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  1 / 7022 MEDLINE  
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[PMID]:28460465
[Au] Autor:McCormick A; Earp E; Elliot K; Cuthbert G; O'Donnell R; Wilson BT; Sutton R; Leeson C; Thomas HD; Blair H; Fordham S; Lunec J; Allan J; Edmondson RJ
[Ad] Endereço:Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, UK.
[Ti] Título:Functional characterisation of a novel ovarian cancer cell line, NUOC-1.
[So] Source:Oncotarget;8(16):26832-26844, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cell lines provide a powerful model to study cancer and here we describe a new spontaneously immortalised epithelial ovarian cancer cell line (NUOC-1) derived from the ascites collected at a time of primary debulking surgery for a mixed endometrioid / clear cell / High Grade Serous (HGS) histology. RESULTS: This spontaneously immortalised cell line was found to maintain morphology and epithelial markers throughout long-term culture. NUOC-1 cells grow as an adherent monolayer with a doubling time of 58 hours. The cells are TP53 wildtype, positive for PTEN, HER2 and HER3 expression but negative for oestrogen, progesterone and androgen receptor expression. NUOC-1 cells are competent in homologous recombination and non-homologous end joining, but base excision repair defective. Karyotype analysis demonstrated a complex tetraploid karyotype. SNP array analysis of parent and derived subpopulations (NUOC-1-A1 and NUOC-1-A2) cells demonstrated heterogeneous cell populations with numerous copy number alterations and a pro-amplification phenotype. The characteristics of this new cell line lends it to be an excellent model for investigation of a number of the identified targets. MATERIALS AND METHODS: The cell line has been characterised for growth, drug sensitivity, expression of common ovarian markers and mutations, clonogenic potential and ability to form xenografts in SCID mice. Copy number changes and clonal evolution were assessed by SNP arrays.
[Mh] Termos MeSH primário: Linhagem Celular Tumoral
Neoplasias Ovarianas/genética
Neoplasias Ovarianas/patologia
[Mh] Termos MeSH secundário: Animais
Bandeamento Cromossômico
Evolução Clonal/genética
Variações do Número de Cópias de DNA
Reparo do DNA
Modelos Animais de Doenças
Feminino
Amplificação de Genes
Genes myc
Xenoenxertos
Seres Humanos
Hibridização in Situ Fluorescente
Camundongos
Camundongos SCID
Meia-Idade
Mutação
Gradação de Tumores
Células-Tronco Neoplásicas/metabolismo
Proteína Supressora de Tumor p53/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tumor Suppressor Protein p53)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15821


  2 / 7022 MEDLINE  
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[PMID]:29225165
[Au] Autor:Chakraborty A; Uechi T; Nakajima Y; Gazda HT; O'Donohue MF; Gleizes PE; Kenmochi N
[Ad] Endereço:Division of Molecular Genetics and Cancer, NU Centre for Science Education & Research, Nitte University, Mangalore 18, India. Electronic address: anirban@nitte.edu.in.
[Ti] Título:Cross talk between TP53 and c-Myc in the pathophysiology of Diamond-Blackfan anemia: Evidence from RPL11-deficient in vivo and in vitro models.
[So] Source:Biochem Biophys Res Commun;495(2):1839-1845, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mutations in genes encoding ribosomal proteins have been identified in Diamond-Blackfan anemia (DBA), a rare genetic disorder that presents with a prominent erythroid phenotype. TP53 has been implicated in the pathophysiology of DBA with ribosomal protein (RP) L11 playing a crucial role in the TP53 response. Interestingly, RPL11 also controls the transcriptional activity of c-Myc, an oncoprotein that positively regulates ribosome biogenesis. In the present study, we analyzed the consequences of rpl11 depletion on erythropoiesis and ribosome biogenesis in zebrafish. As expected, Rpl11-deficient zebrafish exhibited defects in ribosome biogenesis and an anemia phenotype. However, co-inhibition of Tp53 did not alleviate the erythroid aplasia in these fish. Next, we explored the role of c-Myc in RPL11-deficient cellular and animal models. c-Myc and its target nucleolar proteins showed upregulation and increased localization in the head region of Rpl11-deficient zebrafish, where the morphological abnormalities and tp53 expression were more pronounced. Interestingly, in blood cells derived from DBA patients with mutations in RPL11, the biogenesis of ribosomes was defective, but the expression level of c-Myc and its target nucleolar proteins was unchanged. The results suggest a model whereby RPL11 deficiency activates the synthesis of c-Myc target nucleolar proteins, which subsequently triggers a p53 response. These results further demonstrate that the induction of Tp53 mediates the morphological, but not erythroid, defects associated with RPL11 deficiency.
[Mh] Termos MeSH primário: Anemia de Diamond-Blackfan/fisiopatologia
Proteínas Ribossômicas/deficiência
[Mh] Termos MeSH secundário: Anemia de Diamond-Blackfan/genética
Anemia de Diamond-Blackfan/patologia
Animais
Modelos Animais de Doenças
Eritropoese/genética
Proteínas de Peixes/deficiência
Proteínas de Peixes/genética
Genes myc
Genes p53
Seres Humanos
Mutação
Processamento Pós-Transcricional do RNA
Proteínas Ribossômicas/genética
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fish Proteins); 0 (Ribosomal Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE


  3 / 7022 MEDLINE  
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[PMID]:29326336
[Au] Autor:Leong WZ; Tan SH; Ngoc PCT; Amanda S; Yam AWY; Liau WS; Gong Z; Lawton LN; Tenen DG; Sanda T
[Ad] Endereço:Cancer Science Institute of Singapore, National University of Singapore, 117599 Singapore.
[Ti] Título:ARID5B as a critical downstream target of the TAL1 complex that activates the oncogenic transcriptional program and promotes T-cell leukemogenesis.
[So] Source:Genes Dev;31(23-24):2343-2360, 2017 12 01.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The oncogenic transcription factor induces an aberrant transcriptional program in T-cell acute lymphoblastic leukemia (T-ALL) cells. However, the critical factors that are directly activated by TAL1 and contribute to T-ALL pathogenesis are largely unknown. Here, we identified ( ) as a collaborating oncogenic factor involved in the transcriptional program in T-ALL. expression is down-regulated at the double-negative 2-4 stages in normal thymocytes, while it is induced by the TAL1 complex in human T-ALL cells. The enhancer located 135 kb upstream of the gene locus is activated under a superenhancer in T-ALL cells but not in normal T cells. Notably, ARID5B-bound regions are associated predominantly with active transcription. ARID5B and TAL1 frequently co-occupy target genes and coordinately control their expression. ARID5B positively regulates the expression of TAL1 and its regulatory partners. ARID5B also activates the expression of the oncogene Importantly, ARID5B is required for the survival and growth of T-ALL cells and forced expression of ARID5B in immature thymocytes results in thymus retention, differentiation arrest, radioresistance, and tumor formation in zebrafish. Our results indicate that ARID5B reinforces the oncogenic transcriptional program by positively regulating the TAL1-induced regulatory circuit and in T-ALL, thereby contributing to T-cell leukemogenesis.
[Mh] Termos MeSH primário: Carcinogênese/genética
Proteínas de Ligação a DNA/metabolismo
Regulação Neoplásica da Expressão Gênica
Proteína 1 de Leucemia Linfocítica Aguda de Células T/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Sobrevivência Celular/genética
Proteínas de Ligação a DNA/genética
Elementos Facilitadores Genéticos/genética
Perfilação da Expressão Gênica
Genes myc/genética
Células HEK293
Seres Humanos
Leucemia-Linfoma Linfoblástico de Células T Precursoras
Ligação Proteica
Domínios Proteicos/genética
Timócitos/metabolismo
Timo/crescimento & desenvolvimento
Fatores de Transcrição/genética
Ativação Transcricional/genética
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ARID5B protein, human); 0 (DNA-Binding Proteins); 0 (T-Cell Acute Lymphocytic Leukemia Protein 1); 0 (Transcription Factors); 135471-20-4 (TAL1 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE
[do] DOI:10.1101/gad.302646.117


  4 / 7022 MEDLINE  
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[PMID]:28748558
[Au] Autor:Ott G
[Ad] Endereço:Department of Clinical Pathology, Robert-Bosch-Krankenhaus, Stuttgart, Germany.
[Ti] Título:Aggressive B-cell lymphomas in the update of the 4th edition of the World Health Organization classification of haematopoietic and lymphatic tissues: refinements of the classification, new entities and genetic findings.
[So] Source:Br J Haematol;178(6):871-887, 2017 09.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The update of the 4th edition of the World Health Organization Classification of Haematopoietic and Lymphatic Tissues portends important new findings and concepts in the diagnosis, classification and biology of lymphomas. This review summarizes the basic concepts and cornerstones of the classification of aggressive B-cell lymphomas and details the major changes. Of importance, there is a new concept of High-grade B-cell lymphomas (HGBL), partly replacing the provisional entity of B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma (DLBCL) and Burkitt lymphoma, the so-called grey zone lymphomas. They either harbour MYC translocations together with a BCL2 and/or a BCL6 rearrangement (HGBL-Double Hit) or HGBL, not otherwise specified (NOS), lacking a double or triple hit constellation. In addition, the requirement for providing the cell-of-origin classification in the diagnostic work-up of DLBCLs, the role of MYC alterations in DLBCL subtypes, and newer findings in the specific variants/subtypes are highlighted.
[Mh] Termos MeSH primário: Linfoma de Células B/classificação
[Mh] Termos MeSH secundário: Linfoma de Burkitt/classificação
Linfoma de Burkitt/genética
Linfoma de Burkitt/patologia
Genes myc/genética
Seres Humanos
Linfoma de Células B/genética
Linfoma de Células B/patologia
Linfoma Difuso de Grandes Células B/classificação
Linfoma Difuso de Grandes Células B/genética
Linfoma Difuso de Grandes Células B/patologia
Mutação
Gradação de Tumores
Organização Mundial da Saúde
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14744


  5 / 7022 MEDLINE  
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[PMID]:28749548
[Au] Autor:Epperla N; Maddocks KJ; Salhab M; Chavez JC; Reddy N; Karmali R; Umyarova E; Bachanova V; Costa C; Glenn M; Calzada O; Xavier AC; Zhou Z; Hossain NM; Hernandez-Ilizaliturri FJ; Al-Mansour Z; Barta SK; Chhabra S; Lansigan F; Mehta A; Jaglal MV; Evans A; Flowers CR; Cohen JB; Fenske TS; Hamadani M; Costa LJ
[Ad] Endereço:Department of Hematology/Oncology, Medical College of Wisconsin, Milwaukee, Wisconsin.
[Ti] Título:C-MYC-positive relapsed and refractory, diffuse large B-cell lymphoma: Impact of additional "hits" and outcomes with subsequent therapy.
[So] Source:Cancer;123(22):4411-4418, 2017 Nov 15.
[Is] ISSN:1097-0142
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The impact of MYC proto-oncogene, basic helix-loop-helix (MYC) translocations (with or without additional rearrangements involving the B-cell lymphoma 2 [BCL2] or BCL6 genes) on the response to salvage therapy and survival in patients with diffuse large B-cell lymphoma (DLBCL) who experience primary treatment failure is not well defined. METHODS: This was a multicenter, retrospective study of the impact of MYC, BCL2, and BCL6 rearrangements in patients with DLBCL who failed to achieve complete remission or relapsed within 6 months after they completed upfront chemoimmunotherapy. RESULTS: The authors examined response to salvage therapy, receipt of hematopoietic cell transplantation (HCT), and survival outcomes in MYC-negative (n = 120), MYC-positive single hit (SH) (n = 20), and MYC-positive double hit/triple hit (DH/TH) (n = 35) cohorts. The overall response rate in these cohorts to first salvage therapy (51%, 50%, and 54%, respectively) and receipt of HCT (52%, 40%, and 43%, respectively) were comparable between the 3 cohorts. The 2-year overall survival rate was 29.9% in the MYC-negative cohort, 0% in the MYC-positive SH cohort, and 9.9% in the MYC-positive DH/TH cohort (P < .001), and no difference was observed between the SH and DH/TH cohorts (P = .8). The higher risk of death for patients with MYC-positive SH DLBCL (hazard ratio, 1.70; 95% confidence interval, 0.98-2.96; P = .06) and those with MYC-positive DH/TH DLBCL (hazard ratio, 2.22; 95% confidence interval, 1.41-3.50; P = .001) persisted after adjusting for covariates. For patients who underwent autologous HCT, the 2-year overall survival rate was 55.4% in the MYC-negative cohort, 0% in the MYC-positive SH cohort, and 19.4% in the MYC-positive DH/TH cohort (P < .001). All 4 MYC-positive patients who underwent allogeneic HCT relapsed in <4 months. CONCLUSIONS: Patients with MYC-positive DLBCL who experience primary treatment failure have response rates to similar to those achieved by salvage therapy compared with their MYC-negative counterparts, but their survival is dismal irrespective of additional "hits" and HCT, representing an unmet medical need. Cancer 2017;123:4411-8. © 2017 American Cancer Society.
[Mh] Termos MeSH primário: Genes myc
Linfoma Difuso de Grandes Células B/genética
Linfoma Difuso de Grandes Células B/terapia
Translocação Genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Resistência a Medicamentos Antineoplásicos/genética
Feminino
Transplante de Células-Tronco Hematopoéticas
Seres Humanos
Linfoma Difuso de Grandes Células B/mortalidade
Linfoma Difuso de Grandes Células B/patologia
Masculino
Meia-Idade
Recidiva
Estudos Retrospectivos
Terapia de Salvação
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; OBSERVATIONAL STUDY
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1002/cncr.30895


  6 / 7022 MEDLINE  
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[PMID]:29325248
[Au] Autor:Yin WJ; Zhu X; Yang HY; Sun WY; Wu MJ
[Ad] Endereço:Department of Pathology, Zhejiang Cancer Hospital, Hangzhou 310022, China.
[Ti] Título:[Survival of patients with primary central nervous system diffuse large B-cell lymphoma: impact of gene aberrations and protein overexpression of bcl-2 and C-MYC, and selection of chemotherapy regimens].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(1):32-38, 2018 Jan 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the impact of clinicopathological features, gene rearrangements and protein expression of bcl-6, bcl-2, C-MYC and chemotherapy regime on the prognosis of patients with primary central nervous system diffuse large B-cell lymphoma (PCNS-DLBCL). Thirty-three cases of PCNS-DLBCL diagnosed from January 2006 to December 2016 at Zhejiang Cancer Hospital were collected. The expression of CD10, bcl-6, bcl-2, MUM1 and MYC were detected by immunohistochemical staining (IHC). The presence of EB virus was detected by in situ hybridization(EBER). Copy number variation (ICN) and translocation status of bcl-6, bcl-2 and C-MYC genes were detected by fluorescence in situ hybridization (FISH). The relationship between the above indexes and the prognosis was analyzed by univariate, bivariate survival analysis and multiple Cox hazard regression analysis. The study included 33 patients of PCNS-DLBCL, without evidence of primary or secondary immunodeficient disease. Male to female ratio was 1.36∶1.00, and the average age was 56 years. Twenty cases had single lesion while 13 had multiple lesions. Deep brain involvement was seen in 12 cases. All patients underwent partial or total tumor resection. Five patients received whole brain post-surgery radiotherapy, nine patients received high-dose methotrexate (HD-MTX) based chemotherapy, and 12 patients received whole-brain radiotherapy combined with HD-MTX based chemotherapy. Severn patients received no further treatment and rituximab was used in 8 patients. According to the Hans model, 27 cases were classified as non-GCB subtypes (81.8%). Bcl-2 was positive in 25 cases (75.8%, 25/33) and highly expressed in 8 (24.2%). MYC was positive in 12 cases (36.4%) and double expression of bcl-2 and MYC was seen in 6 cases. EBER positive rate was 10.0%(3/30), all of which had multiple lesions. Two bcl-6 gene translocations and 3 amplifications were found in 28 patients. Two translocations, 3 ICN or with both bcl-2 gene translocation and ICN were found in 30 patients. Four ICNs of C-MYC gene were found in 28 patients. Elevated protein in cerebrospinal fluid (CSF) was found in 13 patients. LDH increased in 10 cases. Follow-up period was 2-90 months with the average survival time of (23.0±3.7) months and two-year survival rate of 39.0%. Univariate survival analysis showed that overexpression of bcl-2 protein (≥70%) and MYC protein (≥40%), bcl-2 gene abnormality (including copy number increase and translocation), C-MYC gene copy number increased were adverse factors for survival. C-MYC/ bcl-2 gene double hit was seen in 2 cases. Bivariate survival analysis found that of bcl-2/MYC protein double expression and bcl-2 and C-MYC genes double aberration were significantly associated with adverse outcomes. Cox multivariate risk regression analysis found that gender, cerebrospinal fluid protein increasing, and ICN of C-MYC gene were independent poor prognostic factors. DH-MTX based comprehensive chemotherapy was associated with better prognosis. Double hit at genomic level (copy number variations and gene rearrangements) and double protein expression of bcl-2 and C-MYC in PCNS-DLBCL are significantly associated with an adverse outcome. DH-MTX based comprehensive treatment may prolong the patient survival.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Neoplasias do Sistema Nervoso Central/mortalidade
Rearranjo Gênico
Linfoma Difuso de Grandes Células B/mortalidade
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Proteínas Proto-Oncogênicas c-myc/metabolismo
[Mh] Termos MeSH secundário: Antimetabólitos Antineoplásicos/uso terapêutico
Neoplasias Encefálicas/metabolismo
Neoplasias Encefálicas/mortalidade
Neoplasias Encefálicas/patologia
Neoplasias Encefálicas/terapia
Neoplasias do Sistema Nervoso Central/genética
Neoplasias do Sistema Nervoso Central/metabolismo
Neoplasias do Sistema Nervoso Central/terapia
Variações do Número de Cópias de DNA
Feminino
Dosagem de Genes
Genes bcl-2
Genes myc
Herpesvirus Humano 4/isolamento & purificação
Seres Humanos
Hibridização in Situ Fluorescente
Fatores Reguladores de Interferon/metabolismo
Linfoma Difuso de Grandes Células B/genética
Linfoma Difuso de Grandes Células B/metabolismo
Linfoma Difuso de Grandes Células B/terapia
Masculino
Metotrexato/uso terapêutico
Meia-Idade
Neprilisina/metabolismo
Prognóstico
Proteínas Proto-Oncogênicas c-bcl-6/genética
Proteínas Proto-Oncogênicas c-bcl-6/metabolismo
Análise de Sobrevida
Taxa de Sobrevida
Translocação Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (BCL2 protein, human); 0 (Interferon Regulatory Factors); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Proto-Oncogene Proteins c-bcl-6); 0 (Proto-Oncogene Proteins c-myc); 0 (interferon regulatory factor-4); EC 3.4.24.11 (Neprilysin); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.01.007


  7 / 7022 MEDLINE  
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[PMID]:29325247
[Au] Autor:Zhang XY; Ma ZP; Cui WL; Pang XL; Chen R; Wang L; Zhang W; Li XX
[Ad] Endereço:Department of Pathology, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China.
[Ti] Título:[Impact of PRDM1 gene inactivation on C-MYC regulation in diffuse large B-cell lymphoma].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(1):25-31, 2018 Jan 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the role of PRDM1 gene inactivaion in the regulation of C-MYC in diffuse large B-cell lymphoma (DLBCL), and to explore the correlation of its immunophenotype and prognosis. 100 cases paraffin-embedded DLBCL tissues were collected from January 2009 to December 2015 at the First Affiliated Hospital of Xinjiang Medical University along with 20 cases of reactive proliferative lymph nodes as control. Immunohistochemical methods were used to detect the expression of CD20, CD10, MUM1, Ki-67, bcl-6, PRDM1/Blimp1, C-MYC and PAX5 protein. The tumors were classified into two subtypes according to Hans classification.The expression of PRDM1 and C-MYC gene in tumor group and control group was detected by reverse transcription PCR (RT-PCR) and the relationship between PRDM1 and C-MYC gene was analyzed.OCI-LY1 (GCB subtype) and OCI-LY3 (non-GCB subtype) cell lines were transfected with small interfering RNA by cationic liposome reagent transfection, and the expression of C-MYC in the transfected cell lines was detected by RT-PCR and Western blot. The Kaplan-Meier method was used to analyze the prognostic significance of PRDM1/Blimp1 and C-MYC at protein and mRNA levels. There were 27 cases of GCB subtype and 73 cases of non-GCB subtype according to Hans classification. The positive expression of Blimp1 in DLBCL group and proliferative lymph nodes in control group was seen in 26(26.0%) and 20 cases(100%), respectively. There were 58 cases with high expression of PRDM1 at mRNA level, including 22 cases of GCB subtype and 36 cases non-GCB subtype, and the difference was statistically significant ( =0.004). There were differences in PRDM1 gene expression between the two immunological subtypes, serum lactate dehydrogenase (serum LDH) level, presence of B symptoms, tumor primary sites and other clinical pathological parameters, while C-MYC expression was different in gender, IPI score, and serum LDH levels. Upon PRDM1/Blimp1 gene silencing in the two cell lines, C-MYC protein and gene expression were up-regulated in the transfection group, compared with the blank control group and negative control group by reverse transcription PCR and Western blot analyses. Moreover, PRDM1 expression was significantly associated with C-MYC(χ(2)=7.648, =0.006) at mRNA level. The up-regulation of C-MYC gene expression induced by PRDM1 inactivation in DLBCL may play an important role for the development of DLBCL.PRDM1 protein and mRNA are associated with immunophenotyping and PRDM1 mRNA is a marker of poor prognosis.
[Mh] Termos MeSH primário: Inativação Gênica
Genes myc
Linfoma Difuso de Grandes Células B/genética
Fator 1 de Ligação ao Domínio I Regulador Positivo/genética
[Mh] Termos MeSH secundário: Antígenos CD20/metabolismo
Linhagem Celular Tumoral
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Imunofenotipagem
Linfonodos/patologia
Linfoma Difuso de Grandes Células B/patologia
Fator de Transcrição PAX5/metabolismo
Fator 1 de Ligação ao Domínio I Regulador Positivo/metabolismo
Prognóstico
Proteínas Proto-Oncogênicas c-bcl-6/genética
Proteínas Proto-Oncogênicas c-bcl-6/metabolismo
Proteínas Proto-Oncogênicas c-myc/metabolismo
RNA Mensageiro/metabolismo
Proteínas Repressoras/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD20); 0 (PAX5 Transcription Factor); 0 (PAX5 protein, human); 0 (Proto-Oncogene Proteins c-bcl-6); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, Messenger); 0 (Repressor Proteins); 138415-26-6 (PRDM1 protein, human); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.01.006


  8 / 7022 MEDLINE  
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[PMID]:29325245
[Au] Autor:Gong JY; Zhang YZ; Zhang JD; Zhang W; Li JQ; Ru K; Liu EB
[Ad] Endereço:Department of Pathology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin 300020, China.
[Ti] Título:[Clinical characteristics of high-grade B-cell lymphomas with rearrangement of MYC, bcl-6 and bcl-2].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(1):14-18, 2018 Jan 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the clinicopathologic features of patients with high-grade B-cell lymphomas (HGBL) that have rearrangements of MYC, bcl-6 and bcl-2. One hundred and fifty-eight B-cell lymphomas patients from Institute of Hematology and Blood Diseases Hospital from January 2016 to April 2017 were detected by fluorescence in situ hybridization (FISH) with double color split-apart probes. Among 158 B-cell lymphomas, 3 cases with MYC, bcl-2 and bcl-6 rearrangements were identified, 1 of which also had CCND1/IgH translocation. All three patients were of older age, with poor prognostic parameters, multiple organs involvements, elevated LDH and advanced-tumor stage. Two of the three patients were treated with high-intensity chemotherapy and had no remission with an overall survival of 9 months and 11 months respectively. One patient had follow-up with no treatment. Histologically, all three cases showed a spectrum of morphologic features. Although initially categorized as lymphoblastic lymphoma, diffuse large lymphoma and mantle cell lymphoma respectively, two cases were associated with germinal center B-cell (GCB) immunophenotype and 1 case with non-GCB immunophenotype. They had a high proliferation index as assessed by immunostaining for Ki-67 (60%-90%). MYC(+) bcl-2(+) bcl-6(+) HGBL is an aggressive disease with multiple organ involvement, high serum LDH levels, advanced stage disease, poor prognosis and shorter patient survival. The diagnosis should be made by histopathology combined with FISH analysis. Its separation from other types of B cell large cell lymphoma is of clinical importance.
[Mh] Termos MeSH primário: Rearranjo Gênico
Genes myc
Linfoma Difuso de Grandes Células B/genética
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-6/genética
[Mh] Termos MeSH secundário: Linfócitos B
Ciclina D1/genética
Sondas de DNA
Centro Germinativo
Seres Humanos
Imunofenotipagem
Hibridização in Situ Fluorescente
Linfoma Difuso de Grandes Células B/tratamento farmacológico
Linfoma Difuso de Grandes Células B/patologia
Gradação de Tumores
Prognóstico
Translocação Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCND1 protein, human); 0 (DNA Probes); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Proto-Oncogene Proteins c-bcl-6); 136601-57-5 (Cyclin D1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.01.004


  9 / 7022 MEDLINE  
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[PMID]:28901900
[Au] Autor:Xiang Z; Liang Z; Yanfeng H; Leitao K
[Ad] Endereço:1​Cancer Hospital of China Medical University, 44 Xiaoheyan Road, Dadong Region, Shengyang 110042, Liaoning, PR China.
[Ti] Título:Persistence of RSV promotes proliferation and epithelial-mesenchymal transition of bronchial epithelial cells through Nodal signaling.
[So] Source:J Med Microbiol;66(10):1499-1505, 2017 Oct.
[Is] ISSN:1473-5644
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Nodal may play an important role in the development of cancers. The present study was designed to determine the effects of Nodal induced by respiratory syncytial virus (RSV) infection on the occurrence and development of lung cancer and the underlying mechanisms. METHODOLOGY: After verification of RSV infection by observation of cytopathic effect and indirect immunofluorescence, real-time PCR, Western blot and methylation assays were used to verify the influence of RSV on Nodal expression. Then, a Nodal overexpressed vector was constructed and the effects of Nodal on the proliferation and apoptosis of bronchial epithelial cells (BECs) and epithelial-mesenchymal transition (EMT) were assayed by flow cytometry and Western blot, respectively. Moreover, Lefty and pSmad2/3 were assayed by Western blot and Cyclin D1, CDK4, c-myc and Bcl-2 induced by Nodal overepression or RSV infection were also assayed by real-time PCR. RESULTS: The results showed that Nodal over expression and demethylation of the promoter were observed in BECs after RSV infection. Activation of Nodal promoted proliferation, colony formation and EMT and inhibited apoptosis of BECs. Nodal also promoted malignant change by promoting expression of cyclin D1 and related-dependent kinase and inhibiting apoptosis. Besides, RSV infection inhibited Lefty expression and promoted the activation of pSmad2/3. RSV also promoted Cyclin D1, CDK4, c-myc and Bcl-2 expression through the activation of pSmad2/3. CONCLUSIONS: Our data showed that persistence of RSV promoted the proliferation, epithelial-mesenchymal transition and expression of oncogenes through Nodal signaling, which may be associated with the occurrence and development of lung cancers.
[Mh] Termos MeSH primário: Células Epiteliais/virologia
Transição Epitelial-Mesenquimal/fisiologia
Proteína Nodal/metabolismo
Mucosa Respiratória/citologia
Infecções por Vírus Respiratório Sincicial/complicações
[Mh] Termos MeSH secundário: Ciclina D1/genética
Ciclina D1/metabolismo
Quinase 4 Dependente de Ciclina/genética
Quinase 4 Dependente de Ciclina/metabolismo
Efeito Citopatogênico Viral
Células Epiteliais/fisiologia
Regulação da Expressão Gênica/fisiologia
Genes myc/genética
Genes myc/fisiologia
Células HeLa
Seres Humanos
Proteína Nodal/genética
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Infecções por Vírus Respiratório Sincicial/virologia
Vírus Sinciciais Respiratórios
Proteínas Smad/genética
Proteínas Smad/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NODAL protein, human); 0 (Nodal Protein); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Smad Proteins); 136601-57-5 (Cyclin D1); EC 2.7.11.22 (CDK4 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 4)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE
[do] DOI:10.1099/jmm.0.000581


  10 / 7022 MEDLINE  
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[PMID]:28892090
[Au] Autor:He X; Riceberg J; Soucy T; Koenig E; Minissale J; Gallery M; Bernard H; Yang X; Liao H; Rabino C; Shah P; Xega K; Yan ZH; Sintchak M; Bradley J; Xu H; Duffey M; England D; Mizutani H; Hu Z; Guo J; Chau R; Dick LR; Brownell JE; Newcomb J; Langston S; Lightcap ES; Bence N; Pulukuri SM
[Ad] Endereço:Oncology Drug Discovery Unit, Takeda Pharmaceuticals International Co., Cambridge, Massachusetts, USA.
[Ti] Título:Probing the roles of SUMOylation in cancer cell biology by using a selective SAE inhibitor.
[So] Source:Nat Chem Biol;13(11):1164-1171, 2017 Nov.
[Is] ISSN:1552-4469
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Small ubiquitin-like modifier (SUMO) family proteins regulate target-protein functions by post-translational modification. However, a potent and selective inhibitor targeting the SUMO pathway has been lacking. Here we describe ML-792, a mechanism-based SUMO-activating enzyme (SAE) inhibitor with nanomolar potency in cellular assays. ML-792 selectively blocks SAE enzyme activity and total SUMOylation, thus decreasing cancer cell proliferation. Moreover, we found that induction of the MYC oncogene increased the ML-792-mediated viability effect in cancer cells, thus indicating a potential application of SAE inhibitors in treating MYC-amplified tumors. Using ML-792, we further explored the critical roles of SUMOylation in mitotic progression and chromosome segregation. Furthermore, expression of an SAE catalytic-subunit (UBA2) S95N M97T mutant rescued SUMOylation loss and the mitotic defect induced by ML-792, thus confirming the selectivity of ML-792. As a potent and selective SAE inhibitor, ML-792 provides rapid loss of endogenously SUMOylated proteins, thereby facilitating novel insights into SUMO biology.
[Mh] Termos MeSH primário: Inibidores Enzimáticos/farmacologia
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Proteínas Modificadoras Pequenas Relacionadas à Ubiquitina/antagonistas & inibidores
Sumoilação
[Mh] Termos MeSH secundário: Proliferação Celular/efeitos dos fármacos
Segregação de Cromossomos/efeitos dos fármacos
Dano ao DNA/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Genes myc
Seres Humanos
Mitose/efeitos dos fármacos
Neoplasias/genética
Neoplasias/patologia
Processamento de Proteína Pós-Traducional
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Small Ubiquitin-Related Modifier Proteins)
[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:170912
[St] Status:MEDLINE
[do] DOI:10.1038/nchembio.2463



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