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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]: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]:29330226
[Au] Autor:Chortis V; Johal NJ; Bancos I; Evans M; Skordilis K; Guest P; Cullen MH; Porfiri E; Arlt W
[Ad] Endereço:Institute of Metabolism and Systems ResearchUniversity of Birmingham, Birmingham, UK.
[Ti] Título:Mitotane treatment in patients with metastatic testicular Leydig cell tumor associated with severe androgen excess.
[So] Source:Eur J Endocrinol;178(3):K21-K27, 2018 Mar.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitotane (o,p'DDD) is established in the adjuvant and advanced-stage treatment of adrenocortical carcinoma and counteracts both tumor growth and tumor-related steroid production. Both the adrenal glands and the gonads are steroidogenically active organs and share a common embryogenic origin. Here, we describe the effects of mitotane in two patients with metastatic Leydig cell tumor (LCT) of the testes and associated severe androgen excess (serum testosterone 93 and 88 nmol/L, respectively; male reference range 7-27 nmol/L). Both men suffered from severe restlessness, insomnia and irritability, which they described as intolerable and disrupting normal life activities. Urinary steroid profiling by gas chromatography-mass spectrometry (GC-MS) confirmed excess androgen production and revealed concurrent overproduction of glucocorticoids and glucocorticoid precursors, which under physiological conditions are produced only by the adrenal glands but not by the gonads. In a palliative approach, they were commenced on mitotane, which achieved swift control of the hormone excess and the debilitating clinical symptoms, restoring normal quality of life. GC-MS demonstrated normalization of steroid production and decreased 5α-reductase activity, resulting in decreased androgen activation, and imaging demonstrated disease stabilization for 4-10 months. In conclusion, mitotane can be highly effective in controlling steroid excess in metastatic LCTs, with anti-tumor activity in some cases.
[Mh] Termos MeSH primário: Antineoplásicos Hormonais/uso terapêutico
Hiperandrogenismo/tratamento farmacológico
Tumor de Células de Leydig/tratamento farmacológico
Mitotano/uso terapêutico
Neoplasias Testiculares/tratamento farmacológico
[Mh] Termos MeSH secundário: 3-Oxo-5-alfa-Esteroide 4-Desidrogenase/metabolismo
Androgênios/biossíntese
Cromatografia Gasosa-Espectrometria de Massas
Seres Humanos
Hiperandrogenismo/etiologia
Tumor de Células de Leydig/complicações
Tumor de Células de Leydig/secundário
Masculino
Meia-Idade
Metástase Neoplásica
Qualidade de Vida
Neoplasias Testiculares/complicações
Neoplasias Testiculares/patologia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androgens); 0 (Antineoplastic Agents, Hormonal); 78E4J5IB5J (Mitotane); EC 1.3.99.5 (3-Oxo-5-alpha-Steroid 4-Dehydrogenase)
[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:180114
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0542


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[PMID]:28456766
[Au] Autor:Waszut U; Szyszka P; Dworakowska D
[Ad] Endereço:Department of Nuclear Medicine, Medical University of Gdansk, Gdansk, Poland.
[Ti] Título:Understanding mitotane mode of action.
[So] Source:J Physiol Pharmacol;68(1):13-26, 2017 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Adrenocortical carcinoma is a rare disease with poor prognosis. Mitotane is the most effective agent in post-operative treatment (or when inoperable). It selectively limits growth and bioactivity of adrenal tissue. Despite 60 years of use, the basis for its action has yet to be convincingly established. This review summarizes current knowledge of mitotane effects, based on studies on adrenal tissue and primary cell cultures, with emphasis on more recent studies of cell lines. We consider features of the adrenal cortex that might explain mitotane selectivity, and review effects on non-adrenal cells. Since the most clear-cut mitotane effects have been observed for mitochondria, this topic is the core of the review. Mitochondria present unique characteristics in steroidogenic tissue and are known to be important in malignancy development and apoptosis. We look at the evidence for mitotane activation within mitochondria, its impact on mitochondrial energy metabolism and other cellular processes as well as on downstream effects in the cell, such as apoptosis initiation. Further genomic and proteomic investigative studies are likely to yield useful results.
[Mh] Termos MeSH primário: Antineoplásicos Hormonais/farmacologia
Mitotano/farmacologia
[Mh] Termos MeSH secundário: Córtex Suprarrenal/citologia
Córtex Suprarrenal/metabolismo
Carcinoma Adrenocortical/metabolismo
Animais
Apoptose/efeitos dos fármacos
Morte Celular/efeitos dos fármacos
Seres Humanos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Proteínas/metabolismo
Proteoma
Esteroides/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (Proteins); 0 (Proteome); 0 (Steroids); 78E4J5IB5J (Mitotane)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:29390473
[Au] Autor:Zhao H; Yao Y; Yang H; Ma D; Chen A
[Ad] Endereço:Department of Gynecology, The Affiliated Hospital of Qingdao University, Qingdao, PR China.
[Ti] Título:Hormone therapy as a management strategy for lung metastasis after 5 years of endometrial cancer: A case report and literature review.
[So] Source:Medicine (Baltimore);96(51):e9223, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Endometrial cancer patients with lung metastases are rare, and more rarely with long-term management of progesterone after recurrence. PATIENT CONCERNS: Informed consent of the patients and their families. DIAGNOSES: Endometrial cancer (IVB) (Refer to 2009 FIGO stag of endometrial cancer). INTERVENTIONS: the patient was treated with Megestrol Acetate Dispersible Tablets (trade name Yilizhi), 160 mg, orally, once daily, without interruption. OUTCOMES: The patient has been treated with progesterone therapy for stable conditions and her survival time is already roughly a decade (December 2006-October 2016). LESSONS: Hormone therapy may as a long-term management for hormone receptor-positive patients with recurrent endometrial cancer.
[Mh] Termos MeSH primário: Adenocarcinoma/cirurgia
Neoplasias do Endométrio/cirurgia
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/secundário
Megestrol/uso terapêutico
[Mh] Termos MeSH secundário: Adenocarcinoma/secundário
Administração Oral
Antineoplásicos Hormonais/uso terapêutico
Biópsia por Agulha
Neoplasias do Endométrio/diagnóstico
Feminino
Seguimentos
Seres Humanos
Histerectomia/métodos
Imuno-Histoquímica
Neoplasias Pulmonares/diagnóstico por imagem
Meia-Idade
Invasividade Neoplásica/patologia
Recidiva Local de Neoplasia/tratamento farmacológico
Recidiva Local de Neoplasia/patologia
Estadiamento de Neoplasias
Medição de Risco
Fatores de Tempo
Tomografia Computadorizada por Raios X/métodos
Resultado do Tratamento
Hemorragia Uterina/diagnóstico
Hemorragia Uterina/etiologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); EA6LD1M70M (Megestrol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009223


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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]:29205077
[Au] Autor:Ejlertsen B; Offersen BV; Overgaard J; Christiansen P; Jensen MB; Kroman N; Knoop AS; Mouridsen H
[Ad] Endereço:a Danish Breast Cancer Cooperative Group (DBCG) Secretariat and Statistical Office, Rigshospitalet , Copenhagen University Hospital , Copenhagen , Denmark.
[Ti] Título:Forty years of landmark trials undertaken by the Danish Breast Cancer Cooperative Group (DBCG) nationwide or in international collaboration.
[So] Source:Acta Oncol;57(1):3-12, 2018 Jan.
[Is] ISSN:1651-226X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Over the past 40 years the Danish Breast Cancer Cooperative Group (DBCG) has made significant contributions to improve outcome and to make treatment of patients with early breast cancer more tolerable through nationwide and international trials evaluating loco-regional and systemic treatments. These trials have been instrumental to establish standards for the treatment of early breast cancer. METHODS: The DBCG 82 trials had a global impact by documenting that the significant gain in loco-regional recurrence from postmastectomy radiation added to systemic therapy was associated with a reduction in distant recurrence and mortality in high-risk pre- and postmenopausal patients. The DBCG trials comparing breast conserving surgery and radiotherapy with mastectomy and more recently the trial of internal mammary node irradiation also had a major impact of practice. The trials initiated by the DBCG 40 years ago on tamoxifen and cyclophosphamide based chemotherapy became instrumental for the development of adjuvant systemic therapy not only due to their positive results but by sharing these important data with other members of the Early Breast Cancer Trialist' Collaborative Group (EBCTCG). Trials from the DBCG have also been important for highlighting the relative importance of anthracyclines and taxanes in the adjuvant setting. Furthermore, DBCG has made a major contribution to the development of aromatase inhibitors and targeted adjuvant treatment for human epidermal growth factor receptor 2 positive breast cancers. RESULTS: The substantial impact of these treatment improvements is illustrated by a 46.7% 10-year overall survival of early breast cancer patients treated in 1978-1987 compared to 71.5% for patients treated 2008-2012. CONCLUSIONS: The trials conducted and implemented by the DBCG appear to have a major impact on the substantial survival improvements in breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/mortalidade
Neoplasias da Mama/terapia
[Mh] Termos MeSH secundário: Antineoplásicos Hormonais/uso terapêutico
Antineoplásicos Imunológicos/uso terapêutico
Axila/cirurgia
Neoplasias da Mama/patologia
Quimioterapia Adjuvante
Ensaios Clínicos como Assunto
Dinamarca/epidemiologia
Fracionamento de Dose
Feminino
Seres Humanos
Cooperação Internacional
Excisão de Linfonodo
Metástase Linfática/radioterapia
Mastectomia
Mastectomia Segmentar
Estudos Multicêntricos como Assunto
Recidiva Local de Neoplasia/mortalidade
Recidiva Local de Neoplasia/terapia
Prognóstico
Radioterapia Adjuvante
Receptor ErbB-2/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (Antineoplastic Agents, Immunological); EC 2.7.10.1 (Receptor, ErbB-2)
[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.2017.1408962


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[PMID]:29202611
[Au] Autor:Lykkesfeldt AE; Iversen BR; Jensen MB; Ejlertsen B; Giobbie-Hurder A; Reiter BE; Kirkegaard T; Rasmussen BB
[Ad] Endereço:a Unit of Cell Death and Metabolism , Danish Cancer Society Research Center , Copenhagen , Denmark.
[Ti] Título:Aurora kinase A as a possible marker for endocrine resistance in early estrogen receptor positive breast cancer.
[So] Source:Acta Oncol;57(1):67-73, 2018 Jan.
[Is] ISSN:1651-226X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cell culture studies have disclosed that the mitotic Aurora kinase A is causally involved in both tamoxifen and aromatase inhibitor resistant cell growth and thus may be a potential new marker for endocrine resistance in the clinical setting. MATERIAL AND METHODS: Archival tumor tissue was available from 1323 Danish patients with estrogen receptor (ER) positive primary breast cancer, who participated in the Breast International Group (BIG) 1-98 trial, comparing treatment with tamoxifen and letrozole and both in a sequence. The expression of Aurora A was determined by immunohistochemistry in 980 tumors and semi quantitively scored into three groups; negative/weak, moderate and high. The Aurora A expression levels were compared to other clinico-pathological parameters and outcome, defined as disease-free survival (DFS) and overall survival (OS). RESULTS: High expression of Aurora A was found in 26.9% of patients and moderate in 57.0%. High expression was significantly associated with high malignancy grade and HER2 amplification. High Aurora A expression was significantly more frequent in ductal compared to lobular carcinomas. We found no significant association between Aurora A expression and DFS or OS and no evidence of interaction between Aurora A expression and benefits from tamoxifen versus letrozole. CONCLUSIONS: Aurora A expression in breast tumors was associated with high malignancy grade III and with HER2 amplification. A trend as a prognostic factor for OS was found in patients with high Aurora A expression. No predictive property was observed in this study with early breast cancer.
[Mh] Termos MeSH primário: Aurora Quinase A/metabolismo
Neoplasias da Mama/metabolismo
Neoplasias da Mama/mortalidade
Resistência a Medicamentos Antineoplásicos
Receptores Estrogênicos/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos Hormonais/uso terapêutico
Inibidores da Aromatase/uso terapêutico
Biomarcadores/metabolismo
Neoplasias da Mama/patologia
Neoplasias da Mama/terapia
Carcinoma Ductal de Mama/metabolismo
Carcinoma Ductal de Mama/mortalidade
Carcinoma Ductal de Mama/patologia
Carcinoma Ductal de Mama/terapia
Carcinoma Lobular/metabolismo
Carcinoma Lobular/mortalidade
Carcinoma Lobular/patologia
Carcinoma Lobular/terapia
Dinamarca/epidemiologia
Intervalo Livre de Doença
Feminino
Seres Humanos
Imuno-Histoquímica
Nitrilos/uso terapêutico
Prognóstico
Receptor ErbB-2/metabolismo
Tamoxifeno/uso terapêutico
Triazóis/uso terapêutico
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (Aromatase Inhibitors); 0 (Biomarkers); 0 (Nitriles); 0 (Receptors, Estrogen); 0 (Triazoles); 094ZI81Y45 (Tamoxifen); 7LKK855W8I (letrozole); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2); EC 2.7.11.1 (Aurora Kinase A)
[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.2017.1404126


  10 / 14736 MEDLINE  
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[PMID]:29236425
[Au] Autor:Willenberg V; Bamblett M; Cummins M; Hoberg D
[Ti] Título:Review of a home nursing injection service: SHINE.
[So] Source:Aust Nurs Midwifery J;22(6):30-3, 2014 12.
[Is] ISSN:2202-7114
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:The SHINE home injection service is part of a patient support program run by Novartis. SHINE is for people prescribed octreotide long-acting release (Sandostatin LAR) for neuroendocrine tumours (NETs) and acromegaly. SHINE has been running in Australia since 2009. The service is run by a third-party and administered by homecare (SHINE) nurses. Five hundred people with NETs or acromegaly have been involved since the service started. We review our collective experience of the benefits of SHINE, and make recommendations for future development. We hope this review provides guidance for developing future home injection service.
[Mh] Termos MeSH primário: Acromegalia/tratamento farmacológico
Antineoplásicos Hormonais/administração & dosagem
Assistência Domiciliar
Tumores Neuroendócrinos/tratamento farmacológico
Octreotida/administração & dosagem
[Mh] Termos MeSH secundário: Acromegalia/enfermagem
Austrália
Preparações de Ação Retardada
Esquema de Medicação
Feminino
Seres Humanos
Injeções
Masculino
Tumores Neuroendócrinos/enfermagem
Avaliação de Programas e Projetos de Saúde
[Pt] Tipo de publicação:RESEARCH SUPPORT, NON-U.S. GOV'T; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (Delayed-Action Preparations); RWM8CCW8GP (Octreotide)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE



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