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[PMID]:29429159
[Au] Autor:Liu L; Wang LH; Ren YB; Rao XS; Yang SM
[Ad] Endereço:Department of Pathology, Peking University International Hospital, Beijing 102206, China.
[Ti] Título:[Retroperitoneal dedifferentiated liposarcoma with rhabdomyoblastic differentiation: a clinicopathological analysis].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(2):94-98, 2018 Feb 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the clinicopathological features, differential diagnosis, treatment and prognosis of dedifferentiated liposarcoma with rhabdomyoblastic differentiation. Six cases of retroperitoneal dedifferentiated liposarcoma with rhabdomyoblastic features were collected from December 2014 to August 2017 at Peking University International Hospital. The clinical manifestations, histomorphology, immunophenotype, treatment and follow-up data were analyzed, and relevant literature reviewed. The six patients included two males and four females, with age range of 47 to 66 years (mean 56 years). One case was primary and the five cases were recurred; four cases received radiotherapy and/or chemotherapy. The tumor diameters were 10 to 30 cm. Microscopically, the dedifferentiated areas were well demarcated from the well-differentiated areas, and resembled malignant fibrous histiocytoma, fibrosarcoma or solitary fibrous tumor with obvious mitotic figures or necrosis. Rhabdomyoblastic cells made up 10% to 30% of dedifferentiated area, and were scattered or focally distributed, being rounded, band-like or spindled, mostly with abundant eosinophilic cytoplasm. No striated structure was found, and the nucleis were rounded, oval or irregular shape with central or eccentric prominent nucleoli. Rare rhabdomyoblastic cells were lymphocytoid. The tumors encroached the muscular layer of intestinal wall in two cases and perirenal adipose tissue in one case. By immunohistochemical staining, the rhabdomyoblastic cells of all cases were all positive for desmin, myogenin, myoD1 and SMA; S-100 protein was expressed in one case (1/6). Well-differentiated area in two cases and dedifferentiated areas in all six cases were positive for MDM2, CDK4 and p16. After resection of the tumor and adjacent organs, one case recurred three months later, but there was no distant metastasis. Dedifferentiated liposarcoma with rhabdomyoblastic differentiation is a rare dedifferentiated liposarcoma. Pathological diagnosis is based on morphology, with supplementary immunohistochemical or molecular evaluation for further differential diagnosis. Multiple relapses may occur after surgical ablation plus adjuvant therapy.
[Mh] Termos MeSH primário: Lipossarcoma/patologia
Neoplasias Retroperitoneais/patologia
[Mh] Termos MeSH secundário: Idoso
Contagem de Células
Diferenciação Celular
Diagnóstico Diferencial
Feminino
Fibrossarcoma/patologia
Histiocitoma Fibroso Maligno/patologia
Seres Humanos
Imunofenotipagem
Lipossarcoma/terapia
Masculino
Meia-Idade
Recidiva Local de Neoplasia
Prognóstico
Neoplasias Retroperitoneais/terapia
Tumores Fibrosos Solitários/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[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:180213
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.02.003


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[PMID]:28463157
[Au] Autor:Schaefer IM; Hornick JL; Barysauskas CM; Raut CP; Patel SA; Royce TJ; Fletcher CDM; Baldini EH
[Ad] Endereço:Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
[Ti] Título:Histologic Appearance After Preoperative Radiation Therapy for Soft Tissue Sarcoma: Assessment of the European Organization for Research and Treatment of Cancer-Soft Tissue and Bone Sarcoma Group Response Score.
[So] Source:Int J Radiat Oncol Biol Phys;98(2):375-383, 2017 06 01.
[Is] ISSN:1879-355X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To critically assess the prognostic value of the European Organization for Research and Treatment of Cancer-Soft Tissue and Bone Sarcoma Group (EORTC-STBSG) response score and define histologic appearance after preoperative radiation therapy (RT) for soft tissue sarcoma (STS). METHODS AND MATERIALS: For a cohort of 100 patients with STS of the extremity/trunk treated at our institution with preoperative RT followed by resection, 2 expert sarcoma pathologists evaluated the resected specimens for percent residual viable cells, necrosis, hyalinization/fibrosis, and infarction. The EORTC response score and other predictors of recurrence-free survival (RFS) and overall survival (OS) were assessed by Kaplan-Meier and proportional hazard models. RESULTS: Median tumor size was 7.5 cm; 92% were intermediate or high grade. Most common histologies were unclassified sarcoma (34%) and myxofibrosarcoma (25%). Median follow-up was 60 months. The 5-year local recurrence rate was 5%, 5-year RFS was 68%, and 5-year OS was 75%. Distribution of cases according to EORTC response score tiers was as follows: no residual viable tumor for 9 cases (9% pathologic complete response); <1% viable tumor for 0, ≥1% to <10% for 9, ≥10% to <50% for 44, and ≥50% for 38. There was no association between EORTC-STBSG response score and RFS or OS. Conversely, hyalinization/fibrosis was a significant independent favorable predictor for RFS (hazard ratio 0.49, P=.007) and OS (hazard ratio 0.36, P=.02). CONCLUSION: Histologic evaluation after preoperative RT for STS showed a 9% pathologic complete response rate. The EORTC-STBSG response score and percent viable cells were not prognostic. Hyalinization/fibrosis was associated with favorable outcome, and if validated, may become a valid endpoint for neoadjuvant trials.
[Mh] Termos MeSH primário: Sarcoma/patologia
Sarcoma/radioterapia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Sobrevivência Celular
Intervalo Livre de Doença
Feminino
Fibrossarcoma/mortalidade
Fibrossarcoma/patologia
Fibrossarcoma/radioterapia
Fibrossarcoma/cirurgia
Fibrose/patologia
Seguimentos
Seres Humanos
Infarto/patologia
Estimativa de Kaplan-Meier
Leiomiossarcoma/mortalidade
Leiomiossarcoma/patologia
Leiomiossarcoma/radioterapia
Leiomiossarcoma/cirurgia
Lipossarcoma/mortalidade
Lipossarcoma/patologia
Lipossarcoma/radioterapia
Lipossarcoma/cirurgia
Masculino
Meia-Idade
Necrose/patologia
Neoplasia Residual
Modelos de Riscos Proporcionais
Sarcoma/mortalidade
Sarcoma/cirurgia
Fatores de Tempo
Resultado do Tratamento
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:29390454
[Au] Autor:Zhang S; Ma Y; Ma T; Wang Z
[Ad] Endereço:Department of Oral and Maxillofacial Surgery.
[Ti] Título:Low-grade myofibroblastic sarcoma of the orbit: A case report and literature review.
[So] Source:Medicine (Baltimore);96(51):e9172, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Low-grade myofibroblastic sarcoma (LGMS) is a malignant lesion composed of myofibroblasts. It is an uncommon tumor of unknown etiology that mainly develops in the bone or soft tissue and is most often reported in the head and neck, particularly in the tongue and oral cavity. PATIENT CONCERNS: A 2-year-old girl, previously well and with no significant medical history or family history of other diseases, presented with a 2-week painless swelling of the right orbit. DIAGNOSES: Preoperative computed tomography (CT) revealed a large homogeneous enhanced mass, 21 × 13 mm in size, located on lateral wall of the right orbit with bone absorption. The mass was resected and histopathological examination revealed LGMS of the orbit. INTERVENTIONS: On May 2016, she underwent surgery without the additional postoperative treatment. OUTCOMES: The patient's postoperative course was uneventful, and was discharged on the 6th day after surgery. During a year follow-up period, there was no recurrence of the postoperative CT. The patient and her family were satisfied with the result of the surgery. LESSONS: Based on clinical characteristics and postoperative CT, we considered the mass may be a benign tumor. We completely resected along the capsule without an extensive surgical margin. However, postoperative histopathology diagnose LGMS, which shows a strong potential for local recurrence and vascular invasion. So we should close observation of the patient's symptoms and sign. If the tumor has invaded adjacent tissues, we will use adjuvant chemotherapy or radiotherapy.
[Mh] Termos MeSH primário: Fibrossarcoma/patologia
Fibrossarcoma/cirurgia
Miofibroblastos/patologia
Neoplasias Orbitárias/patologia
Neoplasias Orbitárias/cirurgia
[Mh] Termos MeSH secundário: Biópsia por Agulha
Pré-Escolar
China
Feminino
Fibrossarcoma/diagnóstico por imagem
Seguimentos
Seres Humanos
Imuno-Histoquímica
Invasividade Neoplásica/patologia
Estadiamento de Neoplasias
Neoplasias Orbitárias/diagnóstico por imagem
Tomografia Computadorizada por Raios X/métodos
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009172


  4 / 10777 MEDLINE  
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[PMID]:29390560
[Au] Autor:Wang G; Zhao Z; Wei J; Yang J
[Ad] Endereço:Department of Ultrasound.
[Ti] Título:Fibromyxoid sarcoma in the retroperitoneum: A case report.
[So] Source:Medicine (Baltimore);96(51):e9409, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Low-grade fibromyxoid sarcoma (LGFMS) is a pathological type of fibrosing fibrosarcoma that appears as a distinctive soft tissue masse with bland histological features. It is mostly located in the deep soft tissues of the extremities. Computed tomography (CT) plays an important role in diagnosing fibrosing fibrosarcoma in the abdomen. To date, several studies in the literature have reported on CT features of LGFMS. PATIENT CONCERNS AND DIAGNOSES: We report another case of LGFMS, which presented with certain unique CT feature. The anterolateral region and the wall of the cystic nodules showed gradual enhancement and several nourishing vessels were seen after contrast administration. These imaging features were consistent with the histologic findings of LGFMS. INTERVENTIONS AND OUTCOMES: The patient underwent tumorectomy and implantation of radioactive implants. Two years after the operation, 1 metastasis mass occur in the right psoas major. LESSONS: These CT features in LGFMS may be useful to assess the histological characteristics of LGFMS to facilitate preoperative diagnosis in the clinical setting and provide the supplemental imaging knowledge for future studies.
[Mh] Termos MeSH primário: Fibrossarcoma/diagnóstico por imagem
Neoplasias Retroperitoneais/diagnóstico por imagem
[Mh] Termos MeSH secundário: Braquiterapia
Terapia Combinada
Fibrossarcoma/patologia
Fibrossarcoma/terapia
Seres Humanos
Hidroxietilrutosídeo
Masculino
Meia-Idade
Neoplasias Retroperitoneais/patologia
Neoplasias Retroperitoneais/terapia
Espaço Retroperitoneal/diagnóstico por imagem
Espaço Retroperitoneal/patologia
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydroxyethylrutoside)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009409


  5 / 10777 MEDLINE  
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[PMID]:29072951
[Au] Autor:Lucas DR
[Ad] Endereço:From the Department of Pathology, University of Michigan/Michigan Medicine, Ann Arbor, Michigan.
[Ti] Título:Myxoinflammatory Fibroblastic Sarcoma: Review and Update.
[So] Source:Arch Pathol Lab Med;141(11):1503-1507, 2017 Nov.
[Is] ISSN:1543-2165
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Myxoinflammatory fibroblastic sarcoma is a rare soft tissue tumor with most occurring in the distal extremities of adult patients. It has a high rate of local recurrence and a low rate of metastasis. Because it may appear benign on clinical examination, and because the microscopic features are generally underrecognized, it is often inadequately treated and misdiagnosed. In this review, based upon experience and that of the literature, the intent is to highlight salient clinicopathologic features, detail the broad microscopic spectrum including high-grade aggressive variants, review the molecular features, and discuss its relation to hemosiderotic fibrolipomatous tumor.
[Mh] Termos MeSH primário: Fibrossarcoma/diagnóstico
Mixossarcoma/diagnóstico
[Mh] Termos MeSH secundário: Diagnóstico Diferencial
Emperipolese
Extremidades
Fibrossarcoma/imunologia
Fibrossarcoma/patologia
Fibrossarcoma/terapia
Hemossiderose/diagnóstico
Hemossiderose/imunologia
Hemossiderose/patologia
Seres Humanos
Lipoma/diagnóstico
Lipoma/imunologia
Lipoma/patologia
Mixossarcoma/imunologia
Mixossarcoma/patologia
Mixossarcoma/terapia
Recidiva Local de Neoplasia
Neoplasias de Tecido Fibroso/diagnóstico
Neoplasias de Tecido Fibroso/imunologia
Neoplasias de Tecido Fibroso/patologia
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171027
[St] Status:MEDLINE
[do] DOI:10.5858/arpa.2017-0219-RA


  6 / 10777 MEDLINE  
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[PMID]:29061813
[Au] Autor:Kim H; Kim MM
[Ad] Endereço:Department of Applied Chemistry, Dong-Eui University, Busan, Republic of Korea.
[Ti] Título:Effect of Agmatine Sulfate on Modulation of Matrix Metalloproteinases PI3K/Akt-1 in HT1080 Cells.
[So] Source:Anticancer Res;37(11):6303-6309, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The purpose of this study was to investigate the mechanism by which agmatine sulfate induces an anti-metastatic effect in human HT1080 fibrosarcoma cells, by affecting matrix metalloproteinases (MMPs). MATERIALS AND METHODS: For the experiments, we used a non-toxic concentration of agmatine, below 512 µM, that was determined using an MTT assay. The effect of agmatine sulfate on metastasis was gelatin zymography, western blot, immunofluorescence staining and cell invasion assay. RESULTS: Agmatine sulfate inhibited MMP-2 activity stimulated by phenazine methosulfate (PMS). Furthermore, the expression level of MMP-2 stimulated by PMS, was decreased, but the expression level of TIMP-1 was increased in the presence of agmatine sulfate. Moreover, it was observed that the expression levels of ERK and p38 were increased, but those of PI3K and Akt-1 associated with the modulation of MMP-2 were decreased in this study. Furthermore, agmatine sulfate decreased the invasion level of human fibrosarcoma cells stimulated by VEGF. CONCLUSION: These results suggest that agmatine sulfate could inhibit metastasis through inhibition of MMP-2 via the PI3K/Akt-1 signaling pathway.
[Mh] Termos MeSH primário: Agmatina/farmacologia
Antineoplásicos/farmacologia
Fibrossarcoma/metabolismo
Metaloproteinase 2 da Matriz/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Fibrossarcoma/tratamento farmacológico
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 70J407ZL5Q (Agmatine); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.4.24.24 (MMP2 protein, human); EC 3.4.24.24 (Matrix Metalloproteinase 2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


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[PMID]:28837838
[Au] Autor:Panyutin IG; Panyutin IV; Powell-Castilla I; Felix L; Neumann RD
[Ad] Endereço:Nuclear Medicine Division, Department of Radiology and Imaging Sciences, Clinical Center, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD, 20892, USA. Electronic address: ipanyuting@mail.nih.gov.
[Ti] Título:Single nucleotide variations in cultured cancer cells: Effect of mismatch repair.
[So] Source:Mutat Res;803-805:22-25, 2017 Oct.
[Is] ISSN:1873-135X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We assessed single nucleotide variations (SNVs) between individual cells in two cancer cell lines; DU145, from brain metastasis of prostate tumor with deficient mismatch repair; and HT1080, a fibrosarcoma cell line. Clones of individual cells were isolated, and sequenced using Ion Ampliseq comprehensive cancer panel that covered the exomes of 409 oncogenes and tumor suppressor genes. Five clones of DU145 and four clones of HT1080 cells were analyzed. We found from 7 to 12 unique SNVs between DU145 clones, while HT1080 clones showed no more than one unique SNV. We then sub-cloned individual cells from some of these isolated clones of DU145 and HT1080 cells. The sub-clones were expanded from a single cell to approximately one million cells after about 20 cell divisions. The sub-clones of DU145 cells had from one to four new unique SNVs within the sequenced regions. No unique SNVs were found between sub-clones of HT1080 cells. Our data demonstrate that the extent of genetic variation at the single nucleotide level in cultured cancer cells is significantly affected by the status of the DNA mismatch repair system.
[Mh] Termos MeSH primário: Reparo de Erro de Pareamento de DNA
Fibrossarcoma/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Clonagem Molecular
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE


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[PMID]:28798239
[Au] Autor:Brasher MI; Martynowicz DM; Grafinger OR; Hucik A; Shanks-Skinner E; Uniacke J; Coppolino MG
[Ad] Endereço:From the Department of Molecular and Cellular Biology, University of Guelph, Guelph, Ontario N1G 2W1, Canada.
[Ti] Título:Interaction of Munc18c and syntaxin4 facilitates invadopodium formation and extracellular matrix invasion of tumor cells.
[So] Source:J Biol Chem;292(39):16199-16210, 2017 Sep 29.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor cell invasion involves targeted localization of proteins required for interactions with the extracellular matrix and for proteolysis. The localization of many proteins during these cell-extracellular matrix interactions relies on membrane trafficking mediated in part by SNAREs. The SNARE protein syntaxin4 (Stx4) is involved in the formation of invasive structures called invadopodia; however, it is unclear how Stx4 function is regulated during tumor cell invasion. Munc18c is known to regulate Stx4 activity, and here we show that Munc18c is required for Stx4-mediated invadopodium formation and cell invasion. Biochemical and microscopic analyses revealed a physical association between Munc18c and Stx4, which was enhanced during invadopodium formation, and that a reduction in Munc18c expression decreases invadopodium formation. We also found that an N-terminal Stx4-derived peptide associates with Munc18c and inhibits endogenous interactions of Stx4 with synaptosome-associated protein 23 (SNAP23) and vesicle-associated membrane protein 2 (VAMP2). Furthermore, expression of the Stx4 N-terminal peptide decreased invadopodium formation and cell invasion Of note, cells expressing the Stx4 N-terminal peptide exhibited impaired trafficking of membrane type 1 matrix metalloproteinase (MT1-MMP) and EGF receptor (EGFR) to the cell surface during invadopodium formation. Our findings implicate Munc18c as a regulator of Stx4-mediated trafficking of MT1-MMP and EGFR, advancing our understanding of the role of SNARE function in the localization of proteins that drive tumor cell invasion.
[Mh] Termos MeSH primário: Adenocarcinoma/metabolismo
Matriz Extracelular/metabolismo
Fibrossarcoma/metabolismo
Proteínas Munc18/metabolismo
Proteínas de Neoplasias/metabolismo
Podossomos/metabolismo
Proteínas Qa-SNARE/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/patologia
Ligação Competitiva
Linhagem Celular Tumoral
Matriz Extracelular/patologia
Fibrossarcoma/patologia
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Seres Humanos
Metaloproteinase 14 da Matriz/metabolismo
Proteínas Munc18/antagonistas & inibidores
Proteínas Munc18/química
Proteínas Munc18/genética
Invasividade Neoplásica
Proteínas de Neoplasias/antagonistas & inibidores
Proteínas de Neoplasias/química
Proteínas de Neoplasias/genética
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Podossomos/patologia
Domínios e Motivos de Interação entre Proteínas
Multimerização Proteica
Transporte Proteico
Proteínas Qa-SNARE/química
Proteínas Qa-SNARE/genética
Proteínas Qb-SNARE/antagonistas & inibidores
Proteínas Qb-SNARE/química
Proteínas Qb-SNARE/metabolismo
Proteínas Qc-SNARE/antagonistas & inibidores
Proteínas Qc-SNARE/química
Proteínas Qc-SNARE/metabolismo
Interferência de RNA
Receptor do Fator de Crescimento Epidérmico/metabolismo
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Proteína 2 Associada à Membrana da Vesícula/antagonistas & inibidores
Proteína 2 Associada à Membrana da Vesícula/química
Proteína 2 Associada à Membrana da Vesícula/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Munc18 Proteins); 0 (Neoplasm Proteins); 0 (Peptide Fragments); 0 (Qa-SNARE Proteins); 0 (Qb-SNARE Proteins); 0 (Qc-SNARE Proteins); 0 (Recombinant Fusion Proteins); 0 (SNAP23 protein, human); 0 (VAMP2 protein, human); 0 (Vesicle-Associated Membrane Protein 2); 0 (syntaxin 4, human); 147336-22-9 (Green Fluorescent Proteins); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.4.24.80 (MMP14 protein, human); EC 3.4.24.80 (Matrix Metalloproteinase 14)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.807438


  9 / 10777 MEDLINE  
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[PMID]:28759001
[Au] Autor:Gao Y; Souza-Fonseca-Guimaraes F; Bald T; Ng SS; Young A; Ngiow SF; Rautela J; Straube J; Waddell N; Blake SJ; Yan J; Bartholin L; Lee JS; Vivier E; Takeda K; Messaoudene M; Zitvogel L; Teng MWL; Belz GT; Engwerda CR; Huntington ND; Nakamura K; Hölzel M; Smyth MJ
[Ad] Endereço:Immunology in Cancer and Infection, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.
[Ti] Título:Tumor immunoevasion by the conversion of effector NK cells into type 1 innate lymphoid cells.
[So] Source:Nat Immunol;18(9):1004-1015, 2017 Sep.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Avoiding destruction by immune cells is a hallmark of cancer, yet how tumors ultimately evade control by natural killer (NK) cells remains incompletely defined. Using global transcriptomic and flow-cytometry analyses and genetically engineered mouse models, we identified the cytokine-TGF-ß-signaling-dependent conversion of NK cells (CD49a CD49b Eomes ) into intermediate type 1 innate lymphoid cell (intILC1) (CD49a CD49b Eomes ) populations and ILC1 (CD49a CD49b Eomes ) populations in the tumor microenvironment. Strikingly, intILC1s and ILC1s were unable to control local tumor growth and metastasis, whereas NK cells favored tumor immunosurveillance. Experiments with an antibody that neutralizes the cytokine TNF suggested that escape from the innate immune system was partially mediated by TNF-producing ILC1s. Our findings provide new insight into the plasticity of group 1 ILCs in the tumor microenvironment and suggest that the TGF-ß-driven conversion of NK cells into ILC1s is a previously unknown mechanism by which tumors escape surveillance by the innate immune system.
[Mh] Termos MeSH primário: Reprogramação Celular/imunologia
Fibrossarcoma/imunologia
Neoplasias Gastrointestinais/imunologia
Tumores do Estroma Gastrointestinal/imunologia
Imunidade Inata/imunologia
Células Matadoras Naturais/imunologia
Neoplasias Experimentais/imunologia
Evasão Tumoral/imunologia
[Mh] Termos MeSH secundário: Animais
Estudos de Casos e Controles
Linhagem Celular Tumoral
Ensaio de Imunoadsorção Enzimática
Citometria de Fluxo
Perfilação da Expressão Gênica
Seres Humanos
Células Matadoras Naturais/citologia
Linfócitos/citologia
Linfócitos/imunologia
Camundongos
Análise de Sequência de RNA
Transdução de Sinais
Fator de Crescimento Transformador beta/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transforming Growth Factor beta)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3800


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[PMID]:28756225
[Au] Autor:Guo J; Lam LT; Longenecker KL; Bui MH; Idler KB; Glaser KB; Wilsbacher JL; Tse C; Pappano WN; Huang TH
[Ad] Endereço:AbbVie Inc., 1 North Waukegan Rd., North Chicago, IL 60064, United States.
[Ti] Título:Identification of novel resistance mechanisms to NAMPT inhibition via the de novo NAD biosynthesis pathway and NAMPT mutation.
[So] Source:Biochem Biophys Res Commun;491(3):681-686, 2017 Sep 23.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cancer cells have an unusually high requirement for the central and intermediary metabolite nicotinamide adenine dinucleotide (NAD ), and NAD depletion ultimately results in cell death. The rate limiting step within the NAD salvage pathway required for converting nicotinamide to NAD is catalyzed by nicotinamide phosphoribosyltransferase (NAMPT). Targeting NAMPT has been investigated as an anti-cancer strategy, and several highly selective small molecule inhibitors have been found to potently inhibit NAMPT in cancer cells, resulting in NAD depletion and cytotoxicity. To identify mechanisms that could cause resistance to NAMPT inhibitor treatment, we generated a human fibrosarcoma cell line refractory to the highly potent and selective NAMPT small molecule inhibitor, GMX1778. We uncovered novel and unexpected mechanisms of resistance including significantly increased expression of quinolinate phosphoribosyl transferase (QPRT), a key enzyme in the de novo NAD synthesis pathway. Additionally, exome sequencing of the NAMPT gene in the resistant cells identified a single heterozygous point mutation that was not present in the parental cell line. The combination of upregulation of the NAD de novo synthesis pathway through QPRT over-expression and NAMPT mutation confers resistance to GMX1778, but the cells are only partially resistant to next-generation NAMPT inhibitors. The resistance mechanisms uncovered herein provide a potential avenue to continue exploration of next generation NAMPT inhibitors to treat neoplasms in the clinic.
[Mh] Termos MeSH primário: Cianetos/administração & dosagem
Citocinas/antagonistas & inibidores
Citocinas/genética
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Fibrossarcoma/tratamento farmacológico
Fibrossarcoma/metabolismo
Guanidinas/administração & dosagem
NAD/biossíntese
Nicotinamida Fosforribosiltransferase/antagonistas & inibidores
Nicotinamida Fosforribosiltransferase/genética
[Mh] Termos MeSH secundário: Anilidas
Apoptose/efeitos dos fármacos
Apoptose/genética
Arginina/análogos & derivados
Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos/genética
Fibrossarcoma/genética
Seres Humanos
Mutação/genética
NAD/genética
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anilides); 0 (Cyanides); 0 (Cytokines); 0 (Guanidines); 0 (N-(6-chlorophenoxyhexyl)-N''-cyano-N''-4-pyridylguanidine); 0U46U6E8UK (NAD); 85697-89-8 (N(G)-nitroarginine-4-nitroanilide); 94ZLA3W45F (Arginine); EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase); EC 2.4.2.12 (nicotinamide phosphoribosyltransferase, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170731
[St] Status:MEDLINE



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