pubmed-article:9662255 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9662255 | lifeskim:mentions | umls-concept:C1512505 | lld:lifeskim |
pubmed-article:9662255 | lifeskim:mentions | umls-concept:C0069515 | lld:lifeskim |
pubmed-article:9662255 | lifeskim:mentions | umls-concept:C0008838 | lld:lifeskim |
pubmed-article:9662255 | lifeskim:mentions | umls-concept:C0040845 | lld:lifeskim |
pubmed-article:9662255 | lifeskim:mentions | umls-concept:C0060197 | lld:lifeskim |
pubmed-article:9662255 | lifeskim:mentions | umls-concept:C0312418 | lld:lifeskim |
pubmed-article:9662255 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:9662255 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
pubmed-article:9662255 | lifeskim:mentions | umls-concept:C1704824 | lld:lifeskim |
pubmed-article:9662255 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:9662255 | lifeskim:mentions | umls-concept:C0036667 | lld:lifeskim |
pubmed-article:9662255 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:9662255 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:9662255 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:9662255 | pubmed:dateCreated | 1998-7-20 | lld:pubmed |
pubmed-article:9662255 | pubmed:abstractText | We investigated the effects of all-trans retinoic acid (ATRA) and fenretinide (4-HPR) on c-erbB-2 expression in SK-BR-3, BT-474 and MCF-7 breast cancer cells and on the growth, differentiation, apoptosis and cisplatin (CDDP) sensitivity of SK-BR-3 cells. It has been reported that oestrogen inhibits c-erbB-2 in oestrogen receptor-positive breast cancer cells. Using ELISA, Western and Northern analysis we have demonstrated that ATRA and 4-HPR exert similar effects down-regulating c-erbB-2 protein and mRNA in c-erbB-2-overexpressing SK-BR-3 and BT-474 and in normally expressing MCF-7 cells. Both retinoids inhibit SK-BR-3 cell growth. ATRA induces cellular enlargement and flattening, suggesting epithelial differentiation. 4-HPR causes nuclear and cytoplasmic condensation, DNA fragmentation and externalization of phosphatidylserine, indicating apoptosis. c-erbB-2 expression/activity has been linked to sensitivity against CDDP. Therefore, combinations of ATRA or 4-HPR with CDDP were tested for their anti-proliferative activity. Retinoid-conditioned cells were either exposed to retinoid and CDDP (schedule I, 'continuous retinoid treatment') or to CDDP alone (schedule II, 'retinoid pretreatment'). This retinoid-conditioning followed by CDDP +/- retinoid yields stronger growth inhibition compared with unconditioned cells, which were exposed to CDDP +/- retinoid (schedule III, 'no retinoid pretreatment'). The inefficacy of schedule III indicates that retinoid-conditioning is essential for the improvement of the antiproliferative effect. The interactions in schedules I and II are synergistic for ATRA and CDDP, but slightly antagonistic for 4-HPR and CDDR However, 4-HPR + CDDP is more effective in growth inhibition than each drug alone. | lld:pubmed |
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pubmed-article:9662255 | pubmed:language | eng | lld:pubmed |
pubmed-article:9662255 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9662255 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9662255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9662255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9662255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9662255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:9662255 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9662255 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9662255 | pubmed:month | Jul | lld:pubmed |
pubmed-article:9662255 | pubmed:issn | 0007-0920 | lld:pubmed |
pubmed-article:9662255 | pubmed:author | pubmed-author:HuberHH | lld:pubmed |
pubmed-article:9662255 | pubmed:author | pubmed-author:SchneiderS... | lld:pubmed |
pubmed-article:9662255 | pubmed:author | pubmed-author:DittrichEE | lld:pubmed |
pubmed-article:9662255 | pubmed:author | pubmed-author:OffterdingerM... | lld:pubmed |
pubmed-article:9662255 | pubmed:author | pubmed-author:Grunt ThW | lld:pubmed |
pubmed-article:9662255 | pubmed:author | pubmed-author:DittrichChCh | lld:pubmed |
pubmed-article:9662255 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9662255 | pubmed:volume | 78 | lld:pubmed |
pubmed-article:9662255 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9662255 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9662255 | pubmed:pagination | 79-87 | lld:pubmed |
pubmed-article:9662255 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:9662255 | pubmed:year | 1998 | lld:pubmed |
pubmed-article:9662255 | pubmed:articleTitle | Effects of retinoic acid and fenretinide on the c-erbB-2 expression, growth and cisplatin sensitivity of breast cancer cells. | lld:pubmed |
pubmed-article:9662255 | pubmed:affiliation | Laboratory for Cell Growth and Differentiation, Department of Internal Medicine I, University of Vienna, Austria. | lld:pubmed |
pubmed-article:9662255 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9662255 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |