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[PMID]:28954302
[Au] Autor:Fidler MM; Reulen RC; Winter DL; Allodji RS; Bagnasco F; Bárdi E; Bautz A; Bright CJ; Byrne J; Feijen EAM; Garwicz S; Grabow D; Gudmundsdottir T; Guha J; Haddy N; Jankovic M; Kaatsch P; Kaiser M; Kuonen R; Linge H; Maule M; Merletti F; Øfstaas H; Ronckers CM; Skinner R; Teepen J; Terenziani M; Vu-Bezin G; Wesenberg F; Wiebe T; Jakab Z; Haupt R; Lähteenmäki P; Zaletel LZ; Kuehni CE; Winther JF; de Vathaire F; Kremer LC; Hjorth L; Hawkins MM
[Ad] Endereço:Centre for Childhood Cancer Survivor Studies, Institute of Applied Health Research, University of Birmingham, Birmingham, UK; Section of Cancer Surveillance, International Agency for Research on Cancer, Lyon, France; Cancer and Radiation Team, U1018 INSERM, Villejuif, France; Epidemiology and Biosta
[Ti] Título:Risk of Subsequent Bone Cancers Among 69 460 Five-Year Survivors of Childhood and Adolescent Cancer in Europe.
[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:Introduction: We investigate the risks of subsequent primary bone cancers after childhood and adolescent cancer in 12 European countries. For the first time, we satisfactorily address the risks beyond 40 years from diagnosis and beyond 40 years of age among all survivors. Methods: This largest-ever assembled cohort comprises 69 460 five-year survivors of cancer diagnosed before age 20 years. Standardized incidence ratios, absolute excess risks, and multivariable-adjusted relative risks and relative excess risks were calculated. All statistical tests were two-sided. Results: Overall, survivors were 21.65 times (95% confidence interval = 18.97 to 24.60 times) more likely to be diagnosed with a subsequent primary bone cancer than expected from the general population. The greatest excess numbers of bone cancers were observed after retinoblastoma, bone sarcoma, and soft tissue sarcoma. The excess number of bone cancers declined linearly with both years since diagnosis and attained age (all P < .05). Beyond 40 years from diagnosis and age 40 years, there were at most 0.45 excess bone cancers among all survivors per 10 000 person-years at risk; beyond 30 years from diagnosis and age 30 years, there were at most 5.02 excess bone cancers after each of retinoblastoma, bone sarcoma, and soft tissue sarcoma, per 10 000 person-years at risk. Conclusions: For all survivors combined and the cancer groups with the greatest excess number of bone cancers, the excess numbers observed declined with both age and years from diagnosis. These results provide novel, reliable, and unbiased information about risks and risk factors among long-term survivors of childhood and adolescent cancer.
[Mh] Termos MeSH primário: Neoplasias Ósseas/epidemiologia
Segunda Neoplasia Primária/epidemiologia
Sobreviventes/estatística & dados numéricos
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Estudos de Coortes
Europa (Continente)/epidemiologia
Feminino
Seguimentos
Seres Humanos
Masculino
Osteossarcoma/epidemiologia
Retinoblastoma/epidemiologia
Sarcoma/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[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:170928
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx165


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[PMID]:28454732
[Au] Autor:Yang Z; Su Z; DeWitt JP; Xie L; Chen Y; Li X; Han L; Li D; Xia J; Zhang Y; Yang Y; Jin C; Zhang J; Li S; Li K; Zhang Z; Qu X; He Z; Chen Y; Shen Y; Ren M; Yuan Z
[Ad] Endereço:Bone and Soft Tissue Tumors Research Center of Yunnan Province, Department of Orthopaedics, The Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan 650118, China. Electronic address: yangzuozhang@163.com.
[Ti] Título:Fluvastatin Prevents Lung Adenocarcinoma Bone Metastasis by Triggering Autophagy.
[So] Source:EBioMedicine;19:49-59, 2017 May.
[Is] ISSN:2352-3964
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Bone is one of the most preferred sites of metastasis in lung cancer. Currently, bisphosphonates and denosumab are major agents for controlling tumor-associated skeletal-related events (SREs). However, both bisphosphonates and denosumab significantly increase the risk for jaw osteonecrosis. Statins, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors and the most frequently prescribed cholesterol-lowering agents, have been reported to inhibit tumor progression and induce autophagy in cancer cells. However, the effects of statin and role of autophagy by statin on bone metastasis are unknown. In this study, we report that fluvastatin effectively prevented lung adenocarcinoma bone metastasis in a nude mouse model. We further reveal that fluvastatin-induced anti-bone metastatic property was largely dependent on its ability to induce autophagy in lung adenocarcinoma cells. Atg5 or Atg7 deletion, or 3-methyadenine (3-MA) or Bafilomycin A1 (Baf A1) treatment prevented the fluvastatin-induced suppression of bone metastasis. Furthermore, we reveal that fluvastatin stimulation increased the nuclear p53 expression, and fluvastatin-induced autophagy and anti-bone metastatic activity were mostly dependent on p53.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Antineoplásicos/uso terapêutico
Neoplasias Ósseas/prevenção & controle
Ácidos Graxos Monoinsaturados/uso terapêutico
Indóis/uso terapêutico
Neoplasias Pulmonares/tratamento farmacológico
[Mh] Termos MeSH secundário: Adenocarcinoma/metabolismo
Adenocarcinoma/patologia
Animais
Antineoplásicos/farmacologia
Autofagia/efeitos dos fármacos
Neoplasias Ósseas/metabolismo
Neoplasias Ósseas/secundário
Linhagem Celular Tumoral
Ácidos Graxos Monoinsaturados/farmacologia
Feminino
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Indóis/farmacologia
Neoplasias Pulmonares/metabolismo
Neoplasias Pulmonares/patologia
Camundongos Endogâmicos BALB C
Camundongos Nus
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Fatty Acids, Monounsaturated); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Indoles); 0 (Tumor Suppressor Protein p53); 4L066368AS (fluvastatin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:29489644
[Au] Autor:Attademo L; De Falco S; Rosanova M; Esposito M; Mazio F; Foschini F; Santaniello A; Fiore G; Matano E; Manganelli F; Carlomagno C
[Ad] Endereço:Department of Clinical Medicine and Surgery.
[Ti] Título:A case report of limbic encephalitis in a metastatic colon cancer patient during first-line bevacizumab-combined chemotherapy.
[So] Source:Medicine (Baltimore);97(9):e0011, 2018 Mar.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Paraneoplastic limbic encephalitis (PLE) is one of the most common causes of neurologic paraneoplastic syndromes, with unclear pathogenesis. While several reports published in the last decades showed the occurrence of PLE in a variety of cancers, only a few cases have been associated with colon cancer. PATIENT CONCERNS: In February 2017, a 54-year-old man with clinical history of radically resected colon cancer started first line chemotherapy with FOLFOXIRI plus bevacizumab, after radiological diagnosis of multiple liver and bone metastases. During the third cycle of treatment, the patient developed psychomotor agitation and hallucinations followed by severe consciousness level reduction and cognitive impairment. DIAGNOSES: Magnetic resonance imaging showed hyperintense signals in both hippocampal areas, insula and right cingulate gyrus on fluid attenuated inversion recovery, diffusion weighted imaging, and T2-weighted images, highly suggestive of limbic encephalitis. Other causes (brain metastases, toxicity of chemotherapeutic agents, and infections) were excluded. INTERVENTIONS: Empirical immunosuppressive treatment (high-dose immunoglobulins and corticosteroids) was administered and chemotherapy was resumed. OUTCOMES: A slowly progressive improvement in neurological condition has been observed, even though radiological signs of limbic encephalitis are still evident. LESSONS: The present case highlights the complex diagnostic process of PLE, and the lack of a standard treatment. Moreover, the absence of correlation between PLE and tumor progression or tumor burden, and the opportunity of treating underlying neoplasm is discussed.
[Mh] Termos MeSH primário: Antineoplásicos Imunológicos/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Bevacizumab/uso terapêutico
Neoplasias do Colo/tratamento farmacológico
Neoplasias do Colo/patologia
Encefalite Límbica/diagnóstico
[Mh] Termos MeSH secundário: Neoplasias Ósseas/tratamento farmacológico
Neoplasias Ósseas/secundário
Neoplasias do Colo/complicações
Eletroencefalografia
Seres Humanos
Encefalite Límbica/complicações
Neoplasias Hepáticas/tratamento farmacológico
Neoplasias Hepáticas/secundário
Imagem por Ressonância Magnética
Masculino
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Immunological); 2S9ZZM9Q9V (Bevacizumab)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180301
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000010011


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[PMID]:29303365
[Au] Autor:Xiao Y; Zhao Q; Du B; Chen HY; Zhou DZ
[Ad] Endereço:a Department of Orthopaedic , The People's Hospital of Kaizhou District , Chongqing , PR China.
[Ti] Título:MicroRNA-187 Inhibits Growth and Metastasis of Osteosarcoma by Downregulating S100A4.
[So] Source:Cancer Invest;36(1):1-9, 2018 Jan 02.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Abnormal expression and dysfunction of microRNAs are correlated with osteosarcoma (OS). This study demonstrated that the miR-187 level in OS tissues and cell lines was decreased. The proliferation and metastatic abilities of U-2OS cells were inhibited by miR-187 overexpression and promoted by miR-187 knockdown. Moreover, miR-187 also inhibited growth and metastasis of OS cells in vivo. Furthermore, we revealed that miR-187 could interact with S100A4 3'-UTR and inhibit S100A4 expression in OS cells. In summary, miR-187 inhibits growth and metastasis of OS cells by downregulating S100A4, which might be a potential biomarker and therapeutic target of OS.
[Mh] Termos MeSH primário: Neoplasias Ósseas/genética
Proliferação Celular/genética
Regulação para Baixo/genética
MicroRNAs/genética
Metástase Neoplásica/genética
Osteossarcoma/genética
Proteína A4 de Ligação a Cálcio da Família S100/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas/genética
Neoplasias Ósseas/patologia
Linhagem Celular Tumoral
Movimento Celular/genética
Regulação Neoplásica da Expressão Gênica/genética
Seres Humanos
Metástase Neoplásica/patologia
Osteossarcoma/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (MIRN187 microRNA, human); 0 (MicroRNAs); 0 (S100 Calcium-Binding Protein A4); 142662-27-9 (S100A4 protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2017.1415348


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[PMID]:28460457
[Au] Autor:Trivedi T; Zheng Y; Fournier PGJ; Murthy S; John S; Schillo S; Dunstan CR; Mohammad KS; Zhou H; Seibel MJ; Guise TA
[Ad] Endereço:Bone Research Program, ANZAC Research Institute, University of Sydney, Sydney, Australia.
[Ti] Título:The vitamin D receptor is involved in the regulation of human breast cancer cell growth via a ligand-independent function in cytoplasm.
[So] Source:Oncotarget;8(16):26687-26701, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vitamin D has pleiotropic effects on multiple tissues, including malignant tumors. Vitamin D inhibits breast cancer growth through activation of the vitamin D receptor (VDR) and via classical nuclear signaling pathways. Here, we demonstrate that the VDR can also function in the absence of its ligand to control behaviour of human breast cancer cells both outside and within the bone microenvironment. Stable shRNA expression was used to knock down VDR expression in MCF-7 cells, generating two VDR knockdown clonal lines. In ligand-free culture, knockdown of VDR in MCF-7 cells significantly reduced proliferation and increased apoptosis, suggesting that the VDR plays a ligand-independent role in cancer cell growth. Implantation of these VDR knockdown cells into the mammary fat pad of nude mice resulted in reduced tumor growth in vivo compared with controls. In the intra-tibial xenograft model, VDR knockdown greatly reduced the ability of the cells to form tumors in the bone microenvironment. The in vitro growth of VDR knockdown cells was rescued by the expression of a mutant form of VDR which is unable to translocate to the nucleus and hence accumulates in the cytoplasm. Thus, our data indicate that in the absence of ligand, the VDR promotes breast cancer growth both in vitro and in vivo and that cytoplasmic accumulation of VDR is sufficient to produce this effect in vitro. This new mechanism of VDR action in breast cancer cells contrasts the known anti-proliferative nuclear actions of the VDR-vitamin D ligand complex.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Receptores de Calcitriol/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Neoplasias Ósseas/genética
Neoplasias Ósseas/metabolismo
Neoplasias Ósseas/patologia
Neoplasias da Mama/genética
Linhagem Celular Tumoral
Proliferação Celular
Citoplasma/metabolismo
Modelos Animais de Doenças
Feminino
Expressão Gênica
Técnicas de Silenciamento de Genes
Xenoenxertos
Seres Humanos
Ligantes
Camundongos
Mutação
Osteosclerose/genética
Osteosclerose/metabolismo
Transporte Proteico
Receptores de Calcitriol/genética
Vitamina D/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ligands); 0 (Receptors, Calcitriol); 0 (VDR protein, human); 1406-16-2 (Vitamin D)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15803


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[PMID]:28460435
[Au] Autor:Li ZW; Zhu YR; Zhou XZ; Zhuo BB; Wang XD
[Ad] Endereço:The Center of Diagnosis and Treatment for Children's Bone Diseases, The Children's Hospital Affiliated to Soochow University, Suzhou, China.
[Ti] Título:microRNA-135b expression silences Ppm1e to provoke AMPK activation and inhibit osteoblastoma cell proliferation.
[So] Source:Oncotarget;8(16):26424-26433, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Forced-activation of AMP-activated protein kinase (AMPK) can possibly inhibit osteoblastoma cells. Here, we aim to provoke AMPK activation via microRNA silencing its phosphatase Ppm1e (protein phosphatase Mg2+/Mn2+-dependent 1e). We showed that microRNA-135b-5p ("miR-135b-5p"), the anti-Ppm1e microRNA, was significantly downregulated in human osteoblastoma tissues. It was correlated with Ppm1e upregulation and AMPKα1 de-phosphorylation. Forced-expression of miR-135b-5p in human osteoblastoma cells (MG-63 and U2OS lines) silenced Ppm1e, and induced a profound AMPKα1 phosphorylation (at Thr-172). Osteoblastoma cell proliferation was inhibited after miR-135b-5p expression. Intriguingly, Ppm1e shRNA knockdown similarly induced AMPKα1 phosphorylation, causing osteoblastoma cell proliferation. Reversely, AMPKα1 shRNA knockdown or dominant negative mutation almost abolished miR-135b-5p's actions in osteoblastoma cells. Further in vivo studies demonstrated that U2OS tumor growth in mice was dramatically inhibited after expressing miR-135b-5p or Ppm1e shRNA. Together, our results suggest that miR-135b-induced Ppm1e silence induces AMPK activation to inhibit osteoblastoma cell proliferation.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Neoplasias Ósseas/genética
Neoplasias Ósseas/metabolismo
Inativação Gênica
MicroRNAs/genética
Osteoblastoma/genética
Osteoblastoma/metabolismo
Proteína Fosfatase 2C/genética
[Mh] Termos MeSH secundário: Animais
Neoplasias Ósseas/patologia
Linhagem Celular Tumoral
Proliferação Celular
Modelos Animais de Doenças
Ativação Enzimática
Regulação Neoplásica da Expressão Gênica
Técnicas de Silenciamento de Genes
Seres Humanos
Camundongos
Mutação
Osteoblastoma/patologia
Fosforilação
RNA Interferente Pequeno/genética
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN135 microRNA, human); 0 (MicroRNAs); 0 (RNA, Small Interfering); EC 2.7.11.31 (AMP-Activated Protein Kinases); EC 3.1.3.16 (PPM1E protein, human); EC 3.1.3.16 (Protein Phosphatase 2C)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15477


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[PMID]:28460433
[Au] Autor:Cheng DD; Zhang HZ; Yuan JQ; Li SJ; Yang QC; Fan CY
[Ad] Endereço:Department of Orthopedics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
[Ti] Título:Minichromosome maintenance protein 2 and 3 promote osteosarcoma progression via DHX9 and predict poor patient prognosis.
[So] Source:Oncotarget;8(16):26380-26393, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A label free quantitative proteomic approach (SWATH™ experiment) was performed to identify tumor-associated nuclear proteins that are differentially expressed between osteosarcoma cells and osteoblast cells. By functional screening, minichromosome maintenance protein 2 (MCM2) and minichromosome maintenance protein 3 (MCM3) were found to be related to osteosarcoma cell growth. Here, we show that knockdown of MCM2 or MCM3 inhibits osteosarcoma growth in vitro and in vivo. In co-immunoprecipitation and co-localization experiments, MCM2 and MCM3 were found to interact with DExH-box helicase 9 (DHX9) in osteosarcoma cells. A rescue study showed that the decreased growth of osteosarcoma cells by MCM2 or MCM3 knockdown was reversed by DHX9 overexpression, indicating that MCM2 and MCM3 activity was DHX9-dependent. In addition, the depletion of DHX9 hindered osteosarcoma cell proliferation. Notably, MCM2 and MCM3 expression levels were positively correlated with the DHX9 expression level in tumor samples and were associated with a poor prognosis in patients with osteosarcoma. Taken together, these results suggest that the MCM2/MCM3-DHX9 axis has an important role in osteosarcoma progression.
[Mh] Termos MeSH primário: Neoplasias Ósseas/metabolismo
Neoplasias Ósseas/mortalidade
RNA Helicases DEAD-box/metabolismo
Componente 2 do Complexo de Manutenção de Minicromossomo/metabolismo
Componente 3 do Complexo de Manutenção de Minicromossomo/metabolismo
Proteínas de Neoplasias/metabolismo
Osteossarcoma/metabolismo
Osteossarcoma/mortalidade
[Mh] Termos MeSH secundário: Adolescente
Adulto
Animais
Neoplasias Ósseas/genética
Neoplasias Ósseas/patologia
Linhagem Celular Tumoral
Proliferação Celular/genética
Criança
Modelos Animais de Doenças
Progressão da Doença
Feminino
Expressão Gênica
Técnicas de Silenciamento de Genes
Xenoenxertos
Seres Humanos
Masculino
Camundongos
Componente 2 do Complexo de Manutenção de Minicromossomo/genética
Componente 3 do Complexo de Manutenção de Minicromossomo/genética
Metástase Neoplásica
Estadiamento de Neoplasias
Proteínas Nucleares/metabolismo
Osteossarcoma/genética
Osteossarcoma/patologia
Prognóstico
Modelos de Riscos Proporcionais
Ligação Proteica
Proteoma
Proteômica/métodos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MCM3 protein, human); 0 (Neoplasm Proteins); 0 (Nuclear Proteins); 0 (Proteome); EC 3.6.1.- (DHX9 protein, human); EC 3.6.4.12 (MCM2 protein, human); EC 3.6.4.12 (Minichromosome Maintenance Complex Component 2); EC 3.6.4.12 (Minichromosome Maintenance Complex Component 3); EC 3.6.4.13 (DEAD-box RNA Helicases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15474


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[PMID]:29480835
[Au] Autor:Li L; Tong M; Zhao YT; He Y; Zhou HY; Zhang GF; Zhang YJ
[Ad] Endereço:Department of Orthopedics, Traditional Chinese Medical Hospital of Xinjiang Uygur Autonomous Region, Urumqi.
[Ti] Título:Membrane translocation of Bruton kinase in multiple myeloma cells is associated with osteoclastogenic phenotype in bone metastatic lesions.
[So] Source:Medicine (Baltimore);97(2):e9482, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Using bone biopsy samples, we examined whether osteolytic cytokine profile is changed in situ in bone samples of metastatic multiple myeloma, and whether this creates an environment of lysis within the bone to which it has spread. This also produces the clinical features of increased circulating plasma calcium, and deleterious effects on the kidney.Using multiple myeloma biopsy and cell extracts from bone metastatic lesions, Bruton kinase, a tyrosine kinase, was demonstrated to be translocated to the membrane. Several transcription factors were upregulated included activin A, inflammatory transcription activator like such as nuclear factor kappa B, and specific bone lytic factor such as receptor activator of nuclear factor kappa-B ligand that is known to drive osteoclastogenesis as opposed to a osteogenic environment. The transcript for Bruton kinase was also elevated in its expression.Cytokines that support osteolytic activity such as a proliferation-inducing ligand, RANTES (regulated on activation, normal T cell expressed and secreted), interleukin-8, and activin A were upregulated. Tartrate resistant acid phosphatase (TRAP)-positive osteoclastic enzymatic activity was significantly elevated in the bone microenvironment in metastatic multiple myeloma. Several tyrosine kinase inhibitors, including inhibitors for Bruton kinase such as ibrutinib have been developed. The results of the present study provide evidence that multiple myeloma possess signal transduction mechanisms to support a bone lytic environment.The results provide a preliminary molecular basis to design specific inhibitors for management of bone metastasis of multiple myeloma.
[Mh] Termos MeSH primário: Neoplasias Ósseas/enzimologia
Neoplasias Ósseas/secundário
Membrana Celular/enzimologia
Mieloma Múltiplo/enzimologia
Osteogênese/fisiologia
Proteínas Tirosina Quinases/metabolismo
[Mh] Termos MeSH secundário: Ativinas/metabolismo
Idoso
Quimiocina CCL5/metabolismo
Seres Humanos
Masculino
Meia-Idade
NF-kappa B/metabolismo
RNA Mensageiro/metabolismo
Fosfatase Ácida Resistente a Tartarato/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL5 protein, human); 0 (Chemokine CCL5); 0 (NF-kappa B); 0 (RNA, Messenger); 0 (activin A); 104625-48-1 (Activins); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 3.1.3.2 (Tartrate-Resistant Acid Phosphatase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180227
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009482


  9 / 53280 MEDLINE  
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[PMID]:29370211
[Au] Autor:Hayes AR; Brungs D; Pavlakis N
[Ad] Endereço:Department of Medical Oncology, Royal North Shore Hospital, St Leonards, New South Wales, Australia.
[Ti] Título:Osteoclast inhibitors to prevent bone metastases in men with high-risk, non-metastatic prostate cancer: A systematic review and meta-analysis.
[So] Source:PLoS One;13(1):e0191455, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In advanced prostate cancer, osteoclast inhibitors prevent and palliate skeletal related events associated with bone metastases. However, it is uncertain whether they play a disease-modifying role earlier in the course of the disease. METHODS: Medline, EMBASE, Cochrane Central Register of Controlled Trials and Cochrane Database of Systematic Reviews and ASCO conference proceedings were searched for randomized controlled trials that compared osteoclast inhibitors with placebo and/or standard of care (SOC) in patients with high-risk, non-metastatic prostate cancer. The primary outcome measure was incidence of new bone metastases; secondary outcomes included overall survival (OS), prostate cancer specific survival, mortality unrelated to prostate cancer, toxicity and health related quality of life outcomes. Results are presented as relative risk (RR) with 95% confidence intervals (CI). RESULTS: Six randomized controlled trials (5947 participants) were included, five evaluating bisphosphonates and one denosumab. Overall, there was no difference in incidence of bone metastases between participants treated with osteoclast inhibitors versus placebo/SOC (RR 1.09, 95%CI 0.84-1.41, p = 0.51) however significant heterogeneity was observed between studies. The denosumab trial was the largest and only positive trial amongst the included studies (RR 0.83, 95%CI 0.73-0.95, p = 0.007). No significant difference was observed in OS (RR 0.99 95% CI 0.89-1.10, p = 0.84) nor prostate cancer specific survival (RR 1.12 95%CI 0.93-1.36, p = 0.24). Most studies reported increased rates of osteonecrosis of the jaw (5% or less) and hypocalcemia (2% or less) with osteoclast inhibitors. CONCLUSIONS: While there is limited evidence that bisphosphonates alter the natural history of high-risk, non-metastatic prostate cancer, denosumab delays onset of bone metastases in this patient population. Neither class of osteoclast inhibitor demonstrated an impact on survival outcomes. Future trials with better defined patient selection and a robust definition for high risk disease is critical.
[Mh] Termos MeSH primário: Conservadores da Densidade Óssea/uso terapêutico
Neoplasias Ósseas/prevenção & controle
Neoplasias Ósseas/secundário
Osteoclastos/efeitos dos fármacos
Neoplasias da Próstata/tratamento farmacológico
[Mh] Termos MeSH secundário: Denosumab/uso terapêutico
Difosfonatos/uso terapêutico
Seres Humanos
Masculino
Osteoclastos/patologia
Avaliação de Resultados (Cuidados de Saúde)
Neoplasias da Próstata/patologia
Qualidade de Vida
Ensaios Clínicos Controlados Aleatórios como Assunto
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Bone Density Conservation Agents); 0 (Diphosphonates); 4EQZ6YO2HI (Denosumab)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191455


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[PMID]:29241166
[Au] Autor:De Luca R; Costa RP; Tripoli V; Murabito A; Cicero G
[Ad] Endereço:Department of Surgical, Oncological, and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo, Italy.
[Ti] Título:The Clinical Efficacy of Radium-223 for Bone Metastasis in Patients with Castration-Resistant Prostate Cancer: An Italian Clinical Experience.
[So] Source:Oncology;94(3):161-166, 2018.
[Is] ISSN:1423-0232
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Prostate cancer frequently causes bone metastases and skeletal events that impair quality of life (QoL) and survival. The alpha emitter radium-223 is a new drug that improves treatment in men with castration-resistant prostate cancer (CRPC) and bone metastases. Our aim was to evaluate the effectiveness of radium-223. SUBJECTS AND METHODS: In this retrospective study we enrolled 48 subjects. Pain reduction, alkaline phosphatase (ALP), time to first symptomatic skeletal event, and QoL were the variables we evaluated. RESULTS: Radium-223 was well tolerated, with a manageable toxicity profile and a modest objective response rate. A considerable difference in serum ALP levels before and after treatment was observed, with a significant correlation between pain relief and QoL, which showed a value of R2 to 0.44 with a slope of 1.50 (p = 0.0021). CONCLUSIONS: Radium-223 showed a clinical benefit, with a reduction in pain symptoms in 58% of patients. Radium-223 was shown to be an effective and well-tolerated therapeutic option in patients with metastatic CRPC progressing after docetaxel plus prednisone treatment.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Neoplasias Ósseas/tratamento farmacológico
Neoplasias Ósseas/secundário
Neoplasias de Próstata Resistentes à Castração/patologia
Radioisótopos/uso terapêutico
Rádio (Elemento)/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Seres Humanos
Itália
Masculino
Meia-Idade
Prednisona/uso terapêutico
Neoplasias de Próstata Resistentes à Castração/tratamento farmacológico
Qualidade de Vida
Estudos Retrospectivos
Taxoides/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Radioisotopes); 0 (Radium-223); 0 (Taxoids); 15H5577CQD (docetaxel); VB0R961HZT (Prednisone); W90AYD6R3Q (Radium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1159/000485102



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