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[PMID]:29028222
[Au] Autor:Choi HJ; Joo HS; Won HY; Min KW; Kim HY; Son T; Oh YH; Lee JY; Kong G
[Ad] Endereço:Department of Pathology, College of Medicine, Hanyang University, Seoul, Republic of Korea; Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, Republic of Korea; Institute for Bioengineering and Biopharmaceutical Research (IBBR), Hanyang University,
[Ti] Título:Role of RBP2-Induced ER and IGF1R-ErbB Signaling in Tamoxifen Resistance in Breast Cancer.
[So] Source:J Natl Cancer Inst;110(4), 2018 Apr 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Despite the benefit of endocrine therapy, acquired resistance during or after treatment still remains a major challenge in estrogen receptor (ER)-positive breast cancer. We investigated the potential role of histone demethylase retinoblastoma-binding protein 2 (RBP2) in endocrine therapy resistance of breast cancer. Methods: Survival of breast cancer patients according to RBP2 expression was analyzed in three different breast cancer cohorts including METABRIC (n = 1980) and KM plotter (n = 1764). RBP2-mediated tamoxifen resistance was confirmed by invitro sulforhodamine B (SRB) colorimetric, colony-forming assays, and invivo xenograft models (n = 8 per group). RNA-seq analysis and receptor tyrosine kinase assay were performed to identify the tamoxifen resistance mechanism by RBP2. All statistical tests were two-sided. Results: RBP2 was associated with poor prognosis to tamoxifen therapy in ER-positive breast cancer (P = .04 in HYU cohort, P = .02 in KM plotter, P = .007 in METABRIC, log-rank test). Furthermore, RBP2 expression was elevated in patients with tamoxifen-resistant breast cancer (P = .04, chi-square test). Knockdown of RBP2 conferred tamoxifen sensitivity, whereas overexpression of RBP2 induced tamoxifen resistance invitro and invivo (MCF7 xenograft: tamoxifen-treated control, mean [SD] tumor volume = 70.8 [27.9] mm3, vs tamoxifen-treated RBP2, mean [SD] tumor volume = 387.9 [85.1] mm3, P < .001). Mechanistically, RBP2 cooperated with ER co-activators and corepressors and regulated several tamoxifen resistance-associated genes, including NRIP1, CCND1, and IGFBP4 and IGFBP5. Furthermore, epigenetic silencing of IGFBP4/5 by RBP2-ER-NRIP1-HDAC1 complex led to insulin-like growth factor-1 receptor (IGF1R) activation. RBP2 also increased IGF1R-ErbB crosstalk and subsequent PI3K-AKT activation via demethylase activity-independent ErbB protein stabilization. Combinational treatment with tamoxifen and PI3K inhibitor could overcome RBP2-mediated tamoxifen resistance (RBP2-overexpressing cells: % cell viability [SD], tamoxifen = 89.0 [3.8]%, vs tamoxifen with BKM120 = 41.3 [5.6]%, P < .001). Conclusions: RBP2 activates ER-IGF1R-ErbB signaling cascade in multiple ways to induce tamoxifen resistance, suggesting that RBP2 is a potential therapeutic target for ER-driven cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Carcinoma Ductal de Mama/metabolismo
Resistência a Medicamentos Antineoplásicos
Proteínas de Neoplasias/fisiologia
Receptores Estrogênicos/metabolismo
Proteína 2 de Ligação ao Retinoblastoma/fisiologia
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Análise de Variância
Animais
Antineoplásicos Hormonais/uso terapêutico
Neoplasias da Mama/química
Neoplasias da Mama/tratamento farmacológico
Neoplasias da Mama/patologia
Carcinoma Ductal de Mama/química
Carcinoma Ductal de Mama/tratamento farmacológico
Carcinoma Ductal de Mama/patologia
Proteínas de Transporte/metabolismo
Estudos de Coortes
Colorimetria
Intervalo Livre de Doença
Resistência a Medicamentos Antineoplásicos/genética
Feminino
Xenoenxertos
Seres Humanos
Estimativa de Kaplan-Meier
Células MCF-7
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Proteínas de Neoplasias/metabolismo
Células-Tronco Neoplásicas
Proteínas Nucleares/metabolismo
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/metabolismo
Receptor ErbB-2/metabolismo
Receptor IGF Tipo 1/metabolismo
Proteína 2 de Ligação ao Retinoblastoma/metabolismo
Tamoxifeno/uso terapêutico
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Antineoplastic Agents, Hormonal); 0 (Carrier Proteins); 0 (IGFBP5-interacting protein, human); 0 (Neoplasm Proteins); 0 (Nuclear Proteins); 0 (Receptors, Estrogen); 0 (nuclear receptor interacting protein 1); 094ZI81Y45 (Tamoxifen); EC 1.14.11.27 (Retinoblastoma-Binding Protein 2); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.1 (Receptor, ErbB-2); EC 2.7.10.1 (Receptor, IGF Type 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx207


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[PMID]:28922787
[Au] Autor:Blok EJ; Kroep JR; Meershoek-Klein Kranenbarg E; Duijm-de Carpentier M; Putter H; van den Bosch J; Maartense E; van Leeuwen-Stok AE; Liefers GJ; Nortier JWR; Rutgers EJT; van de Velde CJH; IDEAL Study Group
[Ad] Endereço:Departments of Surgery, Medical Oncology, and Medical Statistics, Leiden University Medical Center, Leiden, Netherlands; Department of Internal Medicine, Albert Schweitzer Hospital, Dordrecht, the Netherlands; Department of Internal Medicine, Reinier de Graaff Hospital, Delft, the Netherlands; Dutch
[Ti] Título:Optimal Duration of Extended Adjuvant Endocrine Therapy for Early Breast Cancer; Results of the IDEAL Trial (BOOG 2006-05).
[So] Source:J Natl Cancer Inst;110(1), 2018 Jan 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: The optimal duration of extended endocrine therapy beyond five years after initial aromatase inhibitor-based adjuvant therapy for postmenopausal women with hormone receptor-positive breast cancer is still unknown. Therefore, we conducted a clinical trial to compare two different extended endocrine therapy durations. Methods: In the randomized phase III IDEAL trial, postmenopausal patients with hormone receptor-positive breast cancer were randomly allocated to either 2.5 or five years of letrozole after the initial five years of any endocrine therapy. The primary end point was disease free survival (DFS), and secondary end points were overall survival (OS), distant metastasis-free interval (DMFi), new primary breast cancer, and safety. Hazard ratios (HRs) were determined using Cox regression analysis. All analyses were by intention-to-treat principle. Results: A total of 1824 patients were assigned to either 2.5 years (n = 909) or five years (n = 915) of letrozole, with a median follow-up of 6.6 years. A DFS event occurred in 152 patients in the five-year group, compared with 163 patients in the 2.5-year group (HR = 0.92, 95% confidence interval [CI] = 0.74 to 1.16). OS (HR = 1.04, 95% CI = 0.78 to 1.38) and DMFi (HR = 1.06, 95% CI = 0.78 to 1.45) were not different between both groups. A reduction in occurrence of second primary breast cancer was observed with five years of treatment (HR = 0.39, 95% CI = 0.19 to 0.81). Subgroup analysis did not identify patients who benefit from five-year extended therapy. Conclusion: This study showed no superiority of five years over 2.5 years of extended adjuvant letrozole after an initial five years of adjuvant endocrine therapy.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Neoplasias da Mama/terapia
Carcinoma Ductal de Mama/terapia
Carcinoma Intraductal não Infiltrante/terapia
Recidiva Local de Neoplasia/prevenção & controle
Segunda Neoplasia Primária/prevenção & controle
Nitrilos/administração & dosagem
Triazóis/administração & dosagem
[Mh] Termos MeSH secundário: Idoso
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Inibidores da Aromatase/administração & dosagem
Neoplasias da Mama/química
Neoplasias da Mama/patologia
Carcinoma Ductal de Mama/química
Carcinoma Ductal de Mama/prevenção & controle
Carcinoma Ductal de Mama/secundário
Carcinoma Intraductal não Infiltrante/prevenção & controle
Quimioterapia Adjuvante/efeitos adversos
Intervalo Livre de Doença
Feminino
Seguimentos
Seres Humanos
Mastectomia Segmentar
Meia-Idade
Nitrilos/efeitos adversos
Pós-Menopausa
Receptores Estrogênicos/análise
Receptores de Progesterona/análise
Taxa de Sobrevida
Tamoxifeno/administração & dosagem
Fatores de Tempo
Triazóis/efeitos adversos
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Aromatase Inhibitors); 0 (Nitriles); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); 0 (Triazoles); 094ZI81Y45 (Tamoxifen); 7LKK855W8I (letrozole)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx134


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[PMID]:28859291
[Au] Autor:Heindl A; Sestak I; Naidoo K; Cuzick J; Dowsett M; Yuan Y
[Ad] Endereço:Centre for Evolution and Cancer, The Institute of Cancer Research, London, UK; Centre for Molecular Pathology, Royal Marsden Hospital, London, UK; Division of Molecular Pathology, The Institute of Cancer Research, London, UK; Centre for Cancer Prevention, Wolfson Institute of Preventive Medicine, Qu
[Ti] Título:Relevance of Spatial Heterogeneity of Immune Infiltration for Predicting Risk of Recurrence After Endocrine Therapy of ER+ Breast Cancer.
[So] Source:J Natl Cancer Inst;110(2), 2018 Feb 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Despite increasing evidence supporting the clinical utility of immune infiltration in the estrogen receptor-negative (ER-) subtype, the prognostic value of immune infiltration for ER+ disease is not well defined. Methods: Quantitative immune scores of cell abundance and spatial heterogeneity were computed using a fully automated hematoxylin and eosin-stained image analysis algorithm and spatial statistics for 1178 postmenopausal patients with ER+ breast cancer treated with five years' tamoxifen or anastrozole. The prognostic significance of immune scores was compared with Oncotype DX 21-gene recurrence score (RS), PAM50 risk of recurrence (ROR) score, IHC4, and clinical treatment score, available for 963 patients. Statistical tests were two-sided. Results: Scores of immune cell abundance were not associated with recurrence-free survival. In contrast, high immune spatial scores indicating increased cell spatial clustering were associated with poor 10-year, early (0-5 years), and late (5-10 years) recurrence-free survival (Immune Hotspot: LR-χ2 = 14.06, P < .001, for 0-10 years; LR-χ2 = 6.24, P = .01, for 0-5 years; LR-χ2 = 7.89, P = .005, for 5-10 years). The prognostic value of spatial scores for late recurrence was similar to that of IHC4 and RS in both populations, but was not as strong as other tests in comparison for recurrence across 10 years. Conclusions: These results provide a missing link between tumor immunity and disease outcome in ER+ disease by examining tumor spatial architecture. The association between spatial scores and late recurrence suggests a lasting memory of protumor immunity that may impact disease progression and evolution of endocrine treatment resistance, which may be exploited for therapeutic advances.
[Mh] Termos MeSH primário: Neoplasias da Mama/imunologia
Neoplasias da Mama/patologia
Linfócitos do Interstício Tumoral/imunologia
Recidiva Local de Neoplasia/imunologia
Receptores Estrogênicos/análise
[Mh] Termos MeSH secundário: Idoso
Antineoplásicos/uso terapêutico
Biomarcadores Tumorais/imunologia
Neoplasias da Mama/química
Neoplasias da Mama/tratamento farmacológico
Intervalo Livre de Doença
Feminino
Seres Humanos
Contagem de Linfócitos
Meia-Idade
Nitrilos/uso terapêutico
Fatores de Risco
Tamoxifeno/uso terapêutico
Triazóis/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biomarkers, Tumor); 0 (Nitriles); 0 (Receptors, Estrogen); 0 (Triazoles); 094ZI81Y45 (Tamoxifen); 2Z07MYW1AZ (anastrozole)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx137


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[PMID]:29344722
[Au] Autor:Generali D; Corona SP; Pusztai L; Rouzier R; Allevi G; Aguggini S; Milani M; Strina C; Frati A
[Ad] Endereço:Department of Medical, Surgery and Health Sciences, University of Trieste, Piazza Ospitale 1, Trieste, 34129, Italy.
[Ti] Título:Benefit of the addition of hormone therapy to neoadjuvant anthracycline-based chemotherapy for breast cancer: comparison of predicted and observed pCR.
[So] Source:J Cancer Res Clin Oncol;144(3):601-606, 2018 Mar.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Neoadjuvant hormonal therapy is generally considered a valid option for hormone receptor positive breast cancer (BC) patients who are unfit for chemotherapy or surgery. AIMS: Whilst numerous studies analyzed efficacy of neoadjuvant chemotherapy (CT) or endocrine therapy (HT) alone in hormone receptor positive patients, there is a lack of research looking at the usefulness of a preoperative combinatorial approach of CT and HT in this patient subgroup. METHODS: Using a predictive model previously described in the literature, developed to analyze the probability of benefit from preoperative chemotherapy, we were able to compare pathological complete response (pCR) rates expected with the use of CT alone with the pCR rates reported in a population of 192 patients treated with the combination of tamoxifen plus anthracycline-based CT at Cremona Hospital between 2003 and 2006. RESULTS: Even with a relatively small patient population, this approach provided insightful information for the selection of hormone receptor positive BC patients most likely to benefit from the use of preoperative HT and CT in combination. Whilst no statistically significant benefit was obtained with the addition of tamoxifen to neoadjuvant chemotherapy in the entire population, or in any of the molecular stratification subgroups, the analysis of the calibration curve showed that a combinatorial approach may improve pCR in patients with luminal B tumors. More specific trials should be designed to confirm our initial results. CONCLUSION: To the best of our knowledge, this is the first report investigating the efficacy of the combination of CT and HT in the neoadjuvant treatment of hormone receptor positive BC.
[Mh] Termos MeSH primário: Antraciclinas/administração & dosagem
Antibióticos Antineoplásicos/administração & dosagem
Antineoplásicos Hormonais/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Neoplasias da Mama/tratamento farmacológico
Tamoxifeno/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Neoplasias da Mama/cirurgia
Quimioterapia Adjuvante
Terapia Combinada
Feminino
Seres Humanos
Meia-Idade
Terapia Neoadjuvante
Período Pré-Operatório
Estudos Retrospectivos
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracyclines); 0 (Antibiotics, Antineoplastic); 0 (Antineoplastic Agents, Hormonal); 094ZI81Y45 (Tamoxifen)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2574-4


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[PMID]:27770345
[Au] Autor:Whitworth P; Beitsch P; Mislowsky A; Pellicane JV; Nash C; Murray M; Lee LA; Dul CL; Rotkis M; Baron P; Stork-Sloots L; de Snoo FA; Beatty J
[Ad] Endereço:Nashville Breast Center, Nashville, TN, USA. patwhitworth@gmail.com.
[Ti] Título:Chemosensitivity and Endocrine Sensitivity in Clinical Luminal Breast Cancer Patients in the Prospective Neoadjuvant Breast Registry Symphony Trial (NBRST) Predicted by Molecular Subtyping.
[So] Source:Ann Surg Oncol;24(3):669-675, 2017 Mar.
[Is] ISSN:1534-4681
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Hormone receptor-positive (HR+) tumors have heterogeneous biology and present a challenge for determining optimal treatment. In the Neoadjuvant Breast Registry Symphony Trial (NBRST) patients were classified according to MammaPrint/BluePrint subtyping to provide insight into the response to neoadjuvant endocrine therapy (NET) or neoadjuvant chemotherapy (NCT). OBJECTIVE: The purpose of this predefined substudy was to compare MammaPrint/BluePrint with conventional 'clinical' immunohistochemistry/fluorescence in situ hybridization (IHC/FISH) subtyping in 'clinical luminal' [HR+/human epidermal growth factor receptor 2-negative (HER2-)] breast cancer patients to predict treatment sensitivity. METHODS: NBRST IHC/FISH HR+/HER2- breast cancer patients (n = 474) were classified into four molecular subgroups by MammaPrint/BluePrint subtyping: Luminal A, Luminal B, HER2, and Basal type. Pathological complete response (pCR) rates were compared with conventional IHC/FISH subtype. RESULTS: The overall pCR rate for 'clinical luminal' patients to NCT was 11 %; however, 87 of these 474 patients were reclassified as Basal type by BluePrint, with a high pCR rate of 32 %. The MammaPrint index was highly associated with the likelihood of pCR (p < 0.001). Fifty-three patients with BluePrint Luminal tumors received NET with an aromatase inhibitor and 36 (68 %) had a clinical response. CONCLUSIONS: With BluePrint subtyping, 18 % of clinical 'luminal' patients are classified in a different subgroup, compared with conventional assessment, and these patients have a significantly higher response rate to NCT compared with BluePrint Luminal patients. MammaPrint/BluePrint subtyping can help allocate effective treatment to appropriate patients. In addition, accurate identification of subtype biology is important in the interpretation of neoadjuvant treatment response since lack of pCR in luminal patients does not portend the worse prognosis associated with residual disease in Basal and HER2 subtypes.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Neoplasias da Mama/classificação
Neoplasias da Mama/tratamento farmacológico
Perfilação da Expressão Gênica
Tipagem Molecular/métodos
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Inibidores da Aromatase/uso terapêutico
Neoplasias da Mama/genética
Neoplasias da Mama/metabolismo
Hidrocarbonetos Aromáticos com Pontes/administração & dosagem
Quimioterapia Adjuvante
Tomada de Decisão Clínica
Ciclofosfamida/administração & dosagem
Doxorrubicina/administração & dosagem
Feminino
Seres Humanos
Imuno-Histoquímica
Hibridização in Situ Fluorescente
Mastectomia Segmentar
Meia-Idade
Terapia Neoadjuvante
Nitrilos/administração & dosagem
Estudos Prospectivos
Receptor ErbB-2/metabolismo
Receptores Estrogênicos/metabolismo
Receptores de Progesterona/metabolismo
Sistema de Registros
Tamoxifeno/administração & dosagem
Taxoides/administração & dosagem
Resultado do Tratamento
Triazóis/administração & dosagem
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE IV; COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Aromatase Inhibitors); 0 (Bridged-Ring Compounds); 0 (Nitriles); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); 0 (Taxoids); 0 (Triazoles); 094ZI81Y45 (Tamoxifen); 15H5577CQD (docetaxel); 1605-68-1 (taxane); 2Z07MYW1AZ (anastrozole); 7LKK855W8I (letrozole); 80168379AG (Doxorubicin); 8N3DW7272P (Cyclophosphamide); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1245/s10434-016-5600-x


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Texto completo
[PMID]:29381962
[Au] Autor:Silva FB; Romero WG; Carvalho ALRA; Souza GAA; Claudio ERG; Abreu GR
[Ad] Endereço:Department of Physiological Sciences.
[Ti] Título:Effects of treatment with chemotherapy and/or tamoxifen on the biomarkers of cardiac injury and oxidative stress in women with breast cancer.
[So] Source:Medicine (Baltimore);96(47):e8723, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There has been an increase in deaths from cardiovascular diseases following breast cancer therapy. Evidence has shown that this outcome is, in part, associated with cardiotoxicity induced by the chemotherapeutic drugs and the increase in oxidative stress. The aim of this study was to evaluate the effects of chemotherapy and hormone therapy with tamoxifen on the biomarkers of cardiac injury and oxidative stress in women with breast cancer.Thirty women were followed-up for 1 year and were divided into 3 groups according to the treatment protocol: women treated only with tamoxifen and clinical follow up for 12 months (Tam, n = 10); women treated only with chemotherapy for 6 months with clinical follow up for an additional 6-month period (Chemo, n = 10); and women who received chemotherapy for 6 months followed by a 6-month period only with tamoxifen therapy and clinical follow up (Chemo + Tam, n = 10). Analysis of the blood levels of cardiac troponin I (cTnI), advanced oxidation protein products (AOPP) and the activity of the plasmatic isoform of the antioxidant enzyme glutathione peroxidase (GPx) was performed before treatment (T0) and at 6 (T6) and 12 (T12) months after treatment.The Chemo group showed higher levels of cTnI (0.065 ±â€Š0.006 ng/mL, P < .05) and AOPP (4.99 ±â€Š0.84 µmol/L, P < .05) and reduced GPx activity (24.4 ±â€Š1.1 nM/min/mL, P < .05) at T12 than the Tam group (cTnI: 0.031 ±â€Š0.001 ng/mL; AOPP: 1.40 ±â€Š0.10 µmol/L; GPx: 28.0 ±â€Š0.7 nM/min/mL) and Chemo + Tam group (cTnI: 0.037 ±â€Š0.002 ng/mL; AOPP: 2.53 ±â€Š0.30 µmol/L; GPx: 29.5 ±â€Š1.0 nM/min/mL).These data support the hypothesis that long-term oxidative stress after chemotherapy may have an impact on cardiovascular diseases and that tamoxifen has cardioprotective effects.
[Mh] Termos MeSH primário: Antineoplásicos/efeitos adversos
Neoplasias da Mama/tratamento farmacológico
Doenças Cardiovasculares/induzido quimicamente
Estresse Oxidativo/efeitos dos fármacos
Tamoxifeno/efeitos adversos
[Mh] Termos MeSH secundário: Produtos da Oxidação Avançada de Proteínas/sangue
Antineoplásicos/uso terapêutico
Biomarcadores
Feminino
Glutationa Peroxidase/sangue
Seres Humanos
Meia-Idade
Tamoxifeno/uso terapêutico
Fatores de Tempo
Troponina I/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Advanced Oxidation Protein Products); 0 (Antineoplastic Agents); 0 (Biomarkers); 0 (Troponin I); 094ZI81Y45 (Tamoxifen); EC 1.11.1.9 (Glutathione Peroxidase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008723


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[PMID]:29180066
[Au] Autor:Tsai CF; Cheng YK; Lu DY; Wang SL; Chang CN; Chang PC; Yeh WL
[Ad] Endereço:Department of Biotechnology, Asia University, No.500 Lioufeng Road, Taichung 41354, Taiwan. Electronic address: tsaicf@asia.edu.tw.
[Ti] Título:Inhibition of estrogen receptor reduces connexin 43 expression in breast cancers.
[So] Source:Toxicol Appl Pharmacol;338:182-190, 2018 01 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Connexins are widely supported as tumor suppressors due to their downregulation in cancers, nevertheless, more recent evidence suggests roles for connexins in facilitating tumor progression in later stages, including metastasis. One of the key factors regulating the expression, modification, stability, and localization of connexins is hormone receptors in hormone-dependent cancers. It is reasonable to consider that hormones/hormone receptors may modulate connexins expression and play critical roles in the cellular control of connexins during breast cancer progression. In estrogen receptor (ER)-positive breast cancers, tamoxifen and fulvestrant are widely used therapeutic agents and are considered to alter ER signaling. In this present study, we investigated the effects of fulvestrant and tamoxifen in Cx43 expression, and we also explored the role of Cx43 in ER-positive breast cancer migration and the relationship between Cx43 and ER. The involvement of estrogen/ER in Cx43 modulation was further verified by administering tyrosine kinase inhibitors and chemotherapeutic agents. We found that inhibition of ER promoted the binding of E3 ligase Nedd4 to Cx43, leading to Cx43 ubiquitination. Furthermore, inhibition of ER by fulvestrant and tamoxifen phosphorylated p38 MAPK, and inhibition of Rac, MKK3/6, and p38 reversed fulvestrant-reduced Cx43 expression. These findings suggest that Cx43 expression which may positively regulate cell migration is ER-dependent in ER-positive breast cancer cells.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Conexina 43/fisiologia
Antagonistas de Estrogênios/farmacologia
[Mh] Termos MeSH secundário: Neoplasias da Mama/química
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Conexina 43/análise
Feminino
Seres Humanos
Ubiquitina-Proteína Ligases Nedd4/metabolismo
Receptores Estrogênicos/fisiologia
Tamoxifeno/análogos & derivados
Tamoxifeno/farmacologia
Proteínas Quinases p38 Ativadas por Mitógeno/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Connexin 43); 0 (Estrogen Antagonists); 0 (GJA1 protein, human); 0 (Receptors, Estrogen); 094ZI81Y45 (Tamoxifen); 17197F0KYM (afimoxifene); EC 2.3.2.26 (Nedd4 Ubiquitin Protein Ligases); EC 2.3.2.26 (Nedd4 protein, human); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE


  8 / 17761 MEDLINE  
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[PMID]:29269484
[Au] Autor:Geter PA; Ernlund AW; Bakogianni S; Alard A; Arju R; Giashuddin S; Gadi A; Bromberg J; Schneider RJ
[Ad] Endereço:Department of Microbiology, Alexandria Center for Life Science, New York University School of Medicine, New York, New York 10016, USA.
[Ti] Título:Hyperactive mTOR and MNK1 phosphorylation of eIF4E confer tamoxifen resistance and estrogen independence through selective mRNA translation reprogramming.
[So] Source:Genes Dev;31(22):2235-2249, 2017 11 15.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The majority of breast cancers expresses the estrogen receptor (ER ) and is treated with anti-estrogen therapies, particularly tamoxifen in premenopausal women. However, tamoxifen resistance is responsible for a large proportion of breast cancer deaths. Using small molecule inhibitors, phospho-mimetic proteins, tamoxifen-sensitive and tamoxifen-resistant breast cancer cells, a tamoxifen-resistant patient-derived xenograft model, patient tumor tissues, and genome-wide transcription and translation studies, we show that tamoxifen resistance involves selective mRNA translational reprogramming to an anti-estrogen state by and other mRNAs. Tamoxifen-resistant translational reprogramming is shown to be mediated by increased expression of eIF4E and its increased availability by hyperactive mTOR and to require phosphorylation of eIF4E at Ser209 by increased MNK activity. Resensitization to tamoxifen is restored only by reducing eIF4E expression or mTOR activity and also blocking MNK1 phosphorylation of eIF4E. mRNAs specifically translationally up-regulated with tamoxifen resistance include , which inhibits ER signaling and estrogen responses and promotes breast cancer metastasis. Silencing significantly restores tamoxifen sensitivity. Tamoxifen-resistant but not tamoxifen-sensitive patient ER breast cancer specimens also demonstrate strongly increased MNK phosphorylation of eIF4E. eIF4E levels, availability, and phosphorylation therefore promote tamoxifen resistance in ER breast cancer through selective mRNA translational reprogramming.
[Mh] Termos MeSH primário: Antineoplásicos Hormonais/farmacologia
Neoplasias da Mama/metabolismo
Antagonistas de Estrogênios/farmacologia
Fator de Iniciação 4E em Eucariotos/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Alvo Mecanístico do Complexo 1 de Rapamicina/metabolismo
Biossíntese de Proteínas
Proteínas Serina-Treonina Quinases/metabolismo
Tamoxifeno/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos
Feminino
Seres Humanos
Fosforilação
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (Estrogen Antagonists); 0 (Eukaryotic Initiation Factor-4E); 0 (Intracellular Signaling Peptides and Proteins); 0 (RNA, Messenger); 094ZI81Y45 (Tamoxifen); EC 2.7.1.- (MKNK1 protein, human); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.1101/gad.305631.117


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[PMID]:29175422
[Au] Autor:Hao M; Weng X; Wang Y; Sun X; Yan T; Li Y; Hou L; Meng X; Wang J
[Ad] Endereço:Department of Biochemistry and Molecular & Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; Department of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
[Ti] Título:Targeting CXCR7 improves the efficacy of breast cancer patients with tamoxifen therapy.
[So] Source:Biochem Pharmacol;147:128-140, 2018 01.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Chemokine (C-X-C motif) receptor 7 (CXCR7) has been established to be involved in breast cancer (BCa) progression. However, the role of CXCR7 in different subtype of BCa still remains unclear. Here we note that CXCR7 expression is significantly amplified in Luminal type BCa tissues as compared with Her2 and TNBC types through data-mining in TCGA datasets, and its protein level positively correlates with ERα expression by staining of human BCa tissue. Interestingly, alteration of CXCR7 expression in Luminal type BCa cells is able to modulate the expression of ERα through ubiquitination at post-translational level. Additionally, overexpression of CXCR7 in these cells greatly induces 4-OHT insensitivity in vitro and is associated with earlier recurrence in patients with tamoxifen therapy. Notably, silencing ERα expression potentially rescues the sensitivity of the above cells to 4-OHT, suggesting that elevated level of ERα is responsible for CXCR7-induced 4-OHT insensitivity in Luminal type BCa. Finally, mechanistic analyses show that the reduced BRCA1 (ubiquitin E3 ligase) and elevated OTUB1 (deubiquitinase) expression, which are regulated by CXCR7/ERK1/2 signaling pathway, are responsible for stabilizing ERα protein. In conclusion, our results suggest that targeting CXCR7 may serve as a potential therapeutic strategy for improving the efficacy of BCa patients with tamoxifen therapy.
[Mh] Termos MeSH primário: Antineoplásicos Hormonais/metabolismo
Neoplasias da Mama/metabolismo
Sistemas de Liberação de Medicamentos/métodos
Receptores CXCR/biossíntese
Tamoxifeno/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos Hormonais/administração & dosagem
Neoplasias da Mama/tratamento farmacológico
Neoplasias da Mama/genética
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/fisiologia
Feminino
Seres Humanos
Células MCF-7
Receptores CXCR/genética
Tamoxifeno/administração & dosagem
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (CXCR7 protein, human); 0 (Receptors, CXCR); 094ZI81Y45 (Tamoxifen)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:29202630
[Au] Autor:Cronin-Fenton D; Lash TL; Ahern TP; Damkier P; Christiansen P; Ejlertsen B; Sørensen HT
[Ad] Endereço:a Department of Clinical Epidemiology , Aarhus University , Aarhus , Denmark.
[Ti] Título:Concurrent new drug prescriptions and prognosis of early breast cancer: studies using the Danish Breast Cancer Group clinical database.
[So] Source:Acta Oncol;57(1):120-128, 2018 Jan.
[Is] ISSN:1651-226X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Myriad reports suggest that frequently used prescription drugs alter the viability of breast cancer cells in pre-clinical studies. Routine use of these drugs, therefore, may impact breast cancer prognosis, and could have important implications for public health. METHODS: The Danish Breast Cancer Group (DBCG) clinical database provides high-quality prospectively collected data on breast cancer diagnosis, treatment, and routine follow-up for breast cancer recurrence. Individual-level linkage of DBCG data to other population-based and medical registries in Denmark, including the Danish National Prescription Registry, has facilitated large population-based pharmacoepidemiology studies. A unique advantage of using DBCG data for such studies is the ability to investigate the association of drugs with breast cancer recurrence rather than breast cancer mortality - which may be misclassified - or all-cause mortality. Here we summarize findings from pharmacoepidemiological studies, based on DBCG data, on the association between routinely used prescription drugs and risk of breast cancer recurrence. RESULTS: Our findings suggest that concurrent use of glucocorticoids, ACE inhibitors, aspirin, NSAIDs, selective COX-2 inhibitors, digoxin, and opioids has little impact on breast cancer recurrence. Similarly, patients who use SSRIs concurrently with tamoxifen treatment are not at increased risk of recurrence. In contrast, post-diagnostic use of simvastatin, a lipophilic statin, correlates with a decreased risk of breast cancer recurrence, providing a rationale for a prospective randomized clinical trial investigating simvastatin as an adjuvant therapy for breast cancer. CONCLUSION: As a whole, findings of pharmacoepidemiological studies based on DBCG data provide reassurance to physicians and healthcare personnel who provide supportive care during and after cancer (including prescriptions for comedications) and to breast cancer survivors for whom the risk of breast cancer recurrence is a major concern.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Progressão da Doença
Recidiva Local de Neoplasia
[Mh] Termos MeSH secundário: Antagonistas Adrenérgicos beta/uso terapêutico
Analgésicos Opioides/uso terapêutico
Inibidores da Enzima Conversora de Angiotensina/uso terapêutico
Anti-Inflamatórios não Esteroides/uso terapêutico
Aspirina/uso terapêutico
Cardiotônicos/uso terapêutico
Inibidores de Ciclo-Oxigenase 2/uso terapêutico
Bases de Dados Factuais
Dinamarca
Digoxina/uso terapêutico
Antagonistas de Estrogênios/uso terapêutico
Feminino
Glucocorticoides/uso terapêutico
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Inibidores da Agregação de Plaquetas/uso terapêutico
Prognóstico
Inibidores da Captação de Serotonina/uso terapêutico
Sinvastatina/uso terapêutico
Tamoxifeno/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Analgesics, Opioid); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cardiotonic Agents); 0 (Cyclooxygenase 2 Inhibitors); 0 (Estrogen Antagonists); 0 (Glucocorticoids); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Platelet Aggregation Inhibitors); 0 (Serotonin Uptake Inhibitors); 094ZI81Y45 (Tamoxifen); 73K4184T59 (Digoxin); AGG2FN16EV (Simvastatin); R16CO5Y76E (Aspirin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1080/0284186X.2017.1407040



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