<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wafai R</submitter><funding>National Health and Medical Research Council</funding><funding>National Breast Cancer Foundation</funding><pagination>136</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7716465</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>22(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Breast cancers acquire aggressive capabilities via epithelial to mesenchymal transition (EMT), in which various integrins/integrin-linked kinase signalling are upregulated.&lt;h4>Methods&lt;/h4>We investigated this in two patient-derived xenografts (PDXs) developed from breast-to-bone metastases, and its functional significance in a breast cancer cell line system. ED03 and EDW01 PDXs were grown subcutaneously in immunocompromised SCID mice through 11 passages and 7 passages, respectively. Tumour tissue was assessed using immunohistochemistry (IHC) for oestrogen receptor (ER)-alpha, E-cadherin, vimentin, Twist1, beta-catenin, P120-RasGAP, CD44, CD24 and Ki67, and RT-qPCR of EMT-related factors (CDH1, VIM, CD44, CD24), integrins beta 1 (ITGB1), alpha 2 (ITGA2) and ILK. Integrin </pubmed_abstract><journal>Breast cancer research : BCR</journal><pubmed_title>Integrin alpha-2 and beta-1 expression increases through multiple generations of the EDW01 patient-derived xenograft model of breast cancer-insight into their role in epithelial mesenchymal transition in vivo gained from an in vitro model system.</pubmed_title><pmcid>PMC7716465</pmcid><funding_grant_id>1027527</funding_grant_id><funding_grant_id>CG-10-04</funding_grant_id><pubmed_authors>Williams ED</pubmed_authors><pubmed_authors>McCart Reed AE</pubmed_authors><pubmed_authors>Waltham M</pubmed_authors><pubmed_authors>Snell CE</pubmed_authors><pubmed_authors>Blick T</pubmed_authors><pubmed_authors>de Souza E</pubmed_authors><pubmed_authors>Wafai R</pubmed_authors><pubmed_authors>Kutasovic JR</pubmed_authors><pubmed_authors>Hugo HJ</pubmed_authors><pubmed_authors>Simpson PT</pubmed_authors><pubmed_authors>Thompson EW</pubmed_authors></additional><is_claimable>false</is_claimable><name>Integrin alpha-2 and beta-1 expression increases through multiple generations of the EDW01 patient-derived xenograft model of breast cancer-insight into their role in epithelial mesenchymal transition in vivo gained from an in vitro model system.</name><description>&lt;h4>Background&lt;/h4>Breast cancers acquire aggressive capabilities via epithelial to mesenchymal transition (EMT), in which various integrins/integrin-linked kinase signalling are upregulated.&lt;h4>Methods&lt;/h4>We investigated this in two patient-derived xenografts (PDXs) developed from breast-to-bone metastases, and its functional significance in a breast cancer cell line system. ED03 and EDW01 PDXs were grown subcutaneously in immunocompromised SCID mice through 11 passages and 7 passages, respectively. Tumour tissue was assessed using immunohistochemistry (IHC) for oestrogen receptor (ER)-alpha, E-cadherin, vimentin, Twist1, beta-catenin, P120-RasGAP, CD44, CD24 and Ki67, and RT-qPCR of EMT-related factors (CDH1, VIM, CD44, CD24), integrins beta 1 (ITGB1), alpha 2 (ITGA2) and ILK. Integrin </description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Dec</publication><modification>2025-04-22T16:52:12.785Z</modification><creation>2021-02-20T10:06:59Z</creation></dates><accession>S-EPMC7716465</accession><cross_references><pubmed>33276802</pubmed><doi>10.1186/s13058-020-01366-8</doi></cross_references></HashMap>