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[PMID]:29318276
[Au] Autor:Plevritis SK; Munoz D; Kurian AW; Stout NK; Alagoz O; Near AM; Lee SJ; van den Broek JJ; Huang X; Schechter CB; Sprague BL; Song J; de Koning HJ; Trentham-Dietz A; van Ravesteyn NT; Gangnon R; Chandler Y; Li Y; Xu C; Ergun MA; Huang H; Berry DA; Mandelblatt JS
[Ad] Endereço:Departments of Radiology and Biomedical Data Science, School of Medicine, Stanford University, Stanford, California.
[Ti] Título:Association of Screening and Treatment With Breast Cancer Mortality by Molecular Subtype in US Women, 2000-2012.
[So] Source:JAMA;319(2):154-164, 2018 01 09.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Given recent advances in screening mammography and adjuvant therapy (treatment), quantifying their separate and combined effects on US breast cancer mortality reductions by molecular subtype could guide future decisions to reduce disease burden. Objective: To evaluate the contributions associated with screening and treatment to breast cancer mortality reductions by molecular subtype based on estrogen-receptor (ER) and human epidermal growth factor receptor 2 (ERBB2, formerly HER2 or HER2/neu). Design, Setting, and Participants: Six Cancer Intervention and Surveillance Network (CISNET) models simulated US breast cancer mortality from 2000 to 2012 using national data on plain-film and digital mammography patterns and performance, dissemination and efficacy of ER/ERBB2-specific treatment, and competing mortality. Multiple US birth cohorts were simulated. Exposures: Screening mammography and treatment. Main Outcomes and Measures: The models compared age-adjusted, overall, and ER/ERBB2-specific breast cancer mortality rates from 2000 to 2012 for women aged 30 to 79 years relative to the estimated mortality rate in the absence of screening and treatment (baseline rate); mortality reductions were apportioned to screening and treatment. Results: In 2000, the estimated reduction in overall breast cancer mortality rate was 37% (model range, 27%-42%) relative to the estimated baseline rate in 2000 of 64 deaths (model range, 56-73) per 100 000 women: 44% (model range, 35%-60%) of this reduction was associated with screening and 56% (model range, 40%-65%) with treatment. In 2012, the estimated reduction in overall breast cancer mortality rate was 49% (model range, 39%-58%) relative to the estimated baseline rate in 2012 of 63 deaths (model range, 54-73) per 100 000 women: 37% (model range, 26%-51%) of this reduction was associated with screening and 63% (model range, 49%-74%) with treatment. Of the 63% associated with treatment, 31% (model range, 22%-37%) was associated with chemotherapy, 27% (model range, 18%-36%) with hormone therapy, and 4% (model range, 1%-6%) with trastuzumab. The estimated relative contributions associated with screening vs treatment varied by molecular subtype: for ER+/ERBB2-, 36% (model range, 24%-50%) vs 64% (model range, 50%-76%); for ER+/ERBB2+, 31% (model range, 23%-41%) vs 69% (model range, 59%-77%); for ER-/ERBB2+, 40% (model range, 34%-47%) vs 60% (model range, 53%-66%); and for ER-/ERBB2-, 48% (model range, 38%-57%) vs 52% (model range, 44%-62%). Conclusions and Relevance: In this simulation modeling study that projected trends in breast cancer mortality rates among US women, decreases in overall breast cancer mortality from 2000 to 2012 were associated with advances in screening and in adjuvant therapy, although the associations varied by breast cancer molecular subtype.
[Mh] Termos MeSH primário: Neoplasias da Mama/mortalidade
Detecção Precoce de Câncer
Mamografia
Modelos Estatísticos
[Mh] Termos MeSH secundário: Neoplasias da Mama/diagnóstico por imagem
Neoplasias da Mama/terapia
Feminino
Seres Humanos
Mamografia/métodos
Mortalidade/tendências
Receptor ErbB-2
Receptores Estrogênicos
Estados Unidos/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Estrogen); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180311
[Lr] Data última revisão:
180311
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.19130


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[PMID]:29175396
[Au] Autor:Wang F; Liu F; Chen W; Xu R; Wang W
[Ad] Endereço:School of Biological Science, Luoyang Normal University, Luoyang, 471022, China; Cold Water Fish Breeding Engineering Technology Research Center of Henan Province, Luoyang, 471022, China. Electronic address: wangfan7677@163.com.
[Ti] Título:Effects of triclosan (TCS) on hormonal balance and genes of hypothalamus-pituitary- gonad axis of juvenile male Yellow River carp (Cyprinus carpio).
[So] Source:Chemosphere;193:695-701, 2018 Feb.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Triclosan (TCS) is a broad spectrum antimicrobial agent which has been widely dispersed and determinated in the aquatic environment. However, the effects of TCS on reproductive endocrine in male fish are poorly understood. In this study, male Yellow River carp (Cyprinus carpio) were exposed to 0, 1/5, 1/10 and 1/20 LC (96 h LC of TCS to carp) TCS under semi-static conditions for 42 d. Vitellogenin (Vtg), 17ß-estradiol (E ), testosterone(T), gonadotropin (GtH), and gonadotropin-releasing hormone (GnRH) levels were measured by enzyme-linked immunosorbent assay (ELISA). Meanwhile, we also examined the mRNA expressions of aromatase, GtHs-ß, GnRH, estrogen receptor (Er), and androgen receptor (Ar) by quantitative Real-time Polymerase Chain Reaction (qRT-PCR). TCS induced Vtg levels of hepatopancreas, E levels of serum, and inhibited Ar and Er mRNA levels, suggesting that the induction of Vtg production by TCS was indirectly caused by non-Er pathways. TCS-induced Vtg levels by interfering with the reproductive axis at plenty of latent loci of male carps: (a) TCS exposure increased the aromatase mRNA expression of hypothalamus and gonad aromatase, consequently increasing serum concentrations of E to induce Vtg in hepatopancreas; (b) TCS treatment changed GtH-ß and GnRH mRNA expression and secretion, causing the disturbance of reproductive endocrine; (c) TCS exposure decreased Ar mRNA levels, indicating potential Ar-mediated antiandrogen action. These mechanisms showed that TCS may induce Vtg production in male carp by non-Er-mediated pathways.
[Mh] Termos MeSH primário: Carpas/metabolismo
Triclosan/toxicidade
Poluentes Químicos da Água/toxicidade
[Mh] Termos MeSH secundário: Animais
Anti-Infecciosos/toxicidade
Aromatase/genética
Sistema Endócrino/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Estradiol/análise
Hormônio Liberador de Gonadotropina/análise
Hormônio Liberador de Gonadotropina/genética
Gônadas/enzimologia
Gônadas/metabolismo
Hepatopâncreas/metabolismo
Hormônios/metabolismo
Hipotálamo/metabolismo
Masculino
Hipófise/metabolismo
RNA Mensageiro/análise
Reação em Cadeia da Polimerase em Tempo Real
Receptores Estrogênicos/genética
Reprodução/efeitos dos fármacos
Testosterona/análise
Vitelogeninas/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Infective Agents); 0 (Hormones); 0 (RNA, Messenger); 0 (Receptors, Estrogen); 0 (Vitellogenins); 0 (Water Pollutants, Chemical); 33515-09-2 (Gonadotropin-Releasing Hormone); 3XMK78S47O (Testosterone); 4NM5039Y5X (Triclosan); 4TI98Z838E (Estradiol); EC 1.14.14.1 (Aromatase); EC 1.14.14.1 (CYP19A1 protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:28457941
[Au] Autor:Menazza S; Sun J; Appachi S; Chambliss KL; Kim SH; Aponte A; Khan S; Katzenellenbogen JA; Katzenellenbogen BS; Shaul PW; Murphy E
[Ad] Endereço:Systems Biology Center, National Heart Lung and Blood Institute, NIH, Bethesda, MD, United States.
[Ti] Título:Non-nuclear estrogen receptor alpha activation in endothelium reduces cardiac ischemia-reperfusion injury in mice.
[So] Source:J Mol Cell Cardiol;107:41-51, 2017 Jun.
[Is] ISSN:1095-8584
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Steroid hormone receptors including estrogen receptors (ER) classically function as ligand-regulated transcription factors. However, estrogens also elicit cellular effects through binding to extra-nuclear ER (ERα, ERß, and G protein-coupled ER or GPER) that are coupled to kinases. How extra-nuclear ER actions impact cardiac ischemia-reperfusion (I/R) injury is unknown. We treated ovariectomized wild-type female mice with estradiol or an estrogen-dendrimer conjugate (EDC), which selectively activates extra-nuclear ER, or vehicle interventions for two weeks. I/R injury was then evaluated in isolated Langendorff perfused hearts. Two weeks of treatment with estradiol significantly decreased infarct size and improved post-ischemic contractile function. Similarly, EDC treatment significantly decreased infarct size and increased post-ischemic functional recovery compared to vehicle-treated hearts. EDC also caused an increase in myocardial protein S-nitrosylation, consistent with previous studies showing a role for this post-translational modification in cardioprotection. In further support of a role for S-nitrosylation, inhibition of nitric oxide synthase, but not soluble guanylyl cyclase blocked the EDC mediated protection. The administration of ICI182,780, which is an agonist of G-protein coupled estrogen receptor (GPER) and an antagonist of ERα and ERß, did not result in protection; however, ICI182,780 significantly blocked EDC-mediated cardioprotection, indicating participation of ERα and/or ERß. In studies determining the specific ER subtype and cellular target involved, EDC decreased infarct size and improved functional recovery in mice lacking ERα in cardiomyocytes. In contrast, protection was lost in mice deficient in endothelial cell ERα. Thus, extra-nuclear ERα activation in endothelium reduces cardiac I/R injury in mice, and this likely entails increased protein S-nitrosylation. Since EDC does not stimulate uterine growth, in the clinical setting EDC-like compounds may provide myocardial protection without undesired uterotrophic and cancer-promoting effects.
[Mh] Termos MeSH primário: Receptor alfa de Estrogênio/genética
Receptor beta de Estrogênio/genética
Isquemia/genética
Traumatismo por Reperfusão/genética
[Mh] Termos MeSH secundário: Animais
Endotélio/metabolismo
Endotélio/patologia
Receptor alfa de Estrogênio/antagonistas & inibidores
Receptor beta de Estrogênio/antagonistas & inibidores
Estrogênios/genética
Estrogênios/metabolismo
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Isquemia/metabolismo
Isquemia/patologia
Camundongos
Ovariectomia
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Receptores Estrogênicos/antagonistas & inibidores
Receptores Acoplados a Proteínas-G/antagonistas & inibidores
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/patologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor alpha); 0 (Estrogen Receptor beta); 0 (Estrogens); 0 (GPR30 protein, mouse); 0 (Receptors, Estrogen); 0 (Receptors, G-Protein-Coupled)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:28470951
[Au] Autor:Posso M; Corominas JM; Serrano L; Román M; Torá-Rocamora I; Domingo L; Romero A; Quintana MJ; Vernet-Tomas M; Baré M; Vidal C; Sánchez M; Saladié F; Natal C; Ferrer J; Servitja S; Sala M; Castells X; BELE Study Group
[Ad] Endereço:Department of Epidemiology and Evaluation, IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain.
[Ti] Título:Biomarkers expression in benign breast diseases and risk of subsequent breast cancer: a case-control study.
[So] Source:Cancer Med;6(6):1482-1489, 2017 Jun.
[Is] ISSN:2045-7634
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Women with benign breast diseases (BBD) have a high risk of breast cancer. However, no biomarkers have been clearly established to predict cancer in these women. Our aim was to explore whether estrogen receptor (ER), progesterone receptor (PR), and Ki67 expression stratify risk of breast cancer in screened women with BBD. We conducted a nested case-control study. Women with breast cancer and prior BBDs (86 cases) were matched to women with prior BBDs who were free from breast cancer (172 controls). The matching factors were age at BBD diagnosis, type of BBD, and follow-up time since BBD diagnosis. ER, PR, and Ki67 expression were obtained from BBDs' specimens. Conditional logistic regression was used to estimate odds ratios (ORs), and 95% confidence intervals (CIs) of breast cancer risk according to ER, PR, and Ki67 expression. Women with >90% of ER expression had a higher risk of breast cancer (OR = 2.63; 95% CI: 1.26-5.51) than women with ≤70% of ER expression. Similarly, women with >80% of PR expression had a higher risk of breast cancer (OR = 2.22; 95% CI: 1.15-4.27) than women with ≤40% of PR expression. Women with proliferative disease and ≥1% of Ki67 expression had a nonsignificantly increased risk of breast cancer (OR = 1.16; 95% CI: 0.46-2.90) than women with <1% of Ki67 expression. A high expression of ER and PR in BBD is associated with an increased risk of subsequent breast cancer. In proliferative disease, high Ki67 expression may also have an increased risk. This information is helpful to better characterize BBD and is one more step toward personalizing the clinical management of these women.
[Mh] Termos MeSH primário: Doenças Mamárias/epidemiologia
Doenças Mamárias/metabolismo
Receptores Estrogênicos/metabolismo
Receptores de Progesterona/metabolismo
[Mh] Termos MeSH secundário: Idoso
Biomarcadores/metabolismo
Mama/metabolismo
Estudos de Casos e Controles
Feminino
Seres Humanos
Antígeno Ki-67/metabolismo
Meia-Idade
Razão de Chances
Fatores de Risco
Espanha/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Ki-67 Antigen); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/cam4.1080


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[PMID]:28456837
[Au] Autor:Ulaner GA; Castillo R; Wills J; Gönen M; Goldman DA
[Ad] Endereço:Department of Radiology, Memorial Sloan Kettering Cancer Center, New York, NY, USA. ulanerg@mskcc.org.
[Ti] Título:F-FDG-PET/CT for systemic staging of patients with newly diagnosed ER-positive and HER2-positive breast cancer.
[So] Source:Eur J Nucl Med Mol Imaging;44(9):1420-1427, 2017 Aug.
[Is] ISSN:1619-7089
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: This study assesses F-FDG-PET/CT for patients with newly diagnosed estrogen receptor-positive/human epidermal growth factor receptor-negative (ER+/HER2-) and human epidermal growth factor receptor-positive (HER2+) breast cancer. METHODS: In this Institutional Review Board-approved retrospective study, our Healthcare Information System was screened for patients with ER+/HER2- and HER2+ breast cancer who underwent F-FDG-PET/CT prior to systemic or radiation therapy. The initial stage was determined from mammography, ultrasound, magnetic resonance imaging, and/or surgery. F-FDG-PET/CT was evaluated to identify unsuspected extra-axillary regional nodal and distant metastases. The proportion of patients upstaged overall and stratified by stage and receptor phenotypes was calculated along with confidence intervals (CI). RESULTS: A total of 238 patients with ER+/HER2- and 245 patients with HER2+ who met inclusion criteria were evaluated. For patients with ER+/HER2-breast cancer, F-FDG-PET/CT revealed unsuspected distant metastases in 3/71 (4%) initial stage IIA, 13/95 (14%) stage IIB, and 15/57 (26%) stage III. For patients with HER2+ breast cancer, F-FDG-PET/CT revealed unsuspected distant metastases in 3/72 (4%) initial stage IIA, 13/93 (14%) stage IIB, and 13/59 (22%) stage III. The overall upstaging rate for IIB was 14% (95% confidence interval (CI): 9-20%). CONCLUSIONS: F-FDG-PET/CT revealed distant metastases in 14% (95% CI: 9-20%) of patients with stage IIB ER+/HER2- and HER2+ breast cancer, which is similar to upstaging rates previously seen in patients with stage IIB triple-negative breast cancer (15%, 95% CI: 9-24%). The detection of unsuspected distant metastases in these patients alters treatment and prognosis. NCCN guidelines should consider adding patients with stage IIB breast cancer for consideration of systemic staging with F-FDG-PET/CT at the time of initial diagnosis.
[Mh] Termos MeSH primário: Neoplasias da Mama/diagnóstico por imagem
Neoplasias da Mama/patologia
Fluordesoxiglucose F18
Tomografia Computadorizada com Tomografia por Emissão de Pósitrons
Receptor ErbB-2/metabolismo
Receptores Estrogênicos/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Neoplasias da Mama/metabolismo
Feminino
Seres Humanos
Meia-Idade
Estadiamento de Neoplasias
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Estrogen); 0Z5B2CJX4D (Fluorodeoxyglucose F18); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE
[do] DOI:10.1007/s00259-017-3709-1


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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]:28859290
[Au] Autor:Troester MA; Sun X; Allott EH; Geradts J; Cohen SM; Tse CK; Kirk EL; Thorne LB; Mathews M; Li Y; Hu Z; Robinson WR; Hoadley KA; Olopade OI; Reeder-Hayes KE; Earp HS; Olshan AF; Carey LA; Perou CM
[Ad] Endereço:Department of Epidemiology, Lineberger Comprehensive Cancer Center; Department of Pathology and Lab Medicine, Department of Nutrition (EHA), and Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC; Dana Farber Cancer Institute, Harvard University, Boston, MA; Center
[Ti] Título:Racial Differences in PAM50 Subtypes in the Carolina Breast Cancer Study.
[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: African American breast cancer patients have lower frequency of hormone receptor-positive (HR+)/human epidermal growth factor receptor 2 (HER2)-negative disease and higher subtype-specific mortality. Racial differences in molecular subtype within clinically defined subgroups are not well understood. Methods: Using data and biospecimens from the population-based Carolina Breast Cancer Study (CBCS) Phase 3 (2008-2013), we classified 980 invasive breast cancers using RNA expression-based PAM50 subtype and recurrence (ROR) score that reflects proliferation and tumor size. Molecular subtypes (Luminal A, Luminal B, HER2-enriched, and Basal-like) and ROR scores (high vs low/medium) were compared by race (blacks vs whites) and age (≤50 years vs > 50 years) using chi-square tests and analysis of variance tests. Results: Black women of all ages had a statistically significantly lower frequency of Luminal A breast cancer (25.4% and 33.6% in blacks vs 42.8% and 52.1% in whites; younger and older, respectively). All other subtype frequencies were higher in black women (case-only odds ratio [OR] = 3.11, 95% confidence interval [CI] = 2.22 to 4.37, for Basal-like; OR = 1.45, 95% CI = 1.02 to 2.06, for Luminal B; OR = 2.04, 95% CI = 1.33 to 3.13, for HER2-enriched). Among clinically HR+/HER2- cases, Luminal A subtype was less common and ROR scores were statistically significantly higher among black women. Conclusions: Multigene assays highlight racial disparities in tumor subtype distribution that persist even in clinically defined subgroups. Differences in tumor biology (eg, HER2-enriched status) may be targetable to reduce disparities among clinically ER+/HER2- cases.
[Mh] Termos MeSH primário: Afroamericanos
Neoplasias da Mama/química
Neoplasias da Mama/etnologia
Grupo com Ancestrais do Continente Europeu
RNA Neoplásico/análise
Receptor ErbB-2/análise
Receptores Estrogênicos/análise
Receptores de Progesterona/análise
[Mh] Termos MeSH secundário: Adulto
Idoso
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Proliferação Celular
Feminino
Seres Humanos
Meia-Idade
Recidiva
Carga Tumoral
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Neoplasm); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2)
[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/djx135


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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]:28460643
[Au] Autor:Clarke CA; Canchola AJ; Moy LM; Neuhausen SL; Chung NT; Lacey JV; Bernstein L
[Ad] Endereço:Cancer Prevention Institute of California, 2201 Walnut Ave. Suite 300, Fremont, CA, 94538, USA.
[Ti] Título:Regular and low-dose aspirin, other non-steroidal anti-inflammatory medications and prospective risk of HER2-defined breast cancer: the California Teachers Study.
[So] Source:Breast Cancer Res;19(1):52, 2017 May 01.
[Is] ISSN:1465-542X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Regular users of aspirin may have reduced risk of breast cancer. Few studies have addressed whether risk reduction pertains to specific breast cancer subtypes defined jointly by hormone receptor (estrogen and progesterone receptor) and human epidermal growth factor receptor 2 (HER2) expression. This study assessed the prospective risk of breast cancer (overall and by subtype) according to use of aspirin and other non-steroidal anti-inflammatory medications (NSAIDs) in a cohort of female public school professionals in California. METHODS: In 1995 - 1996, participants in the California Teachers Study completed a baseline questionnaire on family history of cancer and other conditions, use of NSAIDs, menstrual and reproductive history, self-reported weight and height, living environment, diet, alcohol use, and physical activity. In 2005-2006, 57,164 participants provided some updated information, including use of NSAIDs and 1457 of these participants developed invasive breast cancer before January 2013. Multivariable Cox proportional hazards regression models provided hazard rate ratios (HRR) for the association between NSAID use and risk of invasive breast cancer as well as hormone receptor- and HER2-defined subtypes. RESULTS: Developing breast cancer was associated inversely with taking three or more tablets of low-dose aspirin per week (23% of participants). Among women reporting this exposure, the HRR was 0.84 (95% confidence interval (CI) 0.72-0.98) compared to those not taking NSAIDs and this was particularly evident in women with the hormone receptor-positive/HER2-negative subtype (HRR = 0.80, 95% CI 0.66-0.96). Use of three or more tablets of "other" NSAIDs was marginally associated with lower risk of breast cancer (HRR = 0.79, 95% CI 0.62-1.00). Other associations with NSAIDs were generally null. CONCLUSION: Our observation of reduced risk of breast cancer, among participants who took three or more tablets of low-dose aspirin weekly, is consistent with other reports looking at aspirin without differentiation by dose. This is the first report to suggest that the reduction in risk occurs for low-dose aspirin and not for regular-dose aspirin and only among women with the hormone receptor-positive/HER2-negative subtype. This preliminary study builds on previous knowledge and further supports the need for formal cancer chemoprevention studies of low-dose aspirin.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/uso terapêutico
Aspirina/uso terapêutico
Neoplasias da Mama/tratamento farmacológico
Receptor ErbB-2/genética
[Mh] Termos MeSH secundário: Idoso
Neoplasias da Mama/epidemiologia
Neoplasias da Mama/patologia
California
Relação Dose-Resposta a Droga
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Meia-Idade
Modelos de Riscos Proporcionais
Receptores Estrogênicos/genética
Receptores de Progesterona/genética
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2); R16CO5Y76E (Aspirin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1186/s13058-017-0840-7



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