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dc.contributor.authorKoutsilieris, M.en
dc.contributor.authorReyes-Moreno, C.en
dc.contributor.authorChoki, I.en
dc.contributor.authorSourla, A.en
dc.contributor.authorDoillon, C.en
dc.contributor.authorPavlidis, N.en
dc.date.accessioned2015-11-24T19:30:45Z-
dc.date.available2015-11-24T19:30:45Z-
dc.identifier.issn1076-1551-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/23160-
dc.rightsDefault Licence-
dc.subjectAntineoplastic Agents/*pharmacologyen
dc.subjectApoptosis/drug effectsen
dc.subjectBreast Neoplasms/*drug therapy/*metabolismen
dc.subjectCell Culture Techniques/methodsen
dc.subjectCell Division/drug effectsen
dc.subjectCollagenen
dc.subjectDose-Response Relationship, Drugen
dc.subjectDoxorubicin/*pharmacologyen
dc.subjectFemaleen
dc.subjectGrowth Substances/*metabolismen
dc.subjectHumansen
dc.subjectInsulin-Like Growth Factor I/drug effects/metabolismen
dc.subjectOsteoblasts/drug effects/*metabolismen
dc.subjectReceptors, Estrogen/metabolismen
dc.subjectTransforming Growth Factor beta/drug effects/metabolismen
dc.subjectTumor Cells, Cultured/drug effects/metabolismen
dc.titleChemotherapy cytotoxicity of human MCF-7 and MDA-MB 231 breast cancer cells is altered by osteoblast-derived growth factorsen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/10203574-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate1999-
heal.abstractOne-third of women with breast cancer will develop bone metastases and eventually die from disease progression at these sites. Therefore, we analyzed the ability of human MG-63 osteoblast-like cells (MG-63 cells), MG-63 conditioned media (MG-63 CM), insulin-like growth factor I (IGF-I), and transforming growth factor beta 1 (TGF-beta1) to alter the effects of adriamycin on cell cycle and apoptosis of estrogen receptor negative (ER-) MDA-MB-231 and positive (ER+) MCF-7 breast cancer cells, using cell count, trypan blue exclusion, flow cytometry, detection of DNA fragmentation by simple agarose gel, and the terminal deoxynucleotidyl transferase (TdT)-mediated nick end-labeling method for apoptosis (TUNEL assay). Adriamycin arrested MCF-7 and MDA-MB-231 cells at G2/M phase in the cell cycle and inhibited cell growth. In addition, adriamycin arrested the MCF-7 cells at G1/G0 phase and induced apoptosis of MDA-MB-231 cells. Exogenous IGF-I partially neutralized the adriamycin cytotoxicity/cytostasis of cancer cells. MG-63 CM and TGF-beta1 partially neutralized the adriamycin cytotoxicity of MDA-MB-231 cells but enhanced adriamycin blockade of MCF-7 cells at G1/G0 phase. MG-63 osteoblast-like cells inhibited growth of MCF-7 cells while promoting growth and rescued MDA-MB-231 cells from adriamycin apoptosis in a collagen co-culture system. These data suggest that osteoblast-derived growth factors can alter the chemotherapy response of breast cancer cells. Conceivably, host tissue (bone)-tumor cell interactions can modify the clinical response to chemotherapy in patients with advanced breast cancer.en
heal.journalNameMol Meden
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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