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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/70657
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dc.contributor.authorConde, S. J.-
dc.contributor.authorLuvizotto, R. A M-
dc.contributor.authorSibio, M. T.-
dc.contributor.authorKatayama, M. L H-
dc.contributor.authorBrentani, M. M.-
dc.contributor.authorNogueira, Célia Regina-
dc.date.accessioned2014-05-27T11:23:42Z-
dc.date.accessioned2016-10-25T18:26:13Z-
dc.date.available2014-05-27T11:23:42Z-
dc.date.available2016-10-25T18:26:13Z-
dc.date.issued2008-12-01-
dc.identifierhttp://dx.doi.org/10.1007/BF03345650-
dc.identifier.citationJournal of Endocrinological Investigation, v. 31, n. 12, p. 1047-1051, 2008.-
dc.identifier.issn0391-4097-
dc.identifier.urihttp://hdl.handle.net/11449/70657-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/70657-
dc.description.abstractObjectives: To examine the effects of triiodothyronine (T3), 17β-estradiol (E2), and tamoxifen (TAM) on transforming growth factor (TGF)-α gene expression in primary breast cancer cell cultures and interactions between the different treatments. Methods and results: Patients included in the study (no.=12) had been newly diagnosed with breast cancer. Fresh human breast carcinoma tissue was cut into 0.3-mm slices. These slices were placed in six 35-mm dishes on 2-ml organ culture medium. Dishes received the following treatments: dish 1: ethanol; dish 2: T3; dish 3: T3+TAM; dish 4: TAM; dish 5: E2; dish 6: E2+TAM. TGF-α mRNA content was normalized to glyceraldehyde-3-phosphate dehydrogenase mRNA levels. All tissues included in this study were positive for estrogen receptor (ER) and thyroid hormone receptor expression. Treatment with T3 for 48 h significantly increased TGF-α mRNA levels compared to controls (15-fold), and concomitant treatment with TAM reduced expression to 3.4-fold compared to controls. When only TAM was added to the culture medium, TGF-α mRNA expression increased 5.3-fold, significantly higher than with all other treatment modalities. Conclusion: We demonstrate that TGF-α mRNA expression is more efficiently upregulated by T3 than E2. Concomitant treatment with TAM had a mitigating effect on the T3 effect, while E2 induced TGF-α upregulation. Our findings show some similarities between primary culture and breast cancer cell lines, but also some important differences: a) induction of TGF-α, a mitogenic protein, by TAM; b) a differential effect of TAM that may depend on relative expression of ER α and β; and c) supraphysiological doses of T3 may induce mitogenic signals in breast cancer tissue under conditions of low circulating E2. ©2008, Editrice Kurtis.en
dc.format.extent1047-1051-
dc.language.isoeng-
dc.sourceScopus-
dc.subjectBreast cancer samples-
dc.subjectEstrogen-
dc.subjectTamoxifen-
dc.subjectTGF-α-
dc.subjectTriiodothyronine-
dc.subjectcyclin D1-
dc.subjectestradiol-
dc.subjectestrogen receptor alpha-
dc.subjectestrogen receptor beta-
dc.subjectglyceraldehyde 3 phosphate dehydrogenase-
dc.subjectliothyronine-
dc.subjectmessenger RNA-
dc.subjecttamoxifen-
dc.subjectthyroid hormone receptor-
dc.subjecttransforming growth factor alpha-
dc.subjectadult-
dc.subjectaged-
dc.subjectbreast carcinoma-
dc.subjectcancer cell culture-
dc.subjectclinical article-
dc.subjectcontrolled study-
dc.subjectculture medium-
dc.subjectdrug mechanism-
dc.subjectfemale-
dc.subjectgene expression regulation-
dc.subjecthuman-
dc.subjecthuman cell-
dc.subjecthuman tissue-
dc.subjectmitogenicity-
dc.subjectupregulation-
dc.subjectAdult-
dc.subjectAged-
dc.subjectAged, 80 and over-
dc.subjectBreast Neoplasms-
dc.subjectCarcinoma-
dc.subjectCell Culture Techniques-
dc.subjectDown-Regulation-
dc.subjectDrug Interactions-
dc.subjectEstradiol-
dc.subjectFemale-
dc.subjectGene Expression Regulation, Neoplastic-
dc.subjectHumans-
dc.subjectMiddle Aged-
dc.subjectTransforming Growth Factor alpha-
dc.subjectTumor Cells, Cultured-
dc.titleTamoxifen inhibits transforming growth factor-α gene expression in human breast carcinoma samples treated with triiodothyronineen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionUniversidade de São Paulo (USP)-
dc.description.affiliationDivision of Endocrinology and Metabolism Department of Medical Clinic UNESP, Rubião Junior, s/n, 18618-970 Botucatu, SP-
dc.description.affiliationDivision of Oncology Department of Radiology USP, São Paulo-
dc.description.affiliationUnespDivision of Endocrinology and Metabolism Department of Medical Clinic UNESP, Rubião Junior, s/n, 18618-970 Botucatu, SP-
dc.identifier.doi10.1007/BF03345650-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofJournal of Endocrinological Investigation-
dc.identifier.scopus2-s2.0-63049106959-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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