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Pesquisa : C04.697.045 [Categoria DeCS]
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[PMID]:27741326
[Au] Autor:Ahmed HH; Shousha WG; El-Mezayen HA; El-Toumy SA; Sayed AH; Ramadan AR
[Ad] Endereço:Hormones Department, National Research Centre, Dokki, Giza, Egypt.
[Ti] Título:Biochemical and molecular evidences for the antitumor potential of Ginkgo biloba leaves extract in rodents.
[So] Source:Acta Biochim Pol;64(1):25-33, 2017.
[Is] ISSN:1734-154X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Hepatocellular carcinoma (HCC) is one of the deadliest primary cancers, with a 5-year survival rate of 10% or less. This study was undertaken to elucidate the underlying biochemical and molecular mechanisms in favor of N-nitrosodiethylamine-induced hepatocellular carcinoma. Furthermore, the aim of this work was extended to explore the efficacy of Ginkgo biloba leaves extract in deterioration of HCC in rats. In the current study, HCC group experienced significant downregulation of ING-3 gene expression and upregulation of Foxp-1 gene expression in liver. Treatment of HCC groups with Ginkgo biloba leaves extract resulted in upregulation of ING-3 and downregulation of Foxp-1 gene expression in liver. In addition, there was significant increase in serum alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA) and glypican-3 (GPC-3) levels in HCC group versus the negative control group. In contrast, the groups with HCC subjected to either high or low dose of Ginkgo biloba leaves extract elicited significant reduction (P<0.05) of AFP, CEA and GPC-3 in serum compared to the untreated HCC rats. Besides, histological examination of liver tissue sections of rats in HCC group revealed typical anaplasia. Interestingly, treatment with Ginkgo biloba leaves extract elicited marked improvement in the histological feature of liver tissue in HCC groups. In conclusion, this research indicated that the carcinogenic potency of N-nitrosodiethylamine targeted multiple systems on the cellular and molecular levels. In addition, the results of the current study shed light on the promising anticancer activity of Ginkgo biloba leaves extract in treatment of hepatocellular carcinoma induced chemically in the experimental model through its apoptotic and antiproliferative properties.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/tratamento farmacológico
Ginkgo biloba
Extratos Vegetais/farmacologia
[Mh] Termos MeSH secundário: Anaplasia/tratamento farmacológico
Animais
Carcinoma Hepatocelular/induzido quimicamente
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Dietilnitrosamina
Regulação da Expressão Gênica/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Neoplasias Hepáticas
Metabolismo/efeitos dos fármacos
Extratos Vegetais/uso terapêutico
Folhas de Planta/química
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plant Extracts); 3IQ78TTX1A (Diethylnitrosamine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170417
[Lr] Data última revisão:
170417
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161015
[St] Status:MEDLINE
[do] DOI:10.18388/abp.2015_1200


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[PMID]:27473009
[Au] Autor:Oue T; Koshinaga T; Takimoto T; Okita H; Tanaka Y; Nozaki M; Haruta M; Kaneko Y; Fukuzawa M; Renal Tumor Committee of the Japanese Children's Cancer Group
[Ad] Endereço:Department of Pediatric Surgery, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo, 63-8501, Japan. ta-oue@hyo-med.ac.jp.
[Ti] Título:Anaplastic histology Wilms' tumors registered to the Japan Wilms' Tumor Study Group are less aggressive than that in the National Wilms' Tumor Study 5.
[So] Source:Pediatr Surg Int;32(9):851-5, 2016 Sep.
[Is] ISSN:1437-9813
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To evaluate the clinical features and treatment results of anaplastic histology (AH) Wilms' tumor (WT) patients registered in the Japan Wilms' Tumor Study (JWiTS) group to elucidate the clinical characteristics of AH in the Japanese population. PATIENTS AND METHODS: Of 344 WT patients who were enrolled in JWiTS between 1995 and 2013, 17 had AH. Treatment using the JWiTS protocols was similar to the fifth National Wilms' Tumor Study 5 (NWTS-5) protocols. Clinical characteristics and mutation status of TP53 gene were evaluated and compared with those in NWST-5 study. RESULTS: AH incidences in JWiTS were 4.9 %, lower than that in NWTS-5. Seven tumors had focal AH and 10 had diffuse AH. Clinical stages of AH patients were stage I in seven, stage II in three, stage III in five, stage IV in one and unknown in one. Four-year event-free survival and overall survival rates were 90.9 and 86.7 %, respectively. Two patients with diffuse AH and none with focal AH had TP53 mutation. CONCLUSION: Japanese patients presented with higher incidence, earlier stages and may have better outcomes than American patients, indicating a possible biological heterogeneity of AH WT. Further analysis is necessary to elucidate the different characteristic of AH WT between Japanese and American populations.
[Mh] Termos MeSH primário: Neoplasias Renais/patologia
Rim/patologia
Tumor de Wilms/patologia
[Mh] Termos MeSH secundário: Anaplasia
Pré-Escolar
Feminino
Seres Humanos
Lactente
Japão/epidemiologia
Neoplasias Renais/mortalidade
Masculino
Estadiamento de Neoplasias
Sistema de Registros
Proteína Supressora de Tumor p53/genética
Tumor de Wilms/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160731
[St] Status:MEDLINE
[do] DOI:10.1007/s00383-016-3929-7


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[PMID]:26795126
[Au] Autor:Wang Y; Wang K; Wang J; Li S; Ma J; Dai J; Jiang T
[Ad] Endereço:Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
[Ti] Título:Identifying the association between contrast enhancement pattern, surgical resection, and prognosis in anaplastic glioma patients.
[So] Source:Neuroradiology;58(4):367-74, 2016 Apr.
[Is] ISSN:1432-1920
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Contrast enhancement observable on magnetic resonance (MR) images reflects the destructive features of malignant gliomas. This study aimed to investigate the relationship between radiologic patterns of tumor enhancement, extent of resection, and prognosis in patients with anaplastic gliomas (AGs). METHODS: Clinical data from 268 patients with histologically confirmed AGs were retrospectively analyzed. Contrast enhancement patterns were classified based on preoperative T1-contrast MR images. Univariate and multivariate analyses were performed to evaluate the prognostic value of MR enhancement patterns on progression-free survival (PFS) and overall survival (OS). RESULTS: The pattern of tumor contrast enhancement was associated with the extent of surgical resection in AGs. A gross total resection was more likely to be achieved for AGs with focal enhancement than those with diffuse (p = 0.001) or ring-like (p = 0.024) enhancement. Additionally, patients with focal-enhanced AGs had a significantly longer PFS and OS than those with diffuse (log-rank, p = 0.025 and p = 0.031, respectively) or ring-like (log-rank, p = 0.008 and p = 0.011, respectively) enhanced AGs. Furthermore, multivariate analysis identified the pattern of tumor enhancement as a significant predictor of PFS (p = 0.016, hazard ratio [HR] = 1.485) and OS (p = 0.030, HR = 1.446). CONCLUSION: Our results suggested that the contrast enhancement pattern on preoperative MR images was associated with the extent of resection and predictive of survival outcomes in AG patients.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/diagnóstico por imagem
Neoplasias Encefálicas/cirurgia
Glioma/diagnóstico por imagem
Glioma/cirurgia
Imagem por Ressonância Magnética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Anaplasia
Neoplasias Encefálicas/mortalidade
Meios de Contraste
Feminino
Gadolínio DTPA
Glioma/mortalidade
Seres Humanos
Masculino
Meia-Idade
Estudos Retrospectivos
Taxa de Sobrevida
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Contrast Media); K2I13DR72L (Gadolinium DTPA)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160123
[St] Status:MEDLINE
[do] DOI:10.1007/s00234-016-1640-y


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[PMID]:26710834
[Au] Autor:Jain M
[Ad] Endereço:Department of Oral Pathology and Microbiology, Peoples Dental Academy, Bhopal 462037, Madhya Pradesh, India.
[Ti] Título:An overview on "cellular cannibalism" with special reference to oral squamous cell carcinoma.
[So] Source:Exp Oncol;37(4):242-5, 2015 Dec.
[Is] ISSN:1812-9269
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:Cellular cannibalism has been defined as a large cell engulfing a slightly smaller one within its cytoplasm. It has been described in various cancers like bladder cancer, breast cancer, lung cancer, gastric cancer, oral squamous cell carcinoma. Cellular cannibalism has been well correlated with anaplasia, tumor aggressiveness, grading and metastatic potential. Present review focuses on significance of cannibalism in relation to cancer with special emphasis on oral squamous cell carcinoma.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/patologia
Citofagocitose/fisiologia
Neoplasias Bucais/patologia
[Mh] Termos MeSH secundário: Anaplasia/patologia
Seres Humanos
Metástase Neoplásica/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1611
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151230
[St] Status:MEDLINE


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[PMID]:26544690
[Au] Autor:Shuda M; Guastafierro A; Geng X; Shuda Y; Ostrowski SM; Lukianov S; Jenkins FJ; Honda K; Maricich SM; Moore PS; Chang Y
[Ad] Endereço:Cancer Virology Program, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
[Ti] Título:Merkel Cell Polyomavirus Small T Antigen Induces Cancer and Embryonic Merkel Cell Proliferation in a Transgenic Mouse Model.
[So] Source:PLoS One;10(11):e0142329, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Merkel cell polyomavirus (MCV) causes the majority of human Merkel cell carcinomas (MCC) and encodes a small T (sT) antigen that transforms immortalized rodent fibroblasts in vitro. To develop a mouse model for MCV sT-induced carcinogenesis, we generated transgenic mice with a flox-stop-flox MCV sT sequence homologously recombined at the ROSA locus (ROSAsT), allowing Cre-mediated, conditional MCV sT expression. Standard tamoxifen (TMX) administration to adult UbcCreERT2; ROSAsT mice, in which Cre is ubiquitously expressed, resulted in MCV sT expression in multiple organs that was uniformly lethal within 5 days. Conversely, most adult UbcCreERT2; ROSAsT mice survived low-dose tamoxifen administration but developed ear lobe dermal hyperkeratosis and hypergranulosis. Simultaneous MCV sT expression and conditional homozygous p53 deletion generated multi-focal, poorly-differentiated, highly anaplastic tumors in the spleens and livers of mice after 60 days of TMX treatment. Mouse embryonic fibroblasts from these mice induced to express MCV sT exhibited anchorage-independent cell growth. To examine Merkel cell pathology, MCV sT expression was also induced during mid-embryogenesis in Merkel cells of Atoh1CreERT2/+; ROSAsT mice, which lead to significantly increased Merkel cell numbers in touch domes at late embryonic ages that normalized postnatally. Tamoxifen administration to adult Atoh1CreERT2/+; ROSAsT and Atoh1CreERT2/+; ROSAsT; p53flox/flox mice had no effects on Merkel cell numbers and did not induce tumor formation. Taken together, these results show that MCV sT stimulates progenitor Merkel cell proliferation in embryonic mice and is a bona fide viral oncoprotein that induces full cancer cell transformation in the p53-null setting.
[Mh] Termos MeSH primário: Antígenos Virais de Tumores/genética
Carcinoma de Célula de Merkel/patologia
Transformação Celular Viral
Embrião de Mamíferos/patologia
Células de Merkel/patologia
Poliomavírus das Células de Merkel/fisiologia
Neoplasias Cutâneas/patologia
[Mh] Termos MeSH secundário: Anaplasia
Animais
Carcinoma de Célula de Merkel/virologia
Contagem de Células
Diferenciação Celular
Linhagem Celular Tumoral
Proliferação Celular
Modelos Animais de Doenças
Feminino
Seres Humanos
Fígado/patologia
Masculino
Poliomavírus das Células de Merkel/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Gravidez
Neoplasias Cutâneas/virologia
Baço/patologia
Proteína Supressora de Tumor p53/deficiência
Proteína Supressora de Tumor p53/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antigens, Viral, Tumor); 0 (Tumor Suppressor Protein p53)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151107
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0142329


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[PMID]:26447238
[Au] Autor:Kumar G; Ahluwalia J
[Ti] Título:"Multiple forms" of a myeloma.
[So] Source:Blood;126(5):692, 2015 Jul 30.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Mieloma Múltiplo/patologia
[Mh] Termos MeSH secundário: Anaplasia
Medula Óssea/imunologia
Medula Óssea/patologia
Feminino
Seres Humanos
Imunoglobulina G/sangue
Imunoglobulina G/metabolismo
Cadeias kappa de Imunoglobulina/sangue
Cadeias kappa de Imunoglobulina/metabolismo
Meia-Idade
Mieloma Múltiplo/diagnóstico
Mieloma Múltiplo/imunologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulin G); 0 (Immunoglobulin kappa-Chains)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:151007
[Lr] Data última revisão:
151007
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:151009
[St] Status:MEDLINE


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[PMID]:26276031
[Au] Autor:Krajewski KL; Matschke J; Humke N; Börm W; Westphal M; Schmidt NO
[Ad] Endereço:Department of Neurosurgery, University Medical Center Hamburg-Eppendorf, Martinistr. 52, 20246, Hamburg, Germany.
[Ti] Título:A 19-Year-Old Male with an Intraventricular Tumor.
[So] Source:Brain Pathol;25(5):657-8, 2015 Sep.
[Is] ISSN:1750-3639
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Mh] Termos MeSH primário: Neoplasias do Ventrículo Cerebral/patologia
Hemangiopericitoma/patologia
Tumores Fibrosos Solitários/patologia
[Mh] Termos MeSH secundário: Adulto
Anaplasia
Seres Humanos
Masculino
Neoplasias da Coluna Vertebral/patologia
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1605
[Cu] Atualização por classe:150815
[Lr] Data última revisão:
150815
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150816
[St] Status:MEDLINE
[do] DOI:10.1111/bpa.12287


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[PMID]:26252838
[Au] Autor:Hayashi Y; Osanai M; Lee GH
[Ad] Endereço:Department of Pathology, Kochi University School of Medicine, Kohasu, Oko-cho, Nankoku, Kochi 783-8505, Japan.
[Ti] Título:NOTCH2 signaling confers immature morphology and aggressiveness in human hepatocellular carcinoma cells.
[So] Source:Oncol Rep;34(4):1650-8, 2015 Oct.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:The NOTCH family of membranous receptors plays key roles during development and carcinogenesis. Since NOTCH2, yet not NOTCH1 has been shown essential for murine hepatogenesis, NOTCH2 rather than NOTCH1 may be more relevant to human hepatocarcinogenesis; however, no previous studies have supported this hypothesis. We therefore assessed the role of NOTCH2 in human hepatocellular carcinoma (HCC) by immunohistochemistry and cell culture. Immunohistochemically, 19% of primary HCCs showed nuclear staining for NOTCH2, indicating activated NOTCH2 signaling. NOTCH2-positive HCCs were on average in more advanced clinical stages, and exhibited more immature cellular morphology, i.e. higher nuclear-cytoplasmic ratios and nuclear densities. Such features were not evident in NOTCH1­positive HCCs. In human HCC cell lines, abundant NOTCH2 expression was associated with anaplasia, represented by loss of E-cadherin. When NOTCH2 signaling was stably downregulated in HLF cells, an anaplastic HCC cell line, the cells were attenuated in potential for in vitro invasiveness and migration, as well as in vivo tumorigenicity accompanied by histological maturation. Generally, inverse results were obtained for a differentiated HCC cell line, Huh7, manipulated to overexpress activated NOTCH2. These findings suggested that the NOTCH2 signaling may confer aggressive behavior and immature morphology in human HCC cells.
[Mh] Termos MeSH primário: Carcinogênese/genética
Carcinoma Hepatocelular/genética
Neoplasias Hepáticas/genética
Receptor Notch2/biossíntese
[Mh] Termos MeSH secundário: Anaplasia/genética
Anaplasia/patologia
Animais
Carcinoma Hepatocelular/patologia
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Neoplasias Hepáticas/patologia
Camundongos
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Receptor Notch1/biossíntese
Receptor Notch1/genética
Receptor Notch2/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (NOTCH1 protein, human); 0 (NOTCH2 protein, human); 0 (Receptor, Notch1); 0 (Receptor, Notch2)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:151201
[Lr] Data última revisão:
151201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150808
[St] Status:MEDLINE
[do] DOI:10.3892/or.2015.4171


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[PMID]:25921241
[Au] Autor:Sidhom I; El Nadi E; Taha H; Elkinaai N; Zaghloul MS; Younes A; Labib R; Sabry M
[Ad] Endereço:Pediatric Oncology Department, Children Cancer Hospital Egypt (CCHE), National Cancer Institute, Cairo University, Egypt.
[Ti] Título:Clinical significance of anaplasia in childhood rhabdomyosarcoma.
[So] Source:J Egypt Natl Canc Inst;27(2):83-9, 2015 Jun.
[Is] ISSN:1110-0362
[Cp] País de publicação:Egypt
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The presence of anaplastic features has been known to correlate with poor clinical outcome in various pediatric malignancies, including Wilms tumor and medulloblastoma but not in rhabdomyosarcoma. AIM: Aim was to study the frequency of anaplasia at presentation in childhood rhabdomyosarcoma and its relationship to clinical and pathological characteristics as well as to outcome. PATIENTS AND METHODS: Anaplasia was retrospectively assessed in 105 consecutive pediatric rhabdomyosarcoma patients who were registered at the Children's Cancer Hospital in Egypt (CCHE) during the period from July 2007 till the end of May 2010. RESULTS: Anaplasia was diagnosed in 18 patients (17.1%), focal in 10 (9.5%) and diffuse in 8 (7.6%). The distribution of anaplasia was found to be more common in older patients having age⩾10 years. Also it was more likely to occur in the high risk group and in tumors with unfavorable histology (alveolar subtype), and stage IV. The 3-year failure free survival rates for patients with and without anaplasia were 27.8±10.6% and 53.4±5.8%, respectively (p=0.014) and the 3-year overall survival rates were 35.3±11.6% and 61±6%, respectively (p=0.019). CONCLUSIONS: The frequency of anaplasia in pediatric patients with rhabdomyosarcoma in our study was 17.1%. The presence of anaplasia had statistically significant worse clinical outcome.
[Mh] Termos MeSH primário: Anaplasia/patologia
Rabdomiossarcoma/diagnóstico
Rabdomiossarcoma/patologia
[Mh] Termos MeSH secundário: Adolescente
Fatores Etários
Criança
Pré-Escolar
Progressão da Doença
Egito
Feminino
Seguimentos
Seres Humanos
Lactente
Masculino
Gradação de Tumores
Metástase Neoplásica
Estadiamento de Neoplasias
Prognóstico
Sistema de Registros
Estudos Retrospectivos
Rabdomiossarcoma/mortalidade
Rabdomiossarcoma/terapia
Análise de Sobrevida
Resultado do Tratamento
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1602
[Cu] Atualização por classe:150513
[Lr] Data última revisão:
150513
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150430
[St] Status:MEDLINE


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[PMID]:25818639
[Au] Autor:Yoshida M; Okita H; Tanimoto T; Bitoh Y; Fukuzawa H; Yokoi A; Kozaki A; Kawasaki K; Akasaka Y
[Ad] Endereço:Department of Pathology, Kobe Children's Hospital, Kobe, Japan.
[Ti] Título:Congenital mesoblastic nephroma with focal anaplastic lesion.
[So] Source:Pathol Int;65(9):507-9, 2015 Sep.
[Is] ISSN:1440-1827
[Cp] País de publicação:Australia
[La] Idioma:eng
[Mh] Termos MeSH primário: Neoplasias Renais/patologia
Nefroma Mesoblástico/patologia
Proteínas de Fusão Oncogênicas/genética
[Mh] Termos MeSH secundário: Anaplasia
Seres Humanos
Lactente
Neoplasias Renais/congênito
Neoplasias Renais/genética
Masculino
Nefroma Mesoblástico/congênito
Nefroma Mesoblástico/genética
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (ETV6-NTRK3 fusion protein, human); 0 (Oncogene Proteins, Fusion)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:150903
[Lr] Data última revisão:
150903
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150331
[St] Status:MEDLINE
[do] DOI:10.1111/pin.12293



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