<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>14(2)</volume><submitter>Kluza E</submitter><pubmed_abstract>Inflammation plays a prominent role in tumor growth. Anti-inflammatory drugs have therefore been proposed as anti-cancer therapeutics. In this study, we determined the anti-angiogenic activity of a single dose of liposomal prednisolone phosphate (PLP-L), by monitoring tumor vascular function and viability over a period of one week. C57BL/6 mice were inoculated subcutaneously with B16F10 melanoma cells. Six animals were PLP-L-treated and six served as control. Tumor tissue and vascular function were probed using MRI before and at three timepoints after treatment. DCE-MRI was used to determine K(trans), v(e), time-to-peak, initial slope and the fraction of non-enhancing pixels, complemented with immunohistochemistry. The apparent diffusion coefficient (ADC), T(2) and tumor size were assessed with MRI as well. PLP-L treatment resulted in smaller tumors and caused a significant drop in K(trans) 48 h post-treatment, which was maintained until one week after drug administration. However, this effect was not sufficient to significantly distinguish treated from non-treated animals. The therapy did not affect tumor tissue viability but did prevent the ADC decrease observed in the control group. No evidence for PLP-L-induced tumor vessel normalization was found on histology. Treatment with PLP-L altered tumor vascular function. This effect did not fully explain the tumor growth inhibition, suggesting a broader spectrum of PLP-L activities.</pubmed_abstract><journal>Angiogenesis</journal><pagination>143-53</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3102848</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Multi-parametric assessment of the anti-angiogenic effects of liposomal glucocorticoids.</pubmed_title><pmcid>PMC3102848</pmcid><pubmed_authors>Schmid S</pubmed_authors><pubmed_authors>van der Schaft DW</pubmed_authors><pubmed_authors>ter Haar Romeny BM</pubmed_authors><pubmed_authors>Heisen M</pubmed_authors><pubmed_authors>Kluza E</pubmed_authors><pubmed_authors>Storm G</pubmed_authors><pubmed_authors>Schiffelers RM</pubmed_authors><pubmed_authors>Strijkers GJ</pubmed_authors><pubmed_authors>Nicolay K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Multi-parametric assessment of the anti-angiogenic effects of liposomal glucocorticoids.</name><description>Inflammation plays a prominent role in tumor growth. Anti-inflammatory drugs have therefore been proposed as anti-cancer therapeutics. In this study, we determined the anti-angiogenic activity of a single dose of liposomal prednisolone phosphate (PLP-L), by monitoring tumor vascular function and viability over a period of one week. C57BL/6 mice were inoculated subcutaneously with B16F10 melanoma cells. Six animals were PLP-L-treated and six served as control. Tumor tissue and vascular function were probed using MRI before and at three timepoints after treatment. DCE-MRI was used to determine K(trans), v(e), time-to-peak, initial slope and the fraction of non-enhancing pixels, complemented with immunohistochemistry. The apparent diffusion coefficient (ADC), T(2) and tumor size were assessed with MRI as well. PLP-L treatment resulted in smaller tumors and caused a significant drop in K(trans) 48 h post-treatment, which was maintained until one week after drug administration. However, this effect was not sufficient to significantly distinguish treated from non-treated animals. The therapy did not affect tumor tissue viability but did prevent the ADC decrease observed in the control group. No evidence for PLP-L-induced tumor vessel normalization was found on histology. Treatment with PLP-L altered tumor vascular function. This effect did not fully explain the tumor growth inhibition, suggesting a broader spectrum of PLP-L activities.</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 May</publication><modification>2021-03-11T08:06:00Z</modification><creation>2019-03-27T00:42:03Z</creation></dates><accession>S-EPMC3102848</accession><cross_references><pubmed>21225337</pubmed><doi>10.1007/s10456-010-9198-5</doi></cross_references></HashMap>