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Interleukin 3- receptor targeted exosomes inhibit in vitro and in vivo Chronic Myelogenous Leukemia cell growth

Bellavia, Daniele, Raimondo, Stefania, Calabrese, Giovanna, Forte, Stefano, Cristaldi, Marta, Patinella, Agostina, Memeo, Lorenzo, Manno, Mauro, Raccosta, Samuele, Diana, Patrizia, Cirrincione, Girolamo, Giavaresi, Gianluca, Monteleone, Francesca, Fontana, Simona, De Leo, Giacomo, Alessandro, Riccardo·2017·Theranostics
DOI 10.7150/thno.17092PMC PMC5399597
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Figure 1 Schematic representation of IL3-R-targeted exosomes: (A) HEK293T cells were transfected with a plasmid containing the recombinant human protein IL3-Lamp2b. Transfected cells were treated with Imatinib in order to generate Imatinib-containing IL3L exosomes or, transfected with BCR-ABL siRNA in order to generate siRNA-containing IL3L exosomes. The efficacy of engineered exosomes were tested in vitro and in vivo on Imatinib- sensitive or -resistant CML cells. (B) Schematic representation of Pinco plasmid construct containing IL3-Lamp2b.
Figure 1 Schematic representation of IL3-R-targeted exosomes: (A) HEK293T cells were transfected with a plasmid containing the recombinant human protein IL3-Lamp2b. Transfected cells were treated with Imatinib in order to generate Imatinib-containing IL3L exosomes or, transfected with BCR-ABL siRNA in order to generate siRNA-containing IL3L exosomes. The efficacy of engineered exosomes were tested in vitro and in vivo on Imatinib- sensitive or -resistant CML cells. (B) Schematic representation of Pinco plasmid construct containing IL3-Lamp2b.CC BY-NC · PubMed Central
Figure 2 Generation and characterization of IL3-Lamp2b exosomes. (A) Western blot analysis was performed on HEK293T cells, transfected or not with IL3L, and on released exosomes. Protein levels of IL3-Lamp2b (using 6XHis tag), Alix, CD81 and Tsg101 were evaluated. (B) Exosome size distribution was determined by DLS analysis. (C) Exosome particles were visualized by Atomic Force Microscopy (large square 2 μm, small square 500 nm). The apparent heights are colour coded as in the side bar. (D) Western blot analysis was performed on LAMA84, K562 and K562R cell lines. Protein levels of IL3-Rα (Cd123) were evaluated. Blots were stripped and subsequently re-probed with an antibody against Gapdh to ensure equal loading. (E) Analysis at confocal microscopy of LAMA84 (upper panel) or K562R (lower panel) cells treated, for 3h and 6h, with 10μg/ml of HEK293T-derived exosomes (Exo) and IL3L-HEK293T-derived exosomes (IL3L Exo). Nuclei were stained with Hoechst (blue); exosomes were labeled with PKH26 (red).
Figure 2 Generation and characterization of IL3-Lamp2b exosomes. (A) Western blot analysis was performed on HEK293T cells, transfected or not with IL3L, and on released exosomes. Protein levels of IL3-Lamp2b (using 6XHis tag), Alix, CD81 and Tsg101 were evaluated. (B) Exosome size distribution was determined by DLS analysis. (C) Exosome particles were visualized by Atomic Force Microscopy (large square 2 μm, small square 500 nm). The apparent heights are colour coded as in the side bar. (D) Western blot analysis was performed on LAMA84, K562 and K562R cell lines. Protein levels of IL3-Rα (Cd123) were evaluated. Blots were stripped and subsequently re-probed with an antibody against Gapdh to ensure equal loading. (E) Analysis at confocal microscopy of LAMA84 (upper panel) or K562R (lower panel) cells treated, for 3h and 6h, with 10μg/ml of HEK293T-derived exosomes (Exo) and IL3L-HEK293T-derived exosomes (IL3L Exo). Nuclei were stained with Hoechst (blue); exosomes were labeled with PKH26 (red).CC BY-NC · PubMed Central
Figure 3 In vitro and in vivo effects of Imatinib loaded IL3L-exosomes. (A) LAMA84 (upper panel) and K562 (lower panel) growth was measured by MTT assay after 24, 48 h of treatment with Imatinib (positive control), with 0.1, 0.5, 1 or 10 μg/ml of exosomes derived from HEK293T cells, containing or not Imatinib, and with 0.1, 0.5, 1 or 10 μg/ml of exosomes derived from IL3L-HEK293T cells, containing or not Imatinib. The values were plotted as % of growth vs Ctrl (untreated cells - dot line). Each point represents the mean ± SD of three independent experiments (**, p < 0.005; ***, p < 0.0005): versus Imatinib (a, p < 0.0005; b, p < 0.005); versus Exo-Imatinib (°, p < 0.05; °°°, p < 0.0005). (B) Western blot analysis was performed on LAMA84 and K562 cell lines treated for 24h with Imatinib, with 1 or 10 μg/ml Imatinib loaded exosomes derived from HEK293T cells or from IL3L-HEK293T cells. Protein levels of p-Bcr-Abl or Bcr-Abl were evaluated. Blots were stripped and subsequently re-probed with an antibody against Gapdh to ensure equal loading. (C) Comparison of the median tumor volume was an index of the antitumor efficacy of Imatinib loaded exosomes. Significant differences in terms of tumor volume were observed: IL3L Exo-Imatinib versus IL3L Exo at 17 days (a, p < 0.05), IL3L Exo-Imatinib versus IL3L Exo and Imatinib at 21 days (b, p < 0.005), and IL3L Exo-Imatinib versus IL3L Exo, Exo-Imatinib and Imatinib at 24 days (c, p < 0.0005).
Figure 3 In vitro and in vivo effects of Imatinib loaded IL3L-exosomes. (A) LAMA84 (upper panel) and K562 (lower panel) growth was measured by MTT assay after 24, 48 h of treatment with Imatinib (positive control), with 0.1, 0.5, 1 or 10 μg/ml of exosomes derived from HEK293T cells, containing or not Imatinib, and with 0.1, 0.5, 1 or 10 μg/ml of exosomes derived from IL3L-HEK293T cells, containing or not Imatinib. The values were plotted as % of growth vs Ctrl (untreated cells - dot line). Each point represents the mean ± SD of three independent experiments (**, p < 0.005; ***, p < 0.0005): versus Imatinib (a, p < 0.0005; b, p < 0.005); versus Exo-Imatinib (°, p < 0.05; °°°, p < 0.0005). (B) Western blot analysis was performed on LAMA84 and K562 cell lines treated for 24h with Imatinib, with 1 or 10 μg/ml Imatinib loaded exosomes derived from HEK293T cells or from IL3L-HEK293T cells. Protein levels of p-Bcr-Abl or Bcr-Abl were evaluated. Blots were stripped and subsequently re-probed with an antibody against Gapdh to ensure equal loading. (C) Comparison of the median tumor volume was an index of the antitumor efficacy of Imatinib loaded exosomes. Significant differences in terms of tumor volume were observed: IL3L Exo-Imatinib versus IL3L Exo at 17 days (a, p < 0.05), IL3L Exo-Imatinib versus IL3L Exo and Imatinib at 21 days (b, p < 0.005), and IL3L Exo-Imatinib versus IL3L Exo, Exo-Imatinib and Imatinib at 24 days (c, p < 0.0005).CC BY-NC · PubMed Central
Figure 4 In vitro and in vivo effects of BCR-ABL siRNA loaded IL3L-exosomes. (A) LAMA84, K562 and Imatinib resistant K562 cell growth was measured by MTT assay after 24, 48 or 72 h of treatment with Imatinib (on the right side of each histograms) or with 1 μg/ml of exosomes derived from IL3L-HEK293T containing scrambled siRNA or BCR-ABL siRNA. The values were plotted as % of growth vs Ctrl (untreated cells - dot line). Each point represents the mean ± SD of three independent experiments. Statistically significant differences were found between 1 μg/ml IL3L Exo with BCR-ABL and 1 μg/ml IL3L Exo with scramble values (Sidak test: ***, p < 0.0005). In addition, significant decrease in MTT value was observed in each cell type overtime (Sidak test: a, 48h versus 24h - p < 0.0005; b, 72h versus 48h - p < 0.0005). (B) Real-time PCR analysis was performed on CML cell lines treated for 24 or 48 h with Imatinib (on the right side of each histograms) or with 1 μg/ml of exosomes derived from IL3L-HEK293T containing scrambled siRNA or BCR-ABL siRNA. The values were plotted as fold change compared to control (untreated cells - dot line). Each point represents the mean ± SD of three independent experiments. GLM highlighted a significant influence on PCR data by the treatment effect (***, p < 0.0005), but not by experimental time effect. (C) Western blot analysis was performed on CML cell lines treated for 72h with Imatinib or with 1 μg/ml of exosomes derived from IL3L-HEK293T containing scrambled siRNA or BCR-ABL siRNA. Protein levels of Bcr-Abl were evaluated. Blots were stripped and subsequently re-probed with an antibody against Gapdh to ensure equal loading. (D) Comparison of the mean tumor volume was an index of the anti-tumor efficacy of IL3L-HEK293T derived exosomes containing BCR-ABL siRNA. Significant differences in terms of tumor volume were observed at 28 days: IL3L BCR-ABL siRNA versus Ctrl untreated (a, p < 0.0005), IL3L Exo-scrambled siRNA and Imatinib (b, p < 0.005), and versus Exo-scrambled siRNA (c, p < 0.005).
Figure 4 In vitro and in vivo effects of BCR-ABL siRNA loaded IL3L-exosomes. (A) LAMA84, K562 and Imatinib resistant K562 cell growth was measured by MTT assay after 24, 48 or 72 h of treatment with Imatinib (on the right side of each histograms) or with 1 μg/ml of exosomes derived from IL3L-HEK293T containing scrambled siRNA or BCR-ABL siRNA. The values were plotted as % of growth vs Ctrl (untreated cells - dot line). Each point represents the mean ± SD of three independent experiments. Statistically significant differences were found between 1 μg/ml IL3L Exo with BCR-ABL and 1 μg/ml IL3L Exo with scramble values (Sidak test: ***, p < 0.0005). In addition, significant decrease in MTT value was observed in each cell type overtime (Sidak test: a, 48h versus 24h - p < 0.0005; b, 72h versus 48h - p < 0.0005). (B) Real-time PCR analysis was performed on CML cell lines treated for 24 or 48 h with Imatinib (on the right side of each histograms) or with 1 μg/ml of exosomes derived from IL3L-HEK293T containing scrambled siRNA or BCR-ABL siRNA. The values were plotted as fold change compared to control (untreated cells - dot line). Each point represents the mean ± SD of three independent experiments. GLM highlighted a significant influence on PCR data by the treatment effect (***, p < 0.0005), but not by experimental time effect. (C) Western blot analysis was performed on CML cell lines treated for 72h with Imatinib or with 1 μg/ml of exosomes derived from IL3L-HEK293T containing scrambled siRNA or BCR-ABL siRNA. Protein levels of Bcr-Abl were evaluated. Blots were stripped and subsequently re-probed with an antibody against Gapdh to ensure equal loading. (D) Comparison of the mean tumor volume was an index of the anti-tumor efficacy of IL3L-HEK293T derived exosomes containing BCR-ABL siRNA. Significant differences in terms of tumor volume were observed at 28 days: IL3L BCR-ABL siRNA versus Ctrl untreated (a, p < 0.0005), IL3L Exo-scrambled siRNA and Imatinib (b, p < 0.005), and versus Exo-scrambled siRNA (c, p < 0.005).CC BY-NC · PubMed Central
Figure 5 In vivo distribution of engineered exosomes in Imatinib sensitive mouse xenograft. (A) NOD/SCID mice bearing Imatinib sensitive CML xenograft tumors in the right flank were injected intraperitoneally with Free-DiR, 100 μg of HEK293T exosomes-DiR, 100 μg of IL3L-HEK293T exosomes-DiR in a volume of 150 μl PBS. Mice were imaged at 1, 4 and 24 h post injection. A scale of the radiance efficiency is presented to the right of mice image. Histogram represents in vivo quantification of in vivo fluorescence (B) Tumors were excised and imaged after 24 h. A scale of the radiance efficiency is presented to the right. Histogram represents ex vivo quantification of tumor fluorescence.
Figure 5 In vivo distribution of engineered exosomes in Imatinib sensitive mouse xenograft. (A) NOD/SCID mice bearing Imatinib sensitive CML xenograft tumors in the right flank were injected intraperitoneally with Free-DiR, 100 μg of HEK293T exosomes-DiR, 100 μg of IL3L-HEK293T exosomes-DiR in a volume of 150 μl PBS. Mice were imaged at 1, 4 and 24 h post injection. A scale of the radiance efficiency is presented to the right of mice image. Histogram represents in vivo quantification of in vivo fluorescence (B) Tumors were excised and imaged after 24 h. A scale of the radiance efficiency is presented to the right. Histogram represents ex vivo quantification of tumor fluorescence.CC BY-NC · PubMed Central
Figure 6 In vivo distribution of engineered exosomes in Imatinib resistant mouse xenograft. (A) NOD/SCID mice bearing Imatinib resistant CML xenograft tumors in the right flank were injected intraperitoneally with Free-DiR, 10 μg of HEK293T exosomes-DiR, 10 μg of IL3L-HEK293T exosomes-DiR in a volume of 150 μl PBS. Mice were imaged at 1, 4 and 24 h post injection. A scale of the radiance efficiency is presented to the right of mice image. Histogram represents in vivo quantification of in vivo fluorescence (B) Tumors were excised and imaged after 24 h. A scale of the radiance efficiency is presented to the right. Histogram represents ex vivo quantification of tumor fluorescence.
Figure 6 In vivo distribution of engineered exosomes in Imatinib resistant mouse xenograft. (A) NOD/SCID mice bearing Imatinib resistant CML xenograft tumors in the right flank were injected intraperitoneally with Free-DiR, 10 μg of HEK293T exosomes-DiR, 10 μg of IL3L-HEK293T exosomes-DiR in a volume of 150 μl PBS. Mice were imaged at 1, 4 and 24 h post injection. A scale of the radiance efficiency is presented to the right of mice image. Histogram represents in vivo quantification of in vivo fluorescence (B) Tumors were excised and imaged after 24 h. A scale of the radiance efficiency is presented to the right. Histogram represents ex vivo quantification of tumor fluorescence.CC BY-NC · PubMed Central

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Research works printed but not linked: 41

  1. [1]Faderl S Kantarjian HM Talpaz M Chronic myelogenous leukemia: update on biology and treatment Oncology (Williston Park) 1999 13 169 80 discussion 81, 84 10079468
  2. [2]Smith DL Burthem J Whetton AD Molecular pathogenesis of chronic myeloid leukaemia Expert Rev Mol Med 2003 5 1 27 14987402
  3. [3]Druker BJ Lydon NB Lessons learned from the development of an abl tyrosine kinase inhibitor for chronic myelogenous leukemia J Clin Invest 2000 105 3 7 10619854 PMC382593
  4. [4]Jabbour E Kantarjian H Cortes J Use of second- and third-generation tyrosine kinase inhibitors in the treatment of chronic myeloid leukemia: an evolving treatment paradigm Clin Lymphoma Myeloma Leuk 2015 15 323 34 25971713 PMC5141582
  5. [5]Mughal TI Schrieber A Principal long-term adverse effects of imatinib in patients with chronic myeloid leukemia in chronic phase Biologics 2010 4 315 23 21209726 PMC3010822
  6. [6]Farmer S Horvath-Puho E Vestergaard H Hermann AP Frederiksen H Chronic myeloproliferative neoplasms and risk of osteoporotic fractures; a nationwide population-based cohort study Br J Haematol 2013 163 603 10 24111669
  7. [7]Mahon FX Deininger MW Schultheis B Chabrol J Reiffers J Goldman JM Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor STI571: diverse mechanisms of resistance Blood 2000 96 1070 9 10910924
  8. [8]Pinilla-Ibarz J Sweet K Emole J Fradley M Long-term BCR-ABL1 Tyrosine Kinase Inhibitor Therapy in Chronic Myeloid Leukemia Anticancer Res 2015 35 6355 64 26637844
  9. [9]Koldehoff M Zakrzewski JL Beelen DW Elmaagacli AH Additive antileukemia effects by GFI1B- and BCR-ABL-specific siRNA in advanced phase chronic myeloid leukemic cells Cancer Gene Ther 2013 20 421 7 23788109
  10. [10]Zhao RC McIvor RS Griffin JD Verfaillie CM Gene therapy for chronic myelogenous leukemia (CML): a retroviral vector that renders hematopoietic progenitors methotrexate-resistant and CML progenitors functionally normal and nontumorigenic in vivo Blood 1997 90 4687 98 9389683
  11. [11]Burnett JC Rossi JJ RNA-based therapeutics: current progress and future prospects Chem Biol 2012 19 60 71 22284355 PMC3269031
  12. [12]Yingchoncharoen P Kalinowski DS Richardson DR Lipid-Based Drug Delivery Systems in Cancer Therapy: What Is Available and What Is Yet to Come Pharmacol Rev 2016 68 701 87 27363439 PMC4931871
  13. [13]Raimondo S Corrado C Raimondi L De Leo G Alessandro R Role of Extracellular Vesicles in Hematological Malignancies Biomed Res Int 2015 2015 821613 26583135 PMC4637071
  14. [14]Corrado C Raimondo S Chiesi A Ciccia F De Leo G Alessandro R Exosomes as intercellular signaling organelles involved in health and disease: basic science and clinical applications Int J Mol Sci 2013 14 5338 66 23466882 PMC3634447
  15. [15]Raimondo S Naselli F Fontana S Monteleone F Lo Dico A Saieva L Citrus limon-derived nanovesicles inhibit cancer cell proliferation and suppress CML xenograft growth by inducing TRAIL-mediated cell death Oncotarget 2015 6 19514 27 26098775 PMC4637302
  16. [16]Conigliaro A Costa V Lo Dico A Saieva L Buccheri S Dieli F CD90+ liver cancer cells modulate endothelial cell phenotype through the release of exosomes containing H19 lncRNA Mol Cancer 2015 14 155 26272696 PMC4536801
  17. [17]Simons M Raposo G Exosomes-vesicular carriers for intercellular communication Curr Opin Cell Biol 2009 21 575 81 19442504
  18. [18]El Andaloussi S Lakhal S Mager I Wood MJ Exosomes for targeted siRNA delivery across biological barriers Adv Drug Deliv Rev 2013 65 391 7 22921840
  19. [20]Hu G Drescher KM Chen XM Exosomal miRNAs: Biological Properties and Therapeutic Potential Front Genet 2012 3 56 22529849 PMC3330238
  20. [21]Ohno S Takanashi M Sudo K Ueda S Ishikawa A Matsuyama N Systemically injected exosomes targeted to EGFR deliver antitumor microRNA to breast cancer cells Mol Ther 2013 21 185 91 PMC3538304 23032975
  21. [22]Haney MJ Klyachko NL Zhao Y Gupta R Plotnikova EG He Z Exosomes as drug delivery vehicles for Parkinson's disease therapy J Control Release 2015 207 18 30 25836593 PMC4430381
  22. [23]Saari H Lazaro-Ibanez E Viitala T Vuorimaa-Laukkanen E Siljander P Yliperttula M Microvesicle- and exosome-mediated drug delivery enhances the cytotoxicity of Paclitaxel in autologous prostate cancer cells J Control Release 2015 26390807
  23. [24]Alvarez-Erviti L Seow Y Yin H Betts C Lakhal S Wood MJ Delivery of siRNA to the mouse brain by systemic injection of targeted exosomes Nat Biotechnol 2011 29 341 5 21423189
  24. [25]Nievergall E Ramshaw HS Yong AS Biondo M Busfield SJ Vairo G Monoclonal antibody targeting of IL-3 receptor alpha with CSL362 effectively depletes CML progenitor and stem cells Blood 2014 123 1218 28 24363400
  25. [26]Testa U Riccioni R Militi S Coccia E Stellacci E Samoggia P Elevated expression of IL-3Ralpha in acute myelogenous leukemia is associated with enhanced blast proliferation, increased cellularity, and poor prognosis Blood 2002 100 2980 8 12351411
  26. [27]Testa U Pelosi E Frankel A CD 123 is a membrane biomarker and a therapeutic target in hematologic malignancies Biomark Res 2014 2 4 24513123 PMC3928610
  27. [28]Li J Chen X Yi J Liu Y Li D Wang J Identification and Characterization of 293T Cell-Derived Exosomes by Profiling the Protein, mRNA and MicroRNA Components PLoS One 2016 11 e0163043 27649079 PMC5029934
  28. [29]Bumcrot D Manoharan M Koteliansky V Sah DW RNAi therapeutics: a potential new class of pharmaceutical drugs Nat Chem Biol 2006 2 711 9 17108989 PMC7097247
  29. [30]Mendonca LS Moreira JN de Lima MC Simoes S Co-encapsulation of anti-BCR-ABL siRNA and imatinib mesylate in transferrin receptor-targeted sterically stabilized liposomes for chronic myeloid leukemia treatment Biotechnol Bioeng 2010 107 884 93 20632368
  30. [31]Landry B Valencia-Serna J Gul-Uludag H Jiang X Janowska-Wieczorek A Brandwein J Progress in RNAi-mediated Molecular Therapy of Acute and Chronic Myeloid Leukemia Mol Ther Nucleic Acids 2015 4 e240 25965550
  31. [32]Koldehoff M Steckel NK Beelen DW Elmaagacli AH Therapeutic application of small interfering RNA directed against bcr-abl transcripts to a patient with imatinib-resistant chronic myeloid leukaemia Clin Exp Med 2007 7 47 55 17609876
  32. [33]Greco KA Franzen CA Foreman KE Flanigan RC Kuo PC Gupta GN PLK-1 Silencing in Bladder Cancer by siRNA Delivered With Exosomes Urology 2016 91 241 e1-7 26876462
  33. [34]Cooper JM Wiklander PB Nordin JZ Al-Shawi R Wood MJ Vithlani M Systemic exosomal siRNA delivery reduced alpha-synuclein aggregates in brains of transgenic mice Mov Disord 2014 29 1476 85 25112864 PMC4204174
  34. [35]Tian Y Li S Song J Ji T Zhu M Anderson GJ A doxorubicin delivery platform using engineered natural membrane vesicle exosomes for targeted tumor therapy Biomaterials 2014 35 2383 90 24345736
  35. [36]Kim MS Haney MJ Zhao Y Mahajan V Deygen I Klyachko NL Development of exosome-encapsulated paclitaxel to overcome MDR in cancer cells Nanomedicine 2016 12 655 64 26586551 PMC4809755
  36. [37]Sun D Zhuang X Xiang X Liu Y Zhang S Liu C A novel nanoparticle drug delivery system: the anti-inflammatory activity of curcumin is enhanced when encapsulated in exosomes Mol Ther 2010 18 1606 14 20571541 PMC2956928
  37. [38]Frolova O Benito J Brooks C Wang RY Korchin B Rowinsky EK SL-401 and SL-501, targeted therapeutics directed at the interleukin-3 receptor, inhibit the growth of leukaemic cells and stem cells in advanced phase chronic myeloid leukaemia Br J Haematol 2014 166 862 74 24942980 PMC4146738
  38. [39]Simhadri VR Reiners KS Hansen HP Topolar D Simhadri VL Nohroudi K Dendritic cells release HLA-B-associated transcript-3 positive exosomes to regulate natural killer function PLoS One 2008 3 e3377 18852879 PMC2566590
  39. [40]El-Andaloussi S Lee Y Lakhal-Littleton S Li J Seow Y Gardiner C Exosome-mediated delivery of siRNA in vitro and in vivo Nat Protoc 2012 7 2112 26 23154783
  40. [41]Raimondo S Saieva L Corrado C Fontana S Flugy A Rizzo A Chronic myeloid leukemia-derived exosomes promote tumor growth through an autocrine mechanism Cell Commun Signal 2015 13 8 25644060 PMC4320527
  41. [42]Bende G Kollipara S Sekar V Saha R UV-spectrophotometric determination of imatinib mesylate and its application in solubility studies Pharmazie 2008 63 641 5 18819515

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Metadata

Authors
Bellavia, D., Raimondo, S., Calabrese, G., Forte, S., Cristaldi, M., Patinella, A., Memeo, L., Manno, M., Raccosta, S., Diana, P., Cirrincione, G., Giavaresi, G., Monteleone, F., Fontana, S., De Leo, G., & Alessandro, R.
Venue
Theranostics
Publisher
Ivyspring International Publisher
Published
2017
Volume
7
Issue
5
Pages
1333-1345
ISSN
1838-7640
DOI
10.7150/thno.17092
PMC
PMC5399597
Cited by
368
References
1
Language
en

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