<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7(16)</volume><submitter>Kocijancic D</submitter><pubmed_abstract>To date, virulent bacteria remain the basis of most bacteria mediated cancer therapies. For clinical application attenuation is required. However, this might result in a drastically lowered therapeutic capacity. Herein we argue that the E. coli probiotic Symbioflor-2, with a history of safe application may constitute a viable tumor therapeutic candidate. We demonstrate that Symbioflor-2 displays a highly specific tumor targeting ability as determined in murine CT26 and RenCa tumor models. The excellent specificity was ascribed to reduced levels of adverse colonization. A high safety standard was demonstrated in WT and Rag1-/- mice. Thus, Symbioflor-2 may represent an ideal tumor targeting delivery system for therapeutic molecules. Moreover, Symbioflor-2 was capable of inducing CT26 tumor clearance as result of an adjuvant effect on tumor specific CD8+ T cells analogous to the Salmonella variant SL7207. However, lower therapeutic efficacy against RenCa tumors suggested a generally reduced therapeutic potency for probiotics. Interestingly, concurrent depletion of Gr-1+ or Ly6G+ cells installed therapeutic efficacy equal to SL7207, thus highlighting the role of innate effector cells in restraining the anti-tumor effects of Symbioflor-2. Collectively, our findings argue for a strategy of safe strain application and a more sustainable use of bacteria as a delivery system for therapeutic molecules.</pubmed_abstract><journal>Oncotarget</journal><pagination>22605-22</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5008385</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Therapy of solid tumors using probiotic Symbioflor-2: restraints and potential.</pubmed_title><pmcid>PMC5008385</pmcid><pubmed_authors>Frahm M</pubmed_authors><pubmed_authors>Heise U</pubmed_authors><pubmed_authors>Gunzer F</pubmed_authors><pubmed_authors>Rohde M</pubmed_authors><pubmed_authors>Zimmermann K</pubmed_authors><pubmed_authors>Kocijancic D</pubmed_authors><pubmed_authors>Iljazovic A</pubmed_authors><pubmed_authors>Hammer J</pubmed_authors><pubmed_authors>Komoll RM</pubmed_authors><pubmed_authors>Felgner S</pubmed_authors><pubmed_authors>Weiss S</pubmed_authors><pubmed_authors>Crull K</pubmed_authors><pubmed_authors>Leschner S</pubmed_authors><pubmed_authors>Pawar V</pubmed_authors></additional><is_claimable>false</is_claimable><name>Therapy of solid tumors using probiotic Symbioflor-2: restraints and potential.</name><description>To date, virulent bacteria remain the basis of most bacteria mediated cancer therapies. For clinical application attenuation is required. However, this might result in a drastically lowered therapeutic capacity. Herein we argue that the E. coli probiotic Symbioflor-2, with a history of safe application may constitute a viable tumor therapeutic candidate. We demonstrate that Symbioflor-2 displays a highly specific tumor targeting ability as determined in murine CT26 and RenCa tumor models. The excellent specificity was ascribed to reduced levels of adverse colonization. A high safety standard was demonstrated in WT and Rag1-/- mice. Thus, Symbioflor-2 may represent an ideal tumor targeting delivery system for therapeutic molecules. Moreover, Symbioflor-2 was capable of inducing CT26 tumor clearance as result of an adjuvant effect on tumor specific CD8+ T cells analogous to the Salmonella variant SL7207. However, lower therapeutic efficacy against RenCa tumors suggested a generally reduced therapeutic potency for probiotics. Interestingly, concurrent depletion of Gr-1+ or Ly6G+ cells installed therapeutic efficacy equal to SL7207, thus highlighting the role of innate effector cells in restraining the anti-tumor effects of Symbioflor-2. Collectively, our findings argue for a strategy of safe strain application and a more sustainable use of bacteria as a delivery system for therapeutic molecules.</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Apr</publication><modification>2021-02-21T03:01:06Z</modification><creation>2019-03-27T02:23:19Z</creation></dates><accession>S-EPMC5008385</accession><cross_references><pubmed>26981777</pubmed><doi>10.18632/oncotarget.8027</doi></cross_references></HashMap>