<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Harvey AJ</submitter><funding>Breast Cancer Now</funding><pagination>1226-34</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2731141</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>175(3)</volume><pubmed_abstract>Brk, a tyrosine kinase expressed in a majority of breast tumors, but not normal mammary tissue, promotes breast carcinoma cell proliferation. Normal epithelial cells are dependent on cell-cell or cell-matrix interactions for survival and undergo apoptosis after disruption of these interactions. Tumor cells are less sensitive to the induction of apoptosis and are predicted to have the potential to disseminate. We investigated whether Brk has further roles in breast tumor progression by relating its expression to tumor grade and demonstrating its role in the regulation of carcinoma cell survival under non-adherent conditions. Brk expression was determined by reverse transcription PCR on RNA extracted from surgical samples of human breast cancers. Breast carcinoma cell survival in suspension </pubmed_abstract><journal>The American journal of pathology</journal><pubmed_title>Brk protects breast cancer cells from autophagic cell death induced by loss of anchorage.</pubmed_title><pmcid>PMC2731141</pmcid><funding_grant_id>2002:367</funding_grant_id><funding_grant_id>2001:232</funding_grant_id><pubmed_authors>Pennington CJ</pubmed_authors><pubmed_authors>Harvey AJ</pubmed_authors><pubmed_authors>Court W</pubmed_authors><pubmed_authors>Crompton MR</pubmed_authors><pubmed_authors>Eccles SA</pubmed_authors><pubmed_authors>Burmi RS</pubmed_authors><pubmed_authors>Edwards DR</pubmed_authors><pubmed_authors>Porter S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Brk protects breast cancer cells from autophagic cell death induced by loss of anchorage.</name><description>Brk, a tyrosine kinase expressed in a majority of breast tumors, but not normal mammary tissue, promotes breast carcinoma cell proliferation. Normal epithelial cells are dependent on cell-cell or cell-matrix interactions for survival and undergo apoptosis after disruption of these interactions. Tumor cells are less sensitive to the induction of apoptosis and are predicted to have the potential to disseminate. We investigated whether Brk has further roles in breast tumor progression by relating its expression to tumor grade and demonstrating its role in the regulation of carcinoma cell survival under non-adherent conditions. Brk expression was determined by reverse transcription PCR on RNA extracted from surgical samples of human breast cancers. Breast carcinoma cell survival in suspension </description><dates><release>2009-01-01T00:00:00Z</release><publication>2009 Sep</publication><modification>2025-04-22T06:43:36.058Z</modification><creation>2019-03-27T00:24:26Z</creation></dates><accession>S-EPMC2731141</accession><cross_references><pubmed>19661439</pubmed><doi>10.2353/ajpath.2009.080811</doi></cross_references></HashMap>