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   <dc:title>ApoA-I Mimetic administration, but not increased apoA-I-containing HDL, inhibits tumour growth in a mouse model of inherited breast cancer.</dc:title>
   <dc:creator>Cedó Giné, Lídia</dc:creator>
   <dc:creator>García León, Annabel</dc:creator>
   <dc:creator>Baila Rueda, Lucía</dc:creator>
   <dc:creator>Santos, David</dc:creator>
   <dc:creator>Grijalva, Victor</dc:creator>
   <dc:creator>Martínez Cignoni, Melanie Raquel</dc:creator>
   <dc:creator>Carbó, José M.</dc:creator>
   <dc:creator>Metso, Jari</dc:creator>
   <dc:creator>López Vilaró, Laura</dc:creator>
   <dc:creator>Zorzano Olarte, Antonio</dc:creator>
   <dc:creator>Valledor Fernández, Annabel</dc:creator>
   <dc:creator>Cenarro, Ana</dc:creator>
   <dc:creator>Jauhiainen, Matti</dc:creator>
   <dc:creator>Lerma, Enrique</dc:creator>
   <dc:creator>Fogelman, Alan M.</dc:creator>
   <dc:creator>Reddy, Srinivasa T.</dc:creator>
   <dc:creator>Escolà Gil, Joan Carles</dc:creator>
   <dc:creator>Blanco-Vaca, Francisco</dc:creator>
   <dc:subject>Càncer de mama</dc:subject>
   <dc:subject>Hiperlipoproteïnes</dc:subject>
   <dc:subject>Ratolins transgènics</dc:subject>
   <dc:subject>Pèptids</dc:subject>
   <dc:subject>Breast cancer</dc:subject>
   <dc:subject>High density lipoproteins</dc:subject>
   <dc:subject>Transgenic mice</dc:subject>
   <dc:subject>Peptides</dc:subject>
   <dcterms:abstract>Low levels of high-density lipoprotein cholesterol (HDLc) have been associated with breast cancer risk, but several epidemiologic studies have reported contradictory results with regard to the relationship between apolipoprotein (apo) A-I and breast cancer. We aimed to determine the effects of human apoA-I overexpression and administration of specific apoA-I mimetic peptide (D-4F) on tumour progression by using mammary tumour virus-polyoma middle T-antigen transgenic (PyMT) mice as a model of inherited breast cancer. Expression of human apoA-I in the mice did not affect tumour onset and growth in PyMT transgenic mice, despite an increase in the HDLc level. In contrast, D-4F treatment significantly increased tumour latency and inhibited the development of tumours. The effects of D-4F on tumour development were independent of 27-hydroxycholesterol. However, D-4F treatment reduced the plasma oxidized low-density lipoprotein (oxLDL) levels in mice and prevented oxLDL-mediated proliferative response in human breast adenocarcinoma MCF-7 cells. In conclusion, our study shows that D-4F, but not apoA-I-containing HDL, hinders tumour growth in mice with inherited breast cancer in association with a higher protection against LDL oxidative modification</dcterms:abstract>
   <dcterms:issued>2017-12-12T15:10:33Z</dcterms:issued>
   <dcterms:issued>2017-12-12T15:10:33Z</dcterms:issued>
   <dcterms:issued>2016-11-03</dcterms:issued>
   <dcterms:issued>2017-12-12T15:10:33Z</dcterms:issued>
   <dc:type>info:eu-repo/semantics/article</dc:type>
   <dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
   <dc:relation>Reproducció del document publicat a: https://doi.org/10.1038/srep36387</dc:relation>
   <dc:relation>Scientific Reports, 2016, vol. 6, p. 36387</dc:relation>
   <dc:relation>https://doi.org/10.1038/srep36387</dc:relation>
   <dc:rights>cc-by (c) Cedó et al., 2016</dc:rights>
   <dc:rights>http://creativecommons.org/licenses/by/3.0/es</dc:rights>
   <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
   <dc:publisher>Nature Publishing Group</dc:publisher>
   <dc:source>Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)</dc:source>
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