<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Reader CS</submitter><funding>CRUK Core Facilities at Barts Cancer Institute, London</funding><funding>Cancer Research UK</funding><funding>Training Fellowship</funding><funding>Pancreatic Cancer UK</funding><funding>Medical Research Council</funding><funding>Pancreatic Cancer Research Fund</funding><funding>Wellcome Trust</funding><pagination>332-342</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6852434</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>249(3)</volume><pubmed_abstract>Pancreatic ductal adenocarcinoma (PDAC) has a 5-year survival rate of less than 4% and desperately needs novel effective therapeutics. Integrin αvβ6 has been linked with poor prognosis in cancer but its potential as a target in PDAC remains unclear. We report that transcriptional expression analysis revealed that high levels of β6 mRNA correlated strongly with significantly poorer survival (n = 491 cases, p = 3.17 × 10&lt;sup>-8&lt;/sup> ). In two separate cohorts, we showed that over 80% of PDACs expressed αvβ6 protein and that paired metastases retained αvβ6 expression. In vitro, integrin αvβ6 promoted PDAC cell growth, survival, migration, and invasion. Treatment of both αvβ6-positive human PDAC xenografts and transgenic mice bearing αvβ6-positive PDAC with the αvβ6 blocking antibody 264RAD, </pubmed_abstract><journal>The Journal of pathology</journal><pubmed_title>The integrin αvβ6 drives pancreatic cancer through diverse mechanisms and represents an effective target for therapy.</pubmed_title><pmcid>PMC6852434</pmcid><funding_grant_id>23526</funding_grant_id><funding_grant_id>RIF2015_A06_JAMIESON</funding_grant_id><funding_grant_id>17764</funding_grant_id><funding_grant_id>29996</funding_grant_id><funding_grant_id>G0800825</funding_grant_id><funding_grant_id>FLF2015_04_GLASGOW</funding_grant_id><funding_grant_id>25233</funding_grant_id><funding_grant_id>103721/Z/14/Z</funding_grant_id><funding_grant_id>11650</funding_grant_id><funding_grant_id>20409</funding_grant_id><funding_grant_id>C16420/A18066</funding_grant_id><funding_grant_id>21139</funding_grant_id><pubmed_authors>Chelala C</pubmed_authors><pubmed_authors>Marshall JF</pubmed_authors><pubmed_authors>Keyse SM</pubmed_authors><pubmed_authors>Reader CS</pubmed_authors><pubmed_authors>Moore KM</pubmed_authors><pubmed_authors>Sansom OJ</pubmed_authors><pubmed_authors>Brentnall A</pubmed_authors><pubmed_authors>Lawlor R</pubmed_authors><pubmed_authors>Vallath S</pubmed_authors><pubmed_authors>Barry ST</pubmed_authors><pubmed_authors>Desai A</pubmed_authors><pubmed_authors>Scarpa A</pubmed_authors><pubmed_authors>Evans TJ</pubmed_authors><pubmed_authors>Haider S</pubmed_authors><pubmed_authors>Chang D</pubmed_authors><pubmed_authors>Jamieson NB</pubmed_authors><pubmed_authors>Biankin A</pubmed_authors><pubmed_authors>Morton JP</pubmed_authors><pubmed_authors>Kocher HM</pubmed_authors><pubmed_authors>Steele CW</pubmed_authors><pubmed_authors>Bailey P</pubmed_authors></additional><is_claimable>false</is_claimable><name>The integrin αvβ6 drives pancreatic cancer through diverse mechanisms and represents an effective target for therapy.</name><description>Pancreatic ductal adenocarcinoma (PDAC) has a 5-year survival rate of less than 4% and desperately needs novel effective therapeutics. Integrin αvβ6 has been linked with poor prognosis in cancer but its potential as a target in PDAC remains unclear. We report that transcriptional expression analysis revealed that high levels of β6 mRNA correlated strongly with significantly poorer survival (n = 491 cases, p = 3.17 × 10&lt;sup>-8&lt;/sup> ). In two separate cohorts, we showed that over 80% of PDACs expressed αvβ6 protein and that paired metastases retained αvβ6 expression. In vitro, integrin αvβ6 promoted PDAC cell growth, survival, migration, and invasion. Treatment of both αvβ6-positive human PDAC xenografts and transgenic mice bearing αvβ6-positive PDAC with the αvβ6 blocking antibody 264RAD, </description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Nov</publication><modification>2025-04-04T08:26:57.767Z</modification><creation>2020-05-21T19:10:47Z</creation></dates><accession>S-EPMC6852434</accession><cross_references><pubmed>31259422</pubmed><doi>10.1002/path.5320</doi></cross_references></HashMap>