<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>11</volume><submitter>Ager EI</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Targeting of the renin angiotensin system (RAS) reduces tumour growth in experimental models of cancer. We aimed to establish if combined targeting of the 'classical' and 'alternative' arms of the RAS could result in synergistic inhibition of colorectal cancer (CRC) liver metastases.&lt;h4>Methods&lt;/h4>Immediately following induction of CRC liver metastases through intrasplenic injection of murine CRC cells, treatment with irbesartan (AT1R blocker; 50 mg/kg/day s.c.), captopril (ACE inhibitor; 750 mg/kg/day i.p.), CGP42112A (AT2R agonist; 0.6 μg/kg/hr i.p.), and/or ANG-(1-7) (24 μg/kg/hr i.p.) began and continued for 21 days. Liver to body weight ratio and/or stereology were used as a measure of tumour burden. Immunohistochemistry was used to determine AT1R and VEGF expressi</pubmed_abstract><journal>BMC cancer</journal><pagination>274</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3141779</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Altered efficacy of AT1R-targeted treatment after spontaneous cancer cell-AT1R upregulation.</pubmed_title><pmcid>PMC3141779</pmcid><pubmed_authors>Wen SW</pubmed_authors><pubmed_authors>Chong WW</pubmed_authors><pubmed_authors>Chan J</pubmed_authors><pubmed_authors>Christophi C</pubmed_authors><pubmed_authors>Ager EI</pubmed_authors><pubmed_authors>Neo JH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Altered efficacy of AT1R-targeted treatment after spontaneous cancer cell-AT1R upregulation.</name><description>&lt;h4>Background&lt;/h4>Targeting of the renin angiotensin system (RAS) reduces tumour growth in experimental models of cancer. We aimed to establish if combined targeting of the 'classical' and 'alternative' arms of the RAS could result in synergistic inhibition of colorectal cancer (CRC) liver metastases.&lt;h4>Methods&lt;/h4>Immediately following induction of CRC liver metastases through intrasplenic injection of murine CRC cells, treatment with irbesartan (AT1R blocker; 50 mg/kg/day s.c.), captopril (ACE inhibitor; 750 mg/kg/day i.p.), CGP42112A (AT2R agonist; 0.6 μg/kg/hr i.p.), and/or ANG-(1-7) (24 μg/kg/hr i.p.) began and continued for 21 days. Liver to body weight ratio and/or stereology were used as a measure of tumour burden. Immunohistochemistry was used to determine AT1R and VEGF expressi</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Jun</publication><modification>2025-04-18T13:45:45.275Z</modification><creation>2019-03-27T03:07:19Z</creation></dates><accession>S-EPMC3141779</accession><cross_references><pubmed>21703011</pubmed><doi>10.1186/1471-2407-11-274</doi></cross_references></HashMap>