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[PMID]:29023728
[Au] Autor:Morosi L; Giordano S; Falcetta F; Frapolli R; Licandro SA; Matteo C; Zucchetti M; Ubezio P; Erba E; Visentin S; D'Incalci M; Davoli E
[Ad] Endereço:Department of Oncology, Cancer Pharmacology Laboratory, IRCCS Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy.
[Ti] Título:Application of 3D Mass Spectrometry Imaging to TKIs.
[So] Source:Clin Pharmacol Ther;102(5):748-751, 2017 Nov.
[Is] ISSN:1532-6535
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mass spectrometry imaging (MSI) allows visualization of endogenous and exogenous compound in tissue sections based on its molecular mass. The 3D reconstruction by MSI provides a more informative description of the tumor drug distribution compared to the high-performance liquid chromatography method, highlighting the heterogeneity of intratumor drug concentration. This additional information can be important in understanding chemoresistance to target agents. Here, we present the 3D visualization of the tyrosine kinase inhibitor (TKI), imatinib, in a xenograft model of resistant malignant pleural mesothelioma.
[Mh] Termos MeSH primário: Imagem Tridimensional/métodos
Mesilato de Imatinib/administração & dosagem
Espectrometria de Massas/métodos
Neoplasias Mesoteliais/tratamento farmacológico
Neoplasias Pleurais/tratamento farmacológico
Inibidores de Proteínas Quinases/administração & dosagem
Ensaios Antitumorais Modelo de Xenoenxerto/métodos
[Mh] Termos MeSH secundário: Animais
Ouro/administração & dosagem
Ouro/metabolismo
Seres Humanos
Mesilato de Imatinib/metabolismo
Nanopartículas Metálicas/administração & dosagem
Camundongos
Neoplasias Mesoteliais/diagnóstico por imagem
Neoplasias Mesoteliais/metabolismo
Neoplasias Pleurais/diagnóstico por imagem
Neoplasias Pleurais/metabolismo
Inibidores de Proteínas Quinases/metabolismo
Distribuição Tecidual/efeitos dos fármacos
Distribuição Tecidual/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 7440-57-5 (Gold); 8A1O1M485B (Imatinib Mesylate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1002/cpt.786


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[PMID]:27903930
[Au] Autor:Lu Y; Milchgrub S; Khatri G; Gopal P
[Ad] Endereço:1 University of California Irvine Medical Center, Irvine, CA, USA.
[Ti] Título:Metachronous Uterine Endometrioid Adenocarcinoma and Peritoneal Mesothelioma in Lynch Syndrome: A Case Report.
[So] Source:Int J Surg Pathol;25(3):253-257, 2017 May.
[Is] ISSN:1940-2465
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lynch syndrome is a hereditary disease with germline mutation in a DNA mismatch repair gene, most often presenting with colorectal and/or endometrial carcinomas; however, the spectrum of Lynch syndrome-associated tumors is expanding. In this article, we report a case of a primary peritoneal epithelioid mesothelioma that developed in a Lynch syndrome patient 10 months after diagnosis of uterine endometrioid adenocarcinoma. To our knowledge, this is the first reported case of a Lynch syndrome patient with metachronous uterine endometrioid adenocarcinoma and primary peritoneal mesothelioma.
[Mh] Termos MeSH primário: Carcinoma Endometrioide/patologia
Síndrome de Lynch II/patologia
Neoplasias Mesoteliais/patologia
Neoplasias Peritoneais/patologia
Neoplasias Uterinas/patologia
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/análise
Carcinoma Endometrioide/etiologia
Proteínas de Ligação a DNA/genética
Feminino
Mutação em Linhagem Germinativa
Seres Humanos
Imuno-Histoquímica
Síndrome de Lynch II/complicações
Síndrome de Lynch II/genética
Meia-Idade
Neoplasias Mesoteliais/etiologia
Neoplasias Peritoneais/etiologia
Neoplasias Uterinas/etiologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (DNA-Binding Proteins); 0 (G-T mismatch-binding protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161202
[St] Status:MEDLINE
[do] DOI:10.1177/1066896916680745


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[PMID]:27806842
[Au] Autor:Pandita A; Osipov V
[Ad] Endereço:Department of Anatomic Pathology, Wellington Regional Hospital, New Zealand. Electronic address: panditaarchana@yahoo.com.
[Ti] Título:Mesothelial cell deposits in lymph nodes-a diagnostic pitfall.
[So] Source:Ann Diagn Pathol;25:31-32, 2016 Dec.
[Is] ISSN:1532-8198
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Células Epiteliais/citologia
Epitélio/patologia
Linfonodos/patologia
Linfonodos/cirurgia
Neoplasias Mesoteliais/cirurgia
[Mh] Termos MeSH secundário: Adulto
Seres Humanos
Masculino
Neoplasias Mesoteliais/diagnóstico
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170306
[Lr] Data última revisão:
170306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161104
[St] Status:MEDLINE


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[PMID]:27088640
[Au] Autor:Jiang L; Chew SH; Nakamura K; Ohara Y; Akatsuka S; Toyokuni S
[Ad] Endereço:Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Japan.
[Ti] Título:Dual preventive benefits of iron elimination by desferal in asbestos-induced mesothelial carcinogenesis.
[So] Source:Cancer Sci;107(7):908-15, 2016 Jul.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Asbestos-induced mesothelial carcinogenesis is currently a profound social issue due to its extremely long incubation period and high mortality rate. Therefore, procedures to prevent malignant mesothelioma in people already exposed to asbestos are important. In previous experiments, we established an asbestos-induced rat peritoneal mesothelioma model, which revealed that local iron overload is a major cause of pathogenesis and that the induced genetic alterations are similar to human counterparts. Furthermore, we showed that oral administration of deferasirox modified the histology from sarcomatoid to the more favorable epithelioid subtype. Here, we used i.p. administration of desferal to evaluate its effects on asbestos-induced peritoneal inflammation and iron deposition, as well as oxidative stress. Nitrilotriacetate was used to promote an iron-catalyzed Fenton reaction as a positive control. Desferal significantly decreased peritoneal fibrosis, iron deposition, and nuclear 8-hydroxy-2'-deoxyguanosine levels in mesothelial cells, whereas nitrilotriacetate significantly increased all of them. Desferal was more effective in rat peritoneal mesothelial cells to counteract asbestos-induced cytotoxicity than in murine macrophages (RAW264.7). Furthermore, rat sarcomatoid mesothelioma cells were more dependent on iron for proliferation than rat peritoneal mesothelial cells. Because inflammogenicity of a fiber is proportionally associated with subsequent mesothelial carcinogenesis, iron elimination from the mesothelial environment can confer dual merits for preventing asbestos-induced mesothelial carcinogenesis by suppressing inflammation and mesothelial proliferation simultaneously.
[Mh] Termos MeSH primário: Asbestos/toxicidade
Carcinogênese/efeitos dos fármacos
Desferroxamina/farmacologia
Quelantes de Ferro/farmacologia
Ferro/deficiência
Neoplasias Mesoteliais/induzido quimicamente
Neoplasias Mesoteliais/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Peso Corporal
Proliferação Celular/efeitos dos fármacos
Desoxiguanosina/análogos & derivados
Desoxiguanosina/metabolismo
Ferro/química
Ferro/metabolismo
Macrófagos/efeitos dos fármacos
Masculino
Neoplasias Mesoteliais/metabolismo
Neoplasias Mesoteliais/patologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Iron Chelating Agents); 1332-21-4 (Asbestos); 88847-89-6 (8-oxo-7-hydrodeoxyguanosine); E1UOL152H7 (Iron); G9481N71RO (Deoxyguanosine); J06Y7MXW4D (Deferoxamine)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170425
[Lr] Data última revisão:
170425
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160419
[St] Status:MEDLINE
[do] DOI:10.1111/cas.12947


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[PMID]:26050293
[Au] Autor:Prudnick C; Turnbull J; Jarosz S; Hofeldt M; Richmond B
[Ti] Título:Benign mesothelial mesenteric cyst: case report and literature review.
[So] Source:W V Med J;111(3):20-1, 2015 May-Jun.
[Is] ISSN:0043-3284
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A rare case of a benign mesothelial cyst arising from the mesentery of the descending colon is presented. A 73 year old female presented with an asymptomatic mesenteric cyst on CT scan. Colonoscopy revealed extrinsic compression of the descending colon. Surgical resection of the cyst necessitated partial colon resection due to the adherent nature of the cyst to the colon and its mesentery. The details of the case are presented as well as a brief review of the relevant literature.
[Mh] Termos MeSH primário: Cisto Mesentérico/patologia
Neoplasias Mesoteliais/patologia
[Mh] Termos MeSH secundário: Idoso
Feminino
Seres Humanos
Cisto Mesentérico/cirurgia
Neoplasias Mesoteliais/cirurgia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1506
[Cu] Atualização por classe:150608
[Lr] Data última revisão:
150608
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150609
[St] Status:MEDLINE


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[PMID]:25572813
[Au] Autor:de Lima VA; Sørensen JB
[Ad] Endereço:Department of Oncology, Finsen Centre/National University Hospital, Rigshospitalet/Copenhagen University Hospital, 9 Blegdamsvej, 2100, Copenhagen Ø, Denmark, viniciusablima@gmail.com.
[Ti] Título:Third-line chemotherapy with carboplatin, gemcitabine and liposomised doxorubicin for malignant pleural mesothelioma.
[So] Source:Med Oncol;32(2):458, 2015 Feb.
[Is] ISSN:1559-131X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There is no well-defined standard third-line chemotherapy for advanced malignant pleural mesothelioma (MPM). However, combination of carboplatin, liposomised doxorubicin (Caelyx) and gemcitabine (CCG regimen) has revealed noteworthy activity when used as first-line treatment. The aim of this study is to assess efficacy and toxicity profile for patients with MPM receiving CCG regimen as a third-line treatment. Carboplatin (AUC 5), Caelyx (30 mg/m(2)) and Gemcitabine (1,000 mg/m(2)) day 1, together with Gemcitabine (800 mg/m(2)) day 8, were given in up to six cycles. Patients were unresectable, PS 0-2, and had previously received a first-line platinum-based regimen and either vinorelbine or pemetrexed as second line. Response to treatment was assessed by CT scan using Modified RECIST criteria for mesothelioma. Forty-three patients were treated between 2010 and 2014. Median age was 67 years (47-82), 72 % males, and 79 % had previous asbestos exposure. Ninety per cent had PS 0-1, 58 % had epitheloid subtype and 63 % IMIG stage IV. First-line treatment was platinum and pemetrexed in 42 cases. Second-line treatment was vinorelbine in 42 cases and pemetrexed in one patient. Median lead time from cessation of second-line treatment to start of third CCG was 1 month. Twenty-eight per cent of the patients received six cycles, while treatment was postponed due to toxicities, mainly haematological, in 56 % of cases. No toxicity-related deaths occurred. Partial response (PR) occurred in 14 %, and disease control rate (DCR) was 60 %. Medians of overall survival (OS) from diagnosis and from start of CCG treatment were 25.2 months (18.4-31.5 months) and 6.8 months (5.4-8.4 months), respectively. Progression-free survival (PFS) was 4.1 months (1.7-4.5 months). Third-line CCG revealed a noteworthy efficacy with a DCR of 60.4 %. It was, however, associated with considerable haematological toxicity. Less toxic and more active treatment options are clearly needed.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Mesotelioma/tratamento farmacológico
Neoplasias Mesoteliais/tratamento farmacológico
Neoplasias Pleurais/tratamento farmacológico
Terapia de Salvação/métodos
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Carboplatina/administração & dosagem
Desoxicitidina/administração & dosagem
Desoxicitidina/análogos & derivados
Intervalo Livre de Doença
Doxorrubicina/administração & dosagem
Doxorrubicina/análogos & derivados
Feminino
Seres Humanos
Estimativa de Kaplan-Meier
Masculino
Mesotelioma/mortalidade
Meia-Idade
Neoplasias Mesoteliais/mortalidade
Neoplasias Pleurais/mortalidade
Polietilenoglicóis/administração & dosagem
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (liposomal doxorubicin); 0W860991D6 (Deoxycytidine); 30IQX730WE (Polyethylene Glycols); 80168379AG (Doxorubicin); B76N6SBZ8R (gemcitabine); BG3F62OND5 (Carboplatin)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150110
[St] Status:MEDLINE
[do] DOI:10.1007/s12032-014-0458-x


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[PMID]:25205731
[Au] Autor:Bruney L; Conley KC; Moss NM; Liu Y; Stack MS
[Ti] Título:Membrane-type I matrix metalloproteinase-dependent ectodomain shedding of mucin16/ CA-125 on ovarian cancer cells modulates adhesion and invasion of peritoneal mesothelium.
[So] Source:Biol Chem;395(10):1221-31, 2014 Oct.
[Is] ISSN:1437-4315
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Mucin16 [MUC16/cancer antigen 125 (CA-125)], a high-molecular-weight glycoprotein expressed on the ovarian tumor cell surface, potentiates metastasis via selective binding to mesothelin on peritoneal mesothelial cells. Shed MUC16/CA-125 is detectable in sera from ovarian cancer patients. We investigated the potential role of membrane type 1 matrix metalloproteinase (MT1-MMP, MMP-14), a transmembrane collagenase highly expressed in ovarian cancer cells, in MUC16/CA-125 ectodomain shedding. An inverse correlation between MT1-MMP and MUC16 immunoreactivity was observed in human ovarian tumors and cells. Further, when MUC16-expressing OVCA433 cells were engineered to overexpress MT1-MMP, surface expression of MUC16/CA-125 was lost, whereas cells expressing the inactive E240A mutant retained surface MUC16/CA-125. As a functional consequence, decreased adhesion of cells expressing catalytically active MT1-MMP to three-dimensional meso-mimetic cultures and intact ex vivo peritoneal tissue explants was observed. Nevertheless, meso-mimetic invasion is enhanced in MT1-MMP-expressing cells. Together, these data support a model wherein acquisition of catalytically active MT1-MMP expression in ovarian cancer cells induces MUC16/CA-125 ectodomain shedding, reducing adhesion to meso-mimetic cultures and to intact peritoneal explants. However, proteolytic clearing of MUC16/CA-125, catalyzed by MT1-MMP, may then expose integrins for high-affinity cell binding to peritoneal tissues, thereby anchoring metastatic lesions for subsequent proliferation within the collagen-rich sub-mesothelial matrix.
[Mh] Termos MeSH primário: Antígeno Ca-125/metabolismo
Adesão Celular/fisiologia
Metaloproteinase 14 da Matriz/metabolismo
Proteínas de Membrana/metabolismo
Neoplasias Ovarianas/metabolismo
Cavidade Peritoneal/patologia
[Mh] Termos MeSH secundário: Animais
Antígeno Ca-125/genética
Linhagem Celular Tumoral
Feminino
Seres Humanos
Metaloproteinase 14 da Matriz/genética
Proteínas de Membrana/genética
Camundongos
Camundongos Endogâmicos C57BL
Invasividade Neoplásica/patologia
Metástase Neoplásica/genética
Metástase Neoplásica/patologia
Transplante de Neoplasias
Neoplasias Mesoteliais/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (CA-125 Antigen); 0 (MUC16 protein, human); 0 (Membrane Proteins); EC 3.4.24.80 (MMP14 protein, human); EC 3.4.24.80 (Matrix Metalloproteinase 14)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140911
[St] Status:MEDLINE


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[PMID]:25069783
[Au] Autor:Verardo R; Piazza S; Klaric E; Ciani Y; Bussadori G; Marzinotto S; Mariuzzi L; Cesselli D; Beltrami AP; Mano M; Itoh M; Kawaji H; Lassmann T; Carninci P; Hayashizaki Y; Forrest AR; Beltrami CA; Schneider C; Fantom Consortium
[Ad] Endereço:Laboratorio Nazionale-Consorzio Interuniversitario Biotecnologie (LNCIB), Area Science Park, Trieste, Italy.
[Ti] Título:Specific mesothelial signature marks the heterogeneity of mesenchymal stem cells from high-grade serous ovarian cancer.
[So] Source:Stem Cells;32(11):2998-3011, 2014 Nov.
[Is] ISSN:1549-4918
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mesenchymal stem/stromal cells (MSCs) are the precursors of various cell types that compose both normal and cancer tissue microenvironments. In order to support the widely diversified parenchymal cells and tissue organization, MSCs are characterized by a large degree of heterogeneity, although available analyses of molecular and transcriptional data do not provide clear evidence. We have isolated MSCs from high-grade serous ovarian cancers (HG-SOCs) and various normal tissues (N-MSCs), demonstrated their normal genotype and analyzed their transcriptional activity with respect to the large comprehensive FANTOM5 sample dataset. Our integrative analysis conducted against the extensive panel of primary cells and tissues of the FANTOM5 project allowed us to mark the HG-SOC-MSCs CAGE-seq transcriptional heterogeneity and to identify a cell-type-specific transcriptional activity showing a significant relationship with primary mesothelial cells. Our analysis shows that MSCs isolated from different tissues are highly heterogeneous. The mesothelial-related gene signature identified in this study supports the hypothesis that HG-SOC-MSCs are bona fide representatives of the ovarian district. This finding indicates that HG-SOC-MSCs could actually derive from the coelomic mesothelium, suggesting that they might be linked to the epithelial tumor through common embryological precursors.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Células Mesenquimais Estromais/citologia
Neoplasias Epiteliais e Glandulares/patologia
Neoplasias Mesoteliais/metabolismo
Neoplasias Ovarianas/patologia
Microambiente Tumoral/fisiologia
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Gradação de Tumores/métodos
Neoplasias Epiteliais e Glandulares/metabolismo
Neoplasias Mesoteliais/patologia
Neoplasias Ovarianas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1508
[Cu] Atualização por classe:141015
[Lr] Data última revisão:
141015
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140730
[St] Status:MEDLINE
[do] DOI:10.1002/stem.1791


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[PMID]:24761768
[Au] Autor:Matte I; Lane D; Bachvarov D; Rancourt C; Piché A
[Ti] Título:Role of malignant ascites on human mesothelial cells and their gene expression profiles.
[So] Source:BMC Cancer;14:288, 2014 Apr 24.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Malignant ascites is often present at diagnostic in women with advanced ovarian cancer (OC) and its presence is associated with a worse outcome. Human peritoneal mesothelial cells (HPMCs) are key components of malignant ascites. Although the interplay between HPMCs and OC cells is believed to be critical for tumor progression, it has not been well characterized. The purpose of this study was to assess the effect of ascites on HPMCs and clarify the role of HPMCs in OC progression. METHODS: Human OC ascites and benign peritoneal fluids were assessed for their ability to stimulate HPMC proliferation. Conditioned medium from ascites- and benign fluid-stimulated HPMCs were compared for their ability to attenuate apoptosis induced by TNF-related apoptosis-inducing ligand (TRAIL). We conducted a comparative analysis of global expression changes in ascites-stimulated HPMCs using Agilent oligonucleotide microarrays. RESULTS: As compared to benign peritoneal fluids, malignant ascites stimulated the proliferation of HPMCs. TRAIL-induced apoptosis was attenuated in OC cells exposed to conditioned medium from ascites-stimulated HPMCs as compared to OC cells exposed to conditioned medium from benign fluid-stimulated HPMCs. A total of 649 genes were differentially expressed in ascites-stimulated HPMCs. Based on a ratio of more than 1.5-fold and a P < 0.05, 484 genes were up-regulated and 165 genes were down-regulated in ascites-exposed HPMCs. Stimulation of HPMCs with OC ascites resulted in differential expression of genes mainly associated with the regulation of cell growth and proliferation, cell death, cell cycle and cell assembly and organization, compared to benign peritoneal fluids. Top networks up-regulated by OC ascites included Akt and NF-κB survival pathways whereas vascular endothelial growth factor (VEGF) pathway was down-regulated. CONCLUSIONS: The results of this study not only provide evidence supporting the importance of the interplay between cancer cells and HPMCs but also define the role that the tumor environment plays in these interactions.
[Mh] Termos MeSH primário: Proliferação Celular/genética
Células Epiteliais/metabolismo
Regulação Neoplásica da Expressão Gênica
Neoplasias Mesoteliais/genética
Neoplasias Ovarianas/genética
[Mh] Termos MeSH secundário: Apoptose/genética
Ascite/metabolismo
Ascite/patologia
Células Epiteliais/patologia
Feminino
Seres Humanos
Neoplasias Mesoteliais/complicações
Neoplasias Mesoteliais/patologia
Neoplasias Ovarianas/complicações
Neoplasias Ovarianas/patologia
Cavidade Peritoneal/patologia
Ligante Indutor de Apoptose Relacionado a TNF/genética
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Microambiente Tumoral/genética
Fator A de Crescimento do Endotélio Vascular
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (TNF-Related Apoptosis-Inducing Ligand); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1502
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140426
[St] Status:MEDLINE
[do] DOI:10.1186/1471-2407-14-288


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[PMID]:23584926
[Au] Autor:Geyer SJ
[Ad] Endereço:Geyer Pathology Services, L.L.C., Pittsburgh, PA, 15238.
[Ti] Título:CD147 immunohistochemistry discriminates between reactive mesothelial cells and malignant mesothelioma: an expanded analysis of the data.
[So] Source:Diagn Cytopathol;42(8):734, 2014 Aug.
[Is] ISSN:1097-0339
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Basigina/metabolismo
Imuno-Histoquímica/métodos
Neoplasias Mesoteliais/metabolismo
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
136894-56-9 (Basigin)
[Em] Mês de entrada:1503
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130416
[St] Status:MEDLINE
[do] DOI:10.1002/dc.22985



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BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde