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[PMID]:29480877
[Au] Autor:Zhong S; Zhao Y; Fan C
[Ad] Endereço:Department of Pathology, First Affiliated Hospital and College of Basic Medical Sciences of China Medical University.
[Ti] Título:Hepatoblastoma with pure fetal epithelial differentiation in a 10-year-old boy: A rare case report and review of the literature.
[So] Source:Medicine (Baltimore);97(2):e9647, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Hepatoblastoma is a rare malignant embryonal tumor that only accounts for approximately 1% of all pediatric cancers and mostly develops in children younger than 5 years old. Moreover, the occurrence of hepatoblastoma in adults is extremely rare. PATIENT CONCERNS: Herein, we present a rare case of hepatoblastoma with pure epithelial differentiation in a 10-year-old boy.Pathological examination was performed. The tumor was 15 cm × 15 cm in size with clear margins. The cut surface was multiple nodular and grey-yellow. Histologically, the small cuboidal tumor cells were arranged in trabeculae with 2-3 cell layers. The tumor cells had eosinophilic or clear cytoplasm, formed dark and light areas, and were positive for alpha-fetoprotein, CK, CK8/18, CD10, hepatocyte, and GPC3. CD34 staining revealed that the sinusoids were lined by endothelial cells in the tumor tissues. The Ki67 index was approximately 20%. DIAGNOSES: Based on these findings, the case was diagnosed as hepatoblastoma with pure fetal epithelial differentiation. INTERVENTIONS: The tumor was completely removed. OUTCOMES: No recurrence was found 3 months after the operation. LESSONS: Hepatoblastoma with pure epithelial differentiation can also occur in older children. Children rarely notice and report any physical abnormality, and this may be among the primary reasons for the late diagnosis of the tumor. Annual heath checks may be beneficial in the detection of these rare tumors and improvement of patient outcomes.
[Mh] Termos MeSH primário: Hepatoblastoma/diagnóstico
Hepatoblastoma/patologia
Neoplasias Hepáticas/diagnóstico
Neoplasias Hepáticas/patologia
[Mh] Termos MeSH secundário: Criança
Diagnóstico Diferencial
Hepatoblastoma/cirurgia
Seres Humanos
Neoplasias Hepáticas/cirurgia
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[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:180227
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009647


  2 / 1582 MEDLINE  
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[PMID]:29381980
[Au] Autor:Zhang B; Liu G; Liu X; Zheng S; Dong K; Dong R
[Ad] Endereço:Children's Hospital of Fudan University.
[Ti] Título:Circulating D-dimer level correlates with disease characteristics in hepatoblastoma patients.
[So] Source:Medicine (Baltimore);96(47):e8798, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Hepatoblastoma (HB) is the most common pediatric liver malignancy, typically affecting children within the first 4 years of life. However, only a few validated blood biomarkers are used in clinical evaluation. The current study explored the clinical application and significance of D-dimer levels in patients with HB. METHOD: Forty-four patients with HB were included in this retrospective study. D-dimer and plasma fibrinogen levels were examined, and their correlation with other clinical features was analyzed. D-dimer and plasma fibrinogen levels were examined between HB and other benign hepatic tumors. RESULTS: D-dimer levels were significantly associated with high-risk HB features, such as advanced stage and high α-fetoprotein (AFP) levels. Higher D-dimer levels were observed in stage 4 patients compared with stage 1/2/3 patients (P = .028). Higher D-dimer levels were also observed in patients with higher AFP levels before chemotherapy compared with patients with lower AFP levels after chemotherapy (P< 0.001). In addition, higher D-dimer levels were observed in HB compared with other benign hepatic tumors such as hepatic hemangioma and hepatocellular adenoma (P = .012). No significant difference in D-dimer levels was found between sex (P = .503) and age (≥12 vs <12 months, P = .424). There was no significant difference in plasma fibrinogen levels between sex or age and high-risk HB features, such as advanced stage and high AFP levels. CONCLUSIONS: Elevated D-dimer levels could be a useful determinant biomarker for high-risk features in patients with HB. This finding also supports the clinical application of D-dimer in HB.
[Mh] Termos MeSH primário: Produtos de Degradação da Fibrina e do Fibrinogênio/análise
Hepatoblastoma/sangue
Neoplasias Hepáticas/sangue
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/sangue
Criança
Pré-Escolar
Feminino
Fibrinogênio/análise
Seres Humanos
Lactente
Recém-Nascido
Masculino
Estudos Retrospectivos
alfa-Fetoproteínas/análise
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Fibrin Fibrinogen Degradation Products); 0 (alpha-Fetoproteins); 0 (fibrin fragment D); 9001-32-5 (Fibrinogen)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008798


  3 / 1582 MEDLINE  
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[PMID]:27775819
[Au] Autor:Sumazin P; Chen Y; Treviño LR; Sarabia SF; Hampton OA; Patel K; Mistretta TA; Zorman B; Thompson P; Heczey A; Comerford S; Wheeler DA; Chintagumpala M; Meyers R; Rakheja D; Finegold MJ; Tomlinson G; Parsons DW; López-Terrada D
[Ad] Endereço:Texas Children's Cancer Center, Baylor College of Medicine, Houston, TX.
[Ti] Título:Genomic analysis of hepatoblastoma identifies distinct molecular and prognostic subgroups.
[So] Source:Hepatology;65(1):104-121, 2017 01.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite being the most common liver cancer in children, hepatoblastoma (HB) is a rare neoplasm. Consequently, few pretreatment tumors have been molecularly profiled, and there are no validated prognostic or therapeutic biomarkers for HB patients. We report on the first large-scale effort to profile pretreatment HBs at diagnosis. Our analysis of 88 clinically annotated HBs revealed three risk-stratifying molecular subtypes that are characterized by differential activation of hepatic progenitor cell markers and metabolic pathways: high-risk tumors were characterized by up-regulated nuclear factor, erythroid 2-like 2 activity; high lin-28 homolog B, high mobility group AT-hook 2, spalt-like transcription factor 4, and alpha-fetoprotein expression; and high coordinated expression of oncofetal proteins and stem-cell markers, while low-risk tumors had low lin-28 homolog B and lethal-7 expression and high hepatic nuclear factor 1 alpha activity. CONCLUSION: Analysis of immunohistochemical assays using antibodies targeting these genes in a prospective study of 35 HBs suggested that these candidate biomarkers have the potential to improve risk stratification and guide treatment decisions for HB patients at diagnosis; our results pave the way for clinical collaborative studies to validate candidate biomarkers and test their potential to improve outcome for HB patients. (Hepatology 2017;65:104-121).
[Mh] Termos MeSH primário: Hepatoblastoma/genética
Neoplasias Hepáticas/genética
[Mh] Termos MeSH secundário: Regulação Neoplásica da Expressão Gênica
Genômica
Hepatoblastoma/classificação
Seres Humanos
Neoplasias Hepáticas/classificação
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1002/hep.28888


  4 / 1582 MEDLINE  
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[PMID]:28457172
[Au] Autor:Sayed S; Prabhu S; Fawcett J; Choo K; Alphonso N
[Ad] Endereço:1 Queensland Paediatric Cardiac Services, Lady Cilento Children's Hospital, Brisbane, Australia.
[Ti] Título:A systematic surgical approach to hepatoblastoma with intracardiac extension.
[So] Source:Asian Cardiovasc Thorac Ann;25(4):300-303, 2017 May.
[Is] ISSN:1816-5370
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hepatoblastoma is very uncommon in children, and intracardiac extension is rare. The SIOPEL-4 regime for metastatic hepatoblastoma has extended the surgical options with good results. We successfully treated a boy aged 2 years and 9 months with hepatoblastoma, using a multidisciplinary surgical strategy involving an extended left hepatectomy, left adrenalectomy, biopsy of the paraaortic and coeliac lymph nodes, and resection of the inferior vena caval-right atrial extension of the hepatoblastoma, under cardiopulmonary bypass and deep hypothermia.
[Mh] Termos MeSH primário: Átrios do Coração/cirurgia
Hepatectomia
Hepatoblastoma/cirurgia
Neoplasias Hepáticas/cirurgia
Veia Cava Inferior/cirurgia
[Mh] Termos MeSH secundário: Adrenalectomia
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Biópsia
Ponte Cardiopulmonar
Quimioterapia Adjuvante
Pré-Escolar
Átrios do Coração/patologia
Hepatoblastoma/secundário
Seres Humanos
Hipotermia Induzida
Neoplasias Hepáticas/patologia
Imagem por Ressonância Magnética
Masculino
Terapia Neoadjuvante
Invasividade Neoplásica
Tomografia Computadorizada por Raios X
Resultado do Tratamento
Veia Cava Inferior/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171212
[Lr] Data última revisão:
171212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1177/0218492317705565


  5 / 1582 MEDLINE  
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[PMID]:28921839
[Au] Autor:Dall'Igna P; Brugieres L; Christin AS; Maibach R; Casanova M; Alaggio R; de Goyet JV; Zsiros J; Morland B; Czauderna P; Childs M; Aronson DC; Branchereau S; Brock P; Perilongo G
[Ad] Endereço:Pediatric Surgery Division, Department of Women's and Children's Health, University of Padua, Padua, Italy.
[Ti] Título:Hepatoblastoma in children aged less than six months at diagnosis: A report from the SIOPEL group.
[So] Source:Pediatr Blood Cancer;65(1), 2018 Jan.
[Is] ISSN:1545-5017
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The purpose of this study was to evaluate clinical characteristics, treatment, and survival of children, who were diagnosed with hepatoblastoma (HB) in their first 6 months of age, enrolled in the SIOPEL 2 and 3 protocols. METHODS: Seventy-nine patients, treated between 1994 and 2006, were analyzed after stratification into three age groups: <1 month, between 1 and 3 months, and between 3 and 6 months. All received preoperative chemotherapy. RESULTS: Clinical characteristics were similar in both trials: 4 patients had pulmonary metastases at diagnosis, 4 had α-fetoprotein <100 ng/ml, 68 were operated by partial hepatectomy, and 7 received liver transplant. Chemotherapy courses were delayed in 8.5%, 8.4%, and 11.8% of cycles in the three groups. Doses were calculated according to weight for children <5 and 5-10 kg, and further reduced in 18.1%, 6.8%, and 5.9% of cycles. Acute toxicity was manageable. Long-term hearing loss was the major problem at follow-up occurring in two-thirds of children. Ten patients experienced progression or relapse, and 5 of 10 died. After a median follow-up of 5.6 years, the 5-year overall survival (OS) and event-free survival (EFS) were 91% (95% confidence interval [CI]: 84-96%) and 87% (95% CI: 78-92%), respectively. CONCLUSIONS: The 5-year OS and EFS of children <6 months of age affected by HB seem to be similar to those documented in the elder children. Dose reduction does not seem to jeopardize the long-term outcome and may explain the lower toxicity profile. Ototoxicity though appears as high as in the whole population of SIOPEL 2 and 3. The treatment for these children should be further explored in international studies, particularly focusing on prevention of hearing loss.
[Mh] Termos MeSH primário: Hepatoblastoma
Neoplasias Hepáticas
Neoplasias Pulmonares
[Mh] Termos MeSH secundário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Intervalo Livre de Doença
Feminino
Seguimentos
Hepatectomia
Hepatoblastoma/sangue
Hepatoblastoma/mortalidade
Hepatoblastoma/patologia
Hepatoblastoma/terapia
Seres Humanos
Lactente
Recém-Nascido
Neoplasias Hepáticas/sangue
Neoplasias Hepáticas/mortalidade
Neoplasias Hepáticas/patologia
Neoplasias Hepáticas/terapia
Transplante de Fígado
Neoplasias Pulmonares/sangue
Neoplasias Pulmonares/mortalidade
Neoplasias Pulmonares/secundário
Neoplasias Pulmonares/terapia
Masculino
Metástase Neoplásica
Taxa de Sobrevida
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; MULTICENTER STUDY
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1002/pbc.26791


  6 / 1582 MEDLINE  
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[PMID]:28892430
[Au] Autor:O'Neill AF; Towbin AJ; Krailo MD; Xia C; Gao Y; McCarville MB; Meyers RL; McGahren ED; Tiao GM; Dunn SP; Langham MR; Weldon CB; Finegold MJ; Ranganathan S; Furman WL; Malogolowkin M; Rodriguez-Galindo C; Katzenstein HM
[Ad] Endereço:Allison F. O'Neill and Christopher B. Weldon, Dana-Farber Cancer Institute, Boston Children's Hospital, and Harvard Medical School, Boston, MA; Alexander J. Towbin and Greg M. Tiao, Cincinnati Children's Hospital, Cincinnati, OH; Mark D. Krailo, University of Southern California Keck School of Medic
[Ti] Título:Characterization of Pulmonary Metastases in Children With Hepatoblastoma Treated on Children's Oncology Group Protocol AHEP0731 (The Treatment of Children With All Stages of Hepatoblastoma): A Report From the Children's Oncology Group.
[So] Source:J Clin Oncol;35(30):3465-3473, 2017 Oct 20.
[Is] ISSN:1527-7755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose To determine whether the pattern of lung nodules in children with metastatic hepatoblastoma (HB) correlates with outcome. Methods Thirty-two patients with metastatic HB were enrolled on Children's Oncology Group Protocol AHEP0731 and treated with vincristine and irinotecan (VI). Responders to VI received two additional cycles of VI intermixed with six cycles of cisplatin/fluorouracil/vincristine/doxorubicin (C5VD), and nonresponders received six cycles of C5VD alone. Patients were imaged after every two cycles and at the conclusion of therapy. All computed tomography scans and pathology reports were centrally reviewed, and information was collected regarding lung nodule number, size, laterality, timing of resolution, and pulmonary surgery. Results Among the 29 evaluable patients, only 31% met Response Evaluation Criteria in Solid Tumors (RECIST) for measurable metastatic disease. The presence of measurable disease by RECIST, the sum of nodule diameters greater than or equal to the cumulative cohort median size, bilateral disease, and ≥ 10 nodules were each associated with an increased risk for an event-free survival event ( P = .48, P = .08, P = .065, P = .03, respectively), with nodule number meeting statistical significance. Ten patients underwent pulmonary resection/metastasectomy at various time points, the benefit of which could not be determined because of small patient numbers. Conclusion Children with metastatic HB have a poor prognosis. Overall tumor burden may be an important prognostic factor for these patients. Lesions that fail to meet RECIST size criteria (ie, those < 10 mm) at diagnosis may contain viable tumor, whereas residual lesions at the end of therapy may constitute eradicated tumor/scar tissue. Patients may benefit from risk stratification on the basis of the burden of lung metastatic disease at diagnosis.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Hepatoblastoma/tratamento farmacológico
Neoplasias Hepáticas/tratamento farmacológico
Neoplasias Pulmonares/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Camptotecina/administração & dosagem
Camptotecina/análogos & derivados
Criança
Pré-Escolar
Cisplatino/administração & dosagem
Intervalo Livre de Doença
Doxorrubicina/administração & dosagem
Esquema de Medicação
Feminino
Fluoruracila/administração & dosagem
Hepatoblastoma/diagnóstico por imagem
Hepatoblastoma/patologia
Seres Humanos
Lactente
Neoplasias Hepáticas/diagnóstico por imagem
Neoplasias Hepáticas/patologia
Neoplasias Pulmonares/diagnóstico por imagem
Neoplasias Pulmonares/secundário
Masculino
Pneumonectomia/métodos
Prognóstico
Tomografia Computadorizada por Raios X
Resultado do Tratamento
Vincristina/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
5J49Q6B70F (Vincristine); 7673326042 (irinotecan); 80168379AG (Doxorubicin); Q20Q21Q62J (Cisplatin); U3P01618RT (Fluorouracil); XT3Z54Z28A (Camptothecin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170912
[St] Status:MEDLINE
[do] DOI:10.1200/JCO.2017.73.5654


  7 / 1582 MEDLINE  
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[PMID]:28821606
[Au] Autor:Peters JM
[Ad] Endereço:From the Department of Veterinary and Biomedical Sciences and The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802 jmp21@psu.edu.
[Ti] Título:Flipping a citrate switch on liver cancer cells.
[So] Source:J Biol Chem;292(33):13902-13903, 2017 Aug 18.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Energy homeostasis and oncogenic signaling are critical determinants of the growth of human liver cancer cells, providing a strong rationale to elucidate the regulatory mechanisms for these systems. A new study reports that loss of solute carrier family 13 member 5, which transports citrate across cell membranes, halts liver cancer cell growth by altering both energy production and mammalian target of rapamycin signaling in human liver cancer cell lines and in both an and model of liver tumors, suggesting a new target for liver cancer chemoprevention and/or chemotherapy.
[Mh] Termos MeSH primário: Ciclo do Ácido Cítrico
Hepatoblastoma/terapia
Neoplasias Hepáticas/terapia
Proteínas de Neoplasias/antagonistas & inibidores
Terapêutica com RNAi
Simportadores/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Metabolismo Energético
Hepatoblastoma/metabolismo
Hepatoblastoma/patologia
Seres Humanos
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Camundongos Nus
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Simportadores/genética
Simportadores/metabolismo
Carga Tumoral
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Neoplasm Proteins); 0 (SLC13A5 protein, human); 0 (Symporters)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170820
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.H117.783860


  8 / 1582 MEDLINE  
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[PMID]:28655760
[Au] Autor:Li Z; Li D; Choi EY; Lapidus R; Zhang L; Huang SM; Shapiro P; Wang H
[Ad] Endereço:From the Department of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, Maryland 21201.
[Ti] Título:Silencing of solute carrier family 13 member 5 disrupts energy homeostasis and inhibits proliferation of human hepatocarcinoma cells.
[So] Source:J Biol Chem;292(33):13890-13901, 2017 Aug 18.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The solute carrier family 13 member 5 (SLC13A5), a sodium-coupled citrate transporter, plays a key role in importing citrate from the circulation into liver cells. Recent evidence has revealed that SLC13A5 deletion protects mice from high-fat diet-induced hepatic steatosis and that mutation of the SLC13A5 orthologues in and promotes longevity. However, despite the emerging importance of SLC13A5 in energy homeostasis, whether perturbation of SLC13A5 affects the metabolism and malignancy of hepatocellular carcinoma is unknown. Here, we sought to determine whether SLC13A5 regulates hepatic energy homeostasis and proliferation of hepatoma cells. RNAi-mediated silencing of SLC13A5 expression in two human hepatoma cell lines, HepG2 and Huh7, profoundly suppressed cell proliferation and colony formation, and induced cell cycle arrest accompanied by increased expression of cyclin-dependent kinase inhibitor p21 and decreased expression of cyclin B1. Furthermore, such suppressive effects were also observed on the growth of HepG2 cell-derived xenografts expressing SLC13A5-shRNA in nude mice. Metabolically, knockdown of SLC13A5 in HepG2 and Huh7 cells was associated with a decrease in intracellular levels of citrate, the ratio of ATP/ADP, phospholipid content, and ATP citrate lyase expression. Moreover, both and assays demonstrated that SLC13A5 depletion promotes activation of the AMP-activated protein kinase, which was accompanied by deactivation of oncogenic mechanistic target of rapamycin signaling. Together, our findings expand the role of SLC13A5 from facilitating hepatic energy homeostasis to influencing hepatoma cell proliferation and suggest a potential role of SLC13A5 in the progression of human hepatocellular carcinoma.
[Mh] Termos MeSH primário: Metabolismo Energético
Hepatoblastoma/terapia
Neoplasias Hepáticas/terapia
Proteínas de Neoplasias/antagonistas & inibidores
Terapêutica com RNAi
Simportadores/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Proliferação Celular
Feminino
Regulação Neoplásica da Expressão Gênica
Hepatoblastoma/metabolismo
Hepatoblastoma/patologia
Seres Humanos
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Camundongos Nus
Proteínas de Neoplasias/agonistas
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Interferência de RNA
RNA Interferente Pequeno
Organismos Livres de Patógenos Específicos
Simportadores/genética
Simportadores/metabolismo
Carga Tumoral
Ensaio Tumoral de Célula-Tronco
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neoplasm Proteins); 0 (RNA, Small Interfering); 0 (SLC13A5 protein, human); 0 (Symporters)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.783860


  9 / 1582 MEDLINE  
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[PMID]:28562516
[Au] Autor:Goto H; Kitagawa N; Sekiguchi H; Miyagi Y; Keino D; Sugiyama M; Sarashina T; Miyagawa N; Yokosuka T; Hamanoue S; Iwasaki F; Shiomi M; Goto S; Tanaka Y
[Ad] Endereço:*Division of Hemato-Oncology and Regenerative Medicine †Department of Surgery ∥Division of Pathology, Kanagawa Children's Medical Center ‡Laboratory for Molecular Diagnostics, Kanagawa Cancer Center §Molecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
[Ti] Título:The Collagen Gel Droplet-embedded Culture Drug Sensitivity Test in Relapsed Hepatoblastoma.
[So] Source:J Pediatr Hematol Oncol;39(5):395-401, 2017 Jul.
[Is] ISSN:1536-3678
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There are few treatment options for patients with unresectable or refractory hepatoblastoma which has failed to respond to the standard treatment. The rarity of the disease and lack of experimental materials have hampered the development of new treatments. In this study, the collagen gel droplet-embedded culture drug sensitivity test was used to evaluate the effectiveness of the multikinase inhibitors sorafenib and sunitinib, and other drugs, in relapsed hepatoblastoma tumor tissues. Tumor samples from 6 patients with relapsed hepatoblastoma were tested for drug sensitivity by the collagen gel droplet-embedded culture drug sensitivity test; evaluable results were obtained from 5 of them. All samples were judged to be sensitive to sorafenib with a 50% growth inhibitory concentration (IC50) of 0.5 to 3.1 µg/mL. Sunitinib did not achieve IC50 in 2 of 3 samples within the tested concentration range based on clinically observed serum concentrations. In the drug combination assay using a hepatoblastoma cell line, sorafenib showed synergistic effects with SN-38, an active metabolite of irinotecan. Our results provide the basic science background warranting future clinical trials of a combination of sorafenib and irinotecan for relapsed or refractory hepatoblastoma.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Ensaios de Seleção de Medicamentos Antitumorais
Hepatoblastoma/tratamento farmacológico
Inibidores de Proteínas Quinases/uso terapêutico
[Mh] Termos MeSH secundário: Camptotecina/análogos & derivados
Camptotecina/uso terapêutico
Linhagem Celular Tumoral
Criança
Pré-Escolar
Colágeno
Sinergismo Farmacológico
Feminino
Seres Humanos
Indóis/uso terapêutico
Lactente
Concentração Inibidora 50
Masculino
Niacinamida/análogos & derivados
Niacinamida/uso terapêutico
Compostos de Fenilureia/uso terapêutico
Pirróis/uso terapêutico
Recidiva
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Indoles); 0 (Phenylurea Compounds); 0 (Protein Kinase Inhibitors); 0 (Pyrroles); 25X51I8RD4 (Niacinamide); 7673326042 (irinotecan); 9007-34-5 (Collagen); 9ZOQ3TZI87 (sorafenib); V99T50803M (sunitinib); XT3Z54Z28A (Camptothecin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170601
[St] Status:MEDLINE
[do] DOI:10.1097/MPH.0000000000000865


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[PMID]:28535186
[Au] Autor:Valanejad L; Lewis K; Wright M; Jiang Y; D'Souza A; Karns R; Sheridan R; Gupta A; Bove K; Witte D; Geller J; Tiao G; Nelson DL; Timchenko L; Timchenko N
[Ad] Endereço:Departments of Surgery.
[Ti] Título:FXR-Gankyrin axis is involved in development of pediatric liver cancer.
[So] Source:Carcinogenesis;38(7):738-747, 2017 Jul 01.
[Is] ISSN:1460-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The development of hepatoblastoma (HBL) is associated with failure of hepatic stem cells (HSC) to differentiate into hepatocytes. Despite intensive investigations, mechanisms of the failure of HSC to differentiate are not known. We found that oncogene Gankyrin (Gank) is involved in the inhibition of differentiation of HSC via triggering degradation of tumor suppressor proteins (TSPs) Rb, p53, C/EBPα and HNF4α. Our data show that the activation of a repressor of Gank, farnesoid X receptor, FXR, after initiation of liver cancer by Diethylnitrosamine (DEN) prevents the development of liver cancer by inhibiting Gank and rescuing tumor suppressor proteins. We next analyzed FXR-Gank-Tumor suppressor pathways in a large cohort of HBL patients which include 6 controls and 53 HBL samples. Systemic analysis of these samples and RNA-Seq approach revealed that the FXR-Gank axis is activated; markers of hepatic stem cells are dramatically elevated and hepatocyte markers are reduced in HBL samples. In the course of these studies, we found that RNA binding protein CUGBP1 is a new tumor suppressor protein which is reduced in all HBL samples. Therefore, we generated CUGBP1 KO mice and examined HBL signatures in the liver of these mice. Micro-array studies revealed that the HBL-specific molecular signature is developed in livers of CUGBP1 KO mice at very early ages. Thus, we conclude that FXR-Gank-TSPs-Stem cells pathway is a key determinant of liver cancer in animal models and in pediatric liver cancer. Our data provide a strong basis for development of FXR-Gank-based therapy for treatment of patients with hepatoblastoma.
[Mh] Termos MeSH primário: Proteínas CELF1/genética
Hepatoblastoma/genética
Neoplasias Hepáticas/genética
Complexo de Endopeptidases do Proteassoma/genética
Proteínas Proto-Oncogênicas/genética
Receptores Citoplasmáticos e Nucleares/genética
[Mh] Termos MeSH secundário: Animais
Proteínas CELF1/biossíntese
Diferenciação Celular/genética
Linhagem Celular Tumoral
Dietilnitrosamina/toxicidade
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Hepatoblastoma/induzido quimicamente
Hepatoblastoma/patologia
Hepatócitos/metabolismo
Hepatócitos/patologia
Seres Humanos
Fígado/efeitos dos fármacos
Fígado/patologia
Neoplasias Hepáticas/induzido quimicamente
Neoplasias Hepáticas/patologia
Camundongos
Camundongos Knockout
Proteínas de Neoplasias/genética
Estadiamento de Neoplasias
Pediatria
Receptores Citoplasmáticos e Nucleares/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CELF1 Protein); 0 (CELF1 protein, human); 0 (Neoplasm Proteins); 0 (PSMD10 protein, human); 0 (Proto-Oncogene Proteins); 0 (Receptors, Cytoplasmic and Nuclear); 0 (farnesoid X-activated receptor); 3IQ78TTX1A (Diethylnitrosamine); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1093/carcin/bgx050



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