<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pervin S</submitter><funding>NIA NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>848-58</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3590675</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>108(4)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Breast cancer, a heterogeneous disease has been broadly classified into oestrogen receptor positive (ER+) or oestrogen receptor negative (ER-) tumour types. Each of these tumours is dependent on specific signalling pathways for their progression. While high levels of survivin, an anti-apoptotic protein, increases aggressive behaviour in ER- breast tumours, oxidative stress (OS) promotes the progression of ER+ breast tumours. Mechanisms and molecular targets by which OS promotes tumourigenesis remain poorly understood.&lt;h4>Results&lt;/h4>DETA-NONOate, a nitric oxide (NO)-donor induces OS in breast cancer cell lines by early re-localisation and downregulation of cellular survivin. Using in vivo models of HMLE(HRAS) xenografts and E2-induced breast tumours in ACI rats, we demon</pubmed_abstract><journal>British journal of cancer</journal><pubmed_title>Oxidative stress specifically downregulates survivin to promote breast tumour formation.</pubmed_title><pmcid>PMC3590675</pmcid><funding_grant_id>U54 CA143931</funding_grant_id><funding_grant_id>SC1 AG033407-01A1</funding_grant_id><funding_grant_id>1SC1 CA165865-01A1</funding_grant_id><funding_grant_id>SC1 AG049682</funding_grant_id><funding_grant_id>SC1 AG033407</funding_grant_id><funding_grant_id>SC1 CA165865</funding_grant_id><funding_grant_id>U54CA143931</funding_grant_id><pubmed_authors>Braga M</pubmed_authors><pubmed_authors>Parveen M</pubmed_authors><pubmed_authors>Chaudhuri G</pubmed_authors><pubmed_authors>Urman R</pubmed_authors><pubmed_authors>Singh R</pubmed_authors><pubmed_authors>Tran L</pubmed_authors><pubmed_authors>Pervin S</pubmed_authors><pubmed_authors>Li SA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Oxidative stress specifically downregulates survivin to promote breast tumour formation.</name><description>&lt;h4>Background&lt;/h4>Breast cancer, a heterogeneous disease has been broadly classified into oestrogen receptor positive (ER+) or oestrogen receptor negative (ER-) tumour types. Each of these tumours is dependent on specific signalling pathways for their progression. While high levels of survivin, an anti-apoptotic protein, increases aggressive behaviour in ER- breast tumours, oxidative stress (OS) promotes the progression of ER+ breast tumours. Mechanisms and molecular targets by which OS promotes tumourigenesis remain poorly understood.&lt;h4>Results&lt;/h4>DETA-NONOate, a nitric oxide (NO)-donor induces OS in breast cancer cell lines by early re-localisation and downregulation of cellular survivin. Using in vivo models of HMLE(HRAS) xenografts and E2-induced breast tumours in ACI rats, we demon</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Mar</publication><modification>2026-05-01T05:07:09.928Z</modification><creation>2026-04-07T16:40:24.895Z</creation></dates><accession>S-EPMC3590675</accession><cross_references><pubmed>23403820</pubmed><doi>10.1038/bjc.2013.40</doi></cross_references></HashMap>