolito, Elvira, primary, Plantamura, Ilaria, primary, Bongiovanni, Lucia, primary, Casalini, Patrizia, primary, Baroni, Sara, primary, Piovan, Claudia, primary, Orlandi, Rosaria, primary, Gualeni, Ambra V., primary, Gloghini, Annunziata, primary, Rossini, Anna, primary, Cresta, Sara, primary, Tessari, Anna, primary, De Braud, Filippo, primary, Di Leva, Gianpiero, primary, Tripodo, Claudio, primary, and Iorio, Marilena V., primary

Published
2023
Full Text
View/download PDF

3. Supplementary Figure legends from miR-9 and miR-200 Regulate PDGFRβ-Mediated Endothelial Differentiation of Tumor Cells in Triple-Negative Breast Cancer

Author

D'Ippolito, Elvira, primary, Plantamura, Ilaria, primary, Bongiovanni, Lucia, primary, Casalini, Patrizia, primary, Baroni, Sara, primary, Piovan, Claudia, primary, Orlandi, Rosaria, primary, Gualeni, Ambra V., primary, Gloghini, Annunziata, primary, Rossini, Anna, primary, Cresta, Sara, primary, Tessari, Anna, primary, De Braud, Filippo, primary, Di Leva, Gianpiero, primary, Tripodo, Claudio, primary, and Iorio, Marilena V., primary

Published
2023
Full Text
View/download PDF

4. Data from miR-9 and miR-200 Regulate PDGFRβ-Mediated Endothelial Differentiation of Tumor Cells in Triple-Negative Breast Cancer

Author

D'Ippolito, Elvira, primary, Plantamura, Ilaria, primary, Bongiovanni, Lucia, primary, Casalini, Patrizia, primary, Baroni, Sara, primary, Piovan, Claudia, primary, Orlandi, Rosaria, primary, Gualeni, Ambra V., primary, Gloghini, Annunziata, primary, Rossini, Anna, primary, Cresta, Sara, primary, Tessari, Anna, primary, De Braud, Filippo, primary, Di Leva, Gianpiero, primary, Tripodo, Claudio, primary, and Iorio, Marilena V., primary

Published
2023
Full Text
View/download PDF

12. Human anti-nucleolin recombinant immunoagent for cancer therapy

Author

Palmieri, Dario, Richmond, Timothy, Piovan, Claudia, Sheetz, Tyler, Zanesi, Nicola, Troise, Fulvia, James, Cindy, Wernicke, Dorothee, Nyei, Fata, Gordon, Timothy J., Consiglio, Jessica, Salvatore, Francesco, Coppola, Vincenzo, Pichiorri, Flavia, DeLorenzo, Claudia, and Croce, Carlo M.

Published
2015

21. MicroRNA cluster 221-222 and estrogen receptor [alpha] interactions in breast cancer

Author

Leva, Gianpiero Di, Gasparini, Pierluigi, Piovan, Claudia, Ngankeu, Apollinaire, Garofalo, Michela, Taccioli, Cristian, Iorio, Marilena V., Li, Meng, Volinia, Stefano, Alder, Hansjuerg, Nakamura, Tatsuya, Nuovo, Gerard, Liu, Yunlong, Nephew, Kenneth P., and Croce, Carlo M.

Subjects
MicroRNA -- Health aspects, Breast cancer -- Risk factors, Breast cancer -- Development and progression, Breast cancer -- Genetic aspects, Estrogen -- Receptors, Estrogen -- Health aspects, Estrogen -- Genetic aspects, Health
Abstract

Background Several lines of evidence have suggested that estrogen receptor [alpha] (ER[alpha])--negative breast tumors, which are highly aggressive and nonresponsive to hormonal therapy, arise from ERa-positive precursors through different molecular pathways. Because microRNAs (miRNAs) modulate gene expression, we hypothesized that they may have a role in ER-negative tumor formation. Methods Gene expression profiles were used to highlight the global changes induced by miRNA modulation of ER[alpha] protein, miRNA transfection and luciferase assays enabled us to identify new targets of miRNA 206 (miR-206) and miRNA cluster 221-222 (miR-221-222). Northern blot, luciferase assays, estradiol treatment, and chromatin immunoprecipitation were performed to identify the miR-221-222 transcription unit and the mechanism implicated in its regulation. Results Different global changes in gene expression were induced by overexpression of miR-221-222 and miR-206 in ER-positive cells, miR-221 and -222 increased proliferation of ER[alpha]-positive cells, whereas miR-206 had an inhibitory effect (mean absorbance units [AU]: miR-206:500 AU, 95% confidence interval [CI]) = 480 to 520; miR-221: 850 AU, 95% CI = 810 to 873; miR-222:879 AU, 95% CI = 850 to 893; P < .05). We identified hepatocyte growth factor receptor and forkhead box 03 as new targets of miR-206 and miR-221-222, respectively. We demonstrated that ER[alpha] negatively modulates miR-221 and -222 through the recruitment of transcriptional corepressor partners: nuclear receptor corepressor and silencing mediator of retinoic acid and thyroid hormone receptor. Conclusions These findings suggest that the negative regulatory loop involving miR-221-222 and ER[alpha] may confer proliferative advantage and migratory activity to breast cancer cells and promote the transition from ER-positive to ER-negative tumors. DOI: 10.1093/jnci/djq102

Published
2010

23. MiR-205 as predictive biomarker and adjuvant therapeutic tool in combination with trastuzumab

Author

Cataldo, Alessandra, primary, Piovan, Claudia, additional, Plantamura, Ilaria, additional, D’Ippolito, Elvira, additional, Camelliti, Simone, additional, Casalini, Patrizia, additional, Giussani, Marta, additional, Déas, Olivier, additional, Cairo, Stefano, additional, Judde, Jean-Gabriel, additional, Tagliabue, Elda, additional, and Iorio, Marilena V., additional

Published
2018
Full Text
View/download PDF

26. Correction: In vivo NCL targeting affects breast cancer aggressiveness through miRNA regulation

Author

Pichiorri, Flavia, primary, Palmieri, Dario, additional, De Luca, Luciana, additional, Consiglio, Jessica, additional, You, Jia, additional, Rocci, Alberto, additional, Talabere, Tiffany, additional, Piovan, Claudia, additional, Lagana, Alessandro, additional, Cascione, Luciano, additional, Guan, Jingwen, additional, Gasparini, Pierluigi, additional, Balatti, Veronica, additional, Nuovo, Gerard, additional, Coppola, Vincenzo, additional, Hofmeister, Craig C., additional, Marcucci, Guido, additional, Byrd, John C., additional, Volinia, Stefano, additional, Shapiro, Charles L., additional, Freitas, Michael A., additional, and Croce, Carlo M., additional

Published
2017
Full Text
View/download PDF

27. miR-9 and miR-200 Regulate PDGFRβ-Mediated Endothelial Differentiation of Tumor Cells in Triple-Negative Breast Cancer

Author

D'Ippolito, Elvira, primary, Plantamura, Ilaria, additional, Bongiovanni, Lucia, additional, Casalini, Patrizia, additional, Baroni, Sara, additional, Piovan, Claudia, additional, Orlandi, Rosaria, additional, Gualeni, Ambra V., additional, Gloghini, Annunziata, additional, Rossini, Anna, additional, Cresta, Sara, additional, Tessari, Anna, additional, De Braud, Filippo, additional, Di Leva, Gianpiero, additional, Tripodo, Claudio, additional, and Iorio, Marilena V., additional

Published
2016
Full Text
View/download PDF

29. 130. Purification of Large Scale mRNA Encoding ZFN Nucleases by dHPLC Technology

Author

Giuliani, Erica, primary, Piovan, Claudia, additional, Bossi, Sergio, additional, Corna, Stefano, additional, Scavullo, Cinzia, additional, Pema, Monika, additional, Di Tomaso, Tiziano, additional, Genovese, Pietro, additional, Lombardo, Angelo, additional, Naldini, Luigi, additional, Bordignon, Claudio, additional, Rizzardi, Gian Paolo, additional, and Bovolenta, Chiara, additional

Published
2016
Full Text
View/download PDF

30. 703. Development of RD-MolPack-trLNGFR/dCK.DM.S74E Stable Packaging Cells

Author

Piovan, Claudia, primary, Giuliani, Erica, additional, Corna, Stefano, additional, Scavullo, Cinzia, additional, Bossi, Sergio, additional, Pema, Monika, additional, Medin, Jeffrey A., additional, McKillop, Monty, additional, Au, Bryan, additional, Bordignon, Claudio, additional, Rizzardi, Gian Paolo, additional, and Bovolenta, Chiara, additional

Published
2016
Full Text
View/download PDF

31. Abstract A18: miR-9 and miR-200 regulate PDGFRβ-mediated endothelial differentiation of neoplastic cells in triple-negative breast cancer

Author

D'Ippolito, Elvira, primary, Plantamura, Ilaria, additional, Bongiovanni, Lucia, additional, Casalini, Patrizia, additional, Baroni, Sara, additional, Piovan, Claudia, additional, Orlandi, Rosaria, additional, Gualeni, Ambra V., additional, Gloghini, Annunziata, additional, Rossini, Anna, additional, Braud, Filippo De, additional, Tagliabue, Elda, additional, Tripodo, Claudio, additional, and Iorio, Marilena V., additional

Published
2016
Full Text
View/download PDF

32. RD-MolPack technology for the constitutive production of self-inactivating lentiviral vectors pseudotyped with the nontoxic RD114-TR envelope

Author

Marin, Virna, primary, Stornaiuolo, Anna, additional, Piovan, Claudia, additional, Corna, Stefano, additional, Bossi, Sergio, additional, Pema, Monika, additional, Giuliani, Erica, additional, Scavullo, Cinzia, additional, Zucchelli, Eleonora, additional, Bordignon, Claudio, additional, Rizzardi, Gian Paolo, additional, and Bovolenta, Chiara, additional

Published
2016
Full Text
View/download PDF

37. Abstract A085: miR-222/221 in aggressive breast cancer

Author

Leva, Gianpiero Di, primary, Piovan, Claudia, additional, Cheung, Douglas, additional, Briskin, Daniel, additional, Kumar, Arpan, additional, Nuovo, Gerard, additional, Fassan, Matteo, additional, Coppola, Vincenzo, additional, Garofalo, Michela, additional, and Croce, Carlo, additional

Published
2013
Full Text
View/download PDF

38. In vivo NCL targeting affects breast cancer aggressiveness through miRNA regulation

Author

Pichiorri, Flavia, primary, Palmieri, Dario, additional, Luca, Luciana De, additional, Consiglio, Jessica, additional, You, Jia, additional, Rocci, Alberto, additional, Talabere, Tiffany, additional, Piovan, Claudia, additional, Lagana, Alessandro, additional, Cascione, Luciano, additional, Guan, Jingwen, additional, Gasparini, Pierluigi, additional, Balatti, Veronica, additional, Nuovo, Gerard, additional, Coppola, Vincenzo, additional, Hofmeister, Craig C., additional, Marcucci, Guido, additional, Byrd, John C., additional, Volinia, Stefano, additional, Shapiro, Charles L., additional, Freitas, Michael A., additional, and Croce, Carlo M., additional

Published
2013
Full Text
View/download PDF

39. Correction: Estrogen Mediated-Activation of miR-191/425 Cluster Modulates Tumorigenicity of Breast Cancer Cells Depending on Estrogen Receptor Status

Author

Di Leva, Gianpiero, primary, Piovan, Claudia, additional, Gasparini, Pierluigi, additional, Ngankeu, Apollinaire, additional, Taccioli, Cristian, additional, Briskin, Daniel, additional, Cheung, Douglas G., additional, Bolon, Brad, additional, Anderlucci, Laura, additional, Alder, Hansjuerg, additional, Nuovo, Gerard, additional, Li, Meng, additional, Iorio, Marilena V., additional, Galasso, Marco, additional, Ramasamy, Santhanam, additional, Marcucci, Guido, additional, Perrotti, Danilo, additional, Powell, Kimerly A., additional, Bratasz, Anna, additional, Garofalo, Michela, additional, Nephew, Kenneth P., additional, and Croce, Carlo M., additional

Published
2013
Full Text
View/download PDF

40. Abstract 1122: In vivo NCL-targeting affects breast cancer aggressiveness through miRNA regulation.

Author

Palmieri, Dario, primary, De Luca, Luciana, additional, Consiglio, Jessica, additional, Rocci, Alberto, additional, Talabere, Tiffany, additional, Piovan, Claudia, additional, Lagana, Alessandro, additional, Cascione, Luciano, additional, Guan, Jingwen, additional, Gasparini, Pierluigi, additional, Balatti, Veronica, additional, Coppola, Vincenzo, additional, Hofmeister, Craig, additional, Marcucci, Guido, additional, Byrd, John, additional, Volinia, Stefano, additional, Shapiro, Charles, additional, Freitas, Michael, additional, Croce, Carlo, additional, and Pichiorri, Flavia, additional

Published
2013
Full Text
View/download PDF

41. Estrogen Mediated-Activation of miR-191/425 Cluster Modulates Tumorigenicity of Breast Cancer Cells Depending on Estrogen Receptor Status

Author

Di Leva, Gianpiero, primary, Piovan, Claudia, additional, Gasparini, Pierluigi, additional, Ngankeu, Apollinaire, additional, Taccioli, Cristian, additional, Briskin, Daniel, additional, Cheung, Douglas G., additional, Bolon, Brad, additional, Anderlucci, Laura, additional, Alder, Hansjuerg, additional, Nuovo, Gerard, additional, Li, Meng, additional, Iorio, Marilena V., additional, Galasso, Marco, additional, Ramasamy, Santhanam, additional, Marcucci, Guido, additional, Perrotti, Danilo, additional, Powell, Kimerly A., additional, Bratasz, Anna, additional, Garofalo, Michela, additional, Nephew, Kenneth P., additional, and Croce, Carlo M., additional

Published
2013
Full Text
View/download PDF

43. Abstract 2089: MiR-205 role in triple negative breast cancer

Author

Iorio, Marilena V., primary, Piovan, Claudia, additional, Leva, Gianpiero Di, additional, Casalini, Patrizia, additional, Tortoreto, Monica, additional, Plantamura, Ilaria, additional, Taccioli, Cristian, additional, Croce, Carlo M., additional, and Tagliabue, Elda, additional

Published
2010
Full Text
View/download PDF

44. microRNA-205 Regulates HER3 in Human Breast Cancer

Author

Iorio, Marilena V., primary, Casalini, Patrizia, additional, Piovan, Claudia, additional, Di Leva, Gianpiero, additional, Merlo, Andrea, additional, Triulzi, Tiziana, additional, Ménard, Sylvie, additional, Croce, Carlo M., additional, and Tagliabue, Elda, additional

Published
2009
Full Text
View/download PDF

45. A set of NF-κB-regulated microRNAs induces acquired TRAIL resistance in Lung cancer.

Author

Young-Jun Jeon, Middleton, Justin, Taewan Kim, Laganà, Alessandro, Piovan, Claudia, Secchiero, Paola, Nuovo, Gerard J., Ri Cui, Joshi, Pooja, Romano, Giulia, Di Leva, Gianpiero, Bum-Kyu Lee, Hui-Lung Sun, Yonghwan Kim, Fadda, Paolo, Alder, Hansjuerg, Garofalo, Michela, and Croce, Carlo M.

Subjects
MICRORNA, TUMOR necrosis factors, APOPTOSIS, ANTINEOPLASTIC agents, CANCER cell proliferation, TUMOR suppressor genes, TUMOR suppressor proteins, CASPASES
Abstract

TRAIL (TNF-related apoptosis-inducing ligand) is a promising anticancer agent that can be potentially used as an alternative or complementary therapy because of its specific antitumor activity. However, TRAIL can also stimulate the proliferation of cancer cells through the activation of NF-κB, but the exact mechanism is still poorly understood. In this study, we show that chronic exposure to subtoxic concentrations of TRAIL results in acquired resistance. This resistance is associated with the increase in miR-21, miR-30c, and miR-100 expression, which target tumorsuppressor genes fundamental in the response to TRAIL. Importantly, down-regulation of caspase-8 by miR-21 blocks receptor interacting protein-1 cleavage and induces the activation of NF-κB, which regulates these miRNAs. Thus, TRAIL activates a positive feedback loop that sustains the acquired resistance and causes an aggressive phenotype. Finally, we prove that combinatory treatment of NF-κB inhibitors and TRAIL is able to revert resistance and reduce tumor growth, with important consequences for the clinical practice. [ABSTRACT FROM AUTHOR]

Published
2015
Full Text
View/download PDF

46. MicroRNA cluster 221-222 and estrogen receptor alpha interactions in breast cancer.

Author

Di Leva G, Gasparini P, Piovan C, Ngankeu A, Garofalo M, Taccioli C, Iorio MV, Li M, Volinia S, Alder H, Nakamura T, Nuovo G, Liu Y, Nephew KP, Croce CM, Di Leva, Gianpiero, Gasparini, Pierluigi, Piovan, Claudia, Ngankeu, Apollinaire, and Garofalo, Michela

Abstract

Background: Several lines of evidence have suggested that estrogen receptor alpha (ERalpha)-negative breast tumors, which are highly aggressive and nonresponsive to hormonal therapy, arise from ERalpha-positive precursors through different molecular pathways. Because microRNAs (miRNAs) modulate gene expression, we hypothesized that they may have a role in ER-negative tumor formation.Methods: Gene expression profiles were used to highlight the global changes induced by miRNA modulation of ERalpha protein. miRNA transfection and luciferase assays enabled us to identify new targets of miRNA 206 (miR-206) and miRNA cluster 221-222 (miR-221-222). Northern blot, luciferase assays, estradiol treatment, and chromatin immunoprecipitation were performed to identify the miR-221-222 transcription unit and the mechanism implicated in its regulation.Results: Different global changes in gene expression were induced by overexpression of miR-221-222 and miR-206 in ER-positive cells. miR-221 and -222 increased proliferation of ERalpha-positive cells, whereas miR-206 had an inhibitory effect (mean absorbance units [AU]: miR-206: 500 AU, 95% confidence interval [CI]) = 480 to 520; miR-221: 850 AU, 95% CI = 810 to 873; miR-222: 879 AU, 95% CI = 850 to 893; P < .05). We identified hepatocyte growth factor receptor and forkhead box O3 as new targets of miR-206 and miR-221-222, respectively. We demonstrated that ERalpha negatively modulates miR-221 and -222 through the recruitment of transcriptional corepressor partners: nuclear receptor corepressor and silencing mediator of retinoic acid and thyroid hormone receptor.Conclusions: These findings suggest that the negative regulatory loop involving miR-221-222 and ERalpha may confer proliferative advantage and migratory activity to breast cancer cells and promote the transition from ER-positive to ER-negative tumors. [ABSTRACT FROM AUTHOR]

Published
2010
Full Text
View/download PDF

47. In vivo NCL targeting affects breast cancer aggressiveness through miRNA regulation

Author

Pichiorri, Flavia, Palmieri, Dario, De Luca, Luciana, Consiglio, Jessica, You, Jia, Rocci, Alberto, Talabere, Tiffany, Piovan, Claudia, Lagana, Alessandro, Cascione, Luciano, Guan, Jingwen, Gasparini, Pierluigi, Balatti, Veronica, Nuovo, Gerard, Coppola, Vincenzo, Hofmeister, Craig C., Marcucci, Guido, Byrd, John C., Volinia, Stefano, Shapiro, Charles L., Freitas, Michael A., and Croce, Carlo M.

Abstract

Numerous studies have described the altered expression and the causal role of microRNAs (miRNAs) in human cancer. However, to date, efforts to modulate miRNA levels for therapeutic purposes have been challenging to implement. Here we find that nucleolin (NCL), a major nucleolar protein, posttranscriptionally regulates the expression of a specific subset of miRNAs, including miR-21, miR-221, miR-222, and miR-103, that are causally involved in breast cancer initiation, progression, and drug resistance. We also show that NCL is commonly overexpressed in human breast tumors and that its expression correlates with that of NCL-dependent miRNAs. Finally, inhibition of NCL using guanosine-rich aptamers reduces the levels of NCL-dependent miRNAs and their target genes, thus reducing breast cancer cell aggressiveness both in vitro and in vivo. These findings illuminate a path to novel therapeutic approaches based on NCL-targeting aptamers for the modulation of miRNA expression in the treatment of breast cancer.

Published
2013
Full Text
View/download PDF

48. Vectofusin-1 Promotes RD114-TR-Pseudotyped Lentiviral Vector Transduction of Human HSPCs and T Lymphocytes.

Author

Piovan C, Marin V, Scavullo C, Corna S, Giuliani E, Bossi S, Galy A, Fenard D, Bordignon C, Rizzardi GP, and Bovolenta C

Abstract

Ex vivo transduction of human CD34 + hematopoietic stem/progenitor cells (hCD34 + HSPCs) and T lymphocytes is a key process that requires high efficiency and low toxicity to achieve effective clinical results. So far, several enhancers have been used to improve this process. Among them, Retronectin highly meliorates VSV-G and RD114-TR pseudotyped lentiviral vector delivery in hCD34 + HSPCs and T lymphocytes. However, Retronectin is expensive and requires pre-coating of culture dishes or bags before cell seeding, resulting in a cumbersome procedure. Recently, an alternative transduction adjuvant has been developed, named Vectofusin-1, whose effect has been demonstrated on gene delivery to cell lines and primary hCD34 + HSPCs by lentiviral vectors pseudotyped with different envelope glycoproteins. In this study, we have focused our analysis on the effect of Vectofusin-1 on the transduction of hCD34 + HSPCs and T lymphocytes by using mostly RD114-TR pseudotyped lentivectors and clinical transduction protocols. Here, we have proved that Vectofusin-1 reproducibly enhances gene delivery to hCD34 + HSPCs and activated T cells without cell toxicity and with efficacy comparable to that of Retronectin. The use of Vectofusin-1 will therefore help to shorten and simplify clinical cell manipulation, especially if automated systems are planned for transducing large-scale clinical lots.

Published
2017
Full Text
View/download PDF

49. Codon Optimization Leads to Functional Impairment of RD114-TR Envelope Glycoprotein.

Author

Zucchelli E, Pema M, Stornaiuolo A, Piovan C, Scavullo C, Giuliani E, Bossi S, Corna S, Asperti C, Bordignon C, Rizzardi GP, and Bovolenta C

Abstract

Lentiviral vectors (LVs) are a highly valuable tool for gene transfer currently exploited in basic, applied, and clinical studies. Their optimization is therefore very important for the field of vectorology and gene therapy. A key molecule for LV function is the envelope because it guides cell entry. The most commonly used in transiently produced LVs is the vesicular stomatitis virus glycoprotein (VSV-G) envelope, whose continuous expression is, however, toxic for stable LV producer cells. In contrast, the feline endogenous retroviral RD114-TR envelope is suitable for stable LV manufacturing, being well tolerated by producer cells under constitutive expression. We have previously reported successful, transient and stable production of LVs pseudotyped with RD114-TR for good transduction of T lymphocytes and CD34 + cells. To further improve RD114-TR-pseudotyped LV cell entry by increasing envelope expression, we codon-optimized the RD114-TR open reading frame (ORF). Here we show that, despite the RD114-TRco precursor being produced at a higher level than the wild-type counterpart, it is unexpectedly not duly glycosylated, exported to the cytosol, and processed. Correct cleavage of the precursor in the functional surface and transmembrane subunits is prevented in vivo, and, consequently, the unprocessed precursor is incorporated into LVs, making them inactive.

Published
2017
Full Text
View/download PDF

50. RD-MolPack technology for the constitutive production of self-inactivating lentiviral vectors pseudotyped with the nontoxic RD114-TR envelope.

Author

Marin V, Stornaiuolo A, Piovan C, Corna S, Bossi S, Pema M, Giuliani E, Scavullo C, Zucchelli E, Bordignon C, Rizzardi GP, and Bovolenta C

Abstract

To date, gene therapy with transiently derived lentivectors has been very successful to cure rare infant genetic diseases. However, transient manufacturing is unfeasible to treat adult malignancies because large vector lots are required. By contrast, stable manufacturing is the best option for high-incidence diseases since it reduces the production cost, which is the major current limitation to scale up the transient methods. We have previously developed the proprietary RD2-MolPack technology for the stable production of second-generation lentivectors, based on the RD114-TR envelope. Of note, opposite to vesicular stomatitis virus glycoprotein (VSV-G) envelope, RD114-TR does not need inducible expression thanks to lack of toxicity. Here, we present the construction of RD2- and RD3-MolPack cells for the production of self-inactivating lentivectors expressing green fluorescent protein (GFP) as a proof-of-concept of the feasibility and safety of this technology before its later therapeutic exploitation. We report that human T lymphocytes transduced with self-inactivating lentivectors derived from RD3-MolPack cells or with self-inactivating VSV-G pseudotyped lentivectors derived from transient transfection show identical T-cell memory differentiation phenotype and comparable transduction efficiency in all T-cell subsets. RD-MolPack technology represents, therefore, a straightforward tool to simplify and standardize lentivector manufacturing to engineer T-cells for frontline immunotherapy applications.

Published
2016
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results