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[PMID]:27401254
[Au] Autor:Park S; Hong JP; Lee JK; Park YM; Park Y; Jeon J; Ahn MH; Yoon SC
[Ad] Endereço:Research Planning Division, Mental Health Research Institute, National Center for Mental Health, Seoul, Republic of Korea.
[Ti] Título:Associations between the neuron-specific glucocorticoid receptor (NR3C1) Bcl-1 polymorphisms and suicide in cancer patients within the first year of diagnosis.
[So] Source:Behav Brain Funct;12(1):22, 2016 Jul 11.
[Is] ISSN:1744-9081
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cancer diagnosis is associated with an increased suicide risk, particularly within the first 1 year after diagnosis of cancer. Abnormal function of the hypothalamic-pituitary-adrenal axis has been implicated in the pathophysiology of depression and suicide. We examined genetic associations of the functional Bcl-1 polymorphism of (rs41423247) neuron-specific glucocorticoid receptor (NR3C1) gene, with death by suicide in cancer patients. Suicides occurring within a year of cancer diagnosis ('early suicide') were considered separately from those suicides during the second or subsequent year ('late suicide') after cancer diagnosis. METHODS: The subjects consisted of 343 cancer patients admitted to a general hospital in Seoul, South Korea from 1996 to 2009, of which 182 had died by suicide and 161 were alive on December 31, 2009. Genomic DNA was extracted from formalin-fixed paraffin-embedded tissue sample of patients with cancer. We conducted a case-control association analysis of Bcl-1 polymorphism of NR3C1 gene. RESULTS: Subjects carrying the GG genotype of Bcl-1 polymorphism were at increased risk of early suicide when compared to those carrying the CC genotype (OR 3.80, 95 % CI 1.02-14.16, p = .047). Similarly, those individuals carrying the GG genotype (recessive mode) had an increased risk of early suicide relative to the CC or CG genotype (OR 3.71, 95 % CI 1.03-13.43, p = .045). However, there were no differences in the genotype distributions of the NR3C1 Bcl-1 polymorphism between late suicide cases and controls. CONCLUSIONS: Our findings suggest that the NR3C1 Bcl-1 polymorphisms may be involved in the susceptibility to suicide within the first year after cancer diagnosis among cancer patients in Korean population.
[Mh] Termos MeSH primário: Receptores de Glucocorticoides/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Estudos de Casos e Controles
Depressão/genética
Transtorno Depressivo/genética
Feminino
Frequência do Gene/genética
Genes bcl-1/genética
Predisposição Genética para Doença
Haplótipos
Seres Humanos
Sistema Hipotálamo-Hipofisário
Masculino
Meia-Idade
Neoplasias/psicologia
Neurônios/metabolismo
Sistema Hipófise-Suprarrenal
Polimorfismo de Nucleotídeo Único
Receptores de Glucocorticoides/metabolismo
República da Coreia
Fatores de Risco
Suicídio/psicologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NR3C1 protein, human); 0 (Receptors, Glucocorticoid)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160713
[St] Status:MEDLINE
[do] DOI:10.1186/s12993-016-0104-1


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[PMID]:27156331
[Au] Autor:Nie X; Wang X; Lin Y; Yu Y; Liu W; Xie F; Wang X; Tan J; Huang Q
[Ti] Título:SNP rs1059234 in CDKN1A Gene Correlates with Prognosis in Resected Gastric Adenocarcinoma.
[So] Source:Clin Lab;62(3):409-16, 2016.
[Is] ISSN:1433-6510
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cyclin-dependent kinase inhibitor 1A (CDKN1A) and Cyclin D1 (CCND1) play essential roles in the regulation of cell cycle progression and are closely associated with human cancer. CDKN1A and CCND1 single nucleotide polymorphisms (SNPs) have been demonstrated to influence the prognosis in humans with different cancers. However, their roles in the prognosis of patients with resected gastric adenocarcinoma (RGA) remain to be determined. METHODS: Genotypes of CDKN1A rs1059234 and CCND1 rs603965 SNPs were performed in 235 tissue samples from RGA. The association of the genotypes of these two SNPs with the prognosis in the patients with RGA was analyzed by X2 test, multivariate Cox regression analyses, and Kaplan Meier curves. RESULTS: During the 50 months of median follow-up time, the overall recurrence and survival rate in the whole group was 57.4% and 46.8%, respectively. Whereas, recurrence and survival rate in patients with CC genotype of rs1059234 located in 3'UTR of CDKN1A were 78.0% and 27.1% (p = 0.004; p = 0.006). Multivariate analyses further confirmed that the CC genotype was significantly related with both increased recurrence and death risk (HR 3.33, 95% CI 1.95-5.70; p = 1.07 x 10⁻5, and HR 3.45, 95% CI 1.95-6.10; p = 2.03 x 10⁻5). No significant difference among CCND1 rs603965 SNP with the prognosis was determined. CONCLUSIONS: rs1059234 of CDKN1A is closely associated with the prognosis in patients with RGA.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Inibidor de Quinase Dependente de Ciclina p21/genética
Polimorfismo de Nucleotídeo Único
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/mortalidade
Adulto
Idoso
Feminino
Genes bcl-1
Seres Humanos
Masculino
Meia-Idade
Prognóstico
Neoplasias Gástricas/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CDKN1A protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p21)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:160509
[Lr] Data última revisão:
160509
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160510
[St] Status:MEDLINE


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[PMID]:26573608
[Au] Autor:Xiong M; Wang L; Yu HL; Han H; Mao D; Chen J; Zeng Y; He N; Liu ZG; Wang ZY; Xu SJ; Guo LY; Wang YA
[Ad] Endereço:Department of Orthopedics Institute, Affiliated Dongfeng Hospital, Hubei University of Medicine, Shiyan, Hubei 442008, P.R. China.
[Ti] Título:Ginkgetin exerts growth inhibitory and apoptotic effects on osteosarcoma cells through inhibition of STAT3 and activation of caspase-3/9.
[So] Source:Oncol Rep;35(2):1034-40, 2016 Feb.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Osteosarcoma is composed of tumor osteoblasts and bone-like tissues, with malignant tumors originating from osteogenesis organization. Osteosarcoma is a primary malignant bone tumor. Invasion and metastasis of osteosarcoma affect the prognosis of patients. However, effective therapeutic treatments remain to be identified. The aim of the present study was to investigate the possible inhibitory and apoptotic effects of ginkgetin in osteosarcoma cells. 3.3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays were used to determine the effect ginkgetin exerted on the growth of osteosarcoma cells. Flow cytometry was used to determine cell apoptosis. STAT3 protein expression and activation of caspase-3/9 were measured using western blot analysis and the MTT and LDH assays, respectively. The results showed that ginkgetin inhibited cell growth and induced cell cytotoxicity in osteosarcoma cells in a dose-dependent manner. Treatment with ginkgetin significantly activated the apoptosis of osteosarcoma cells in a concentration-dependent manner. The anticancer activity of ginkgetin significantly inhibited STAT3 and promoted caspase-3/9 activation in osteosarcoma cells. The findings demonstrated that ginkgetin exerts growth inhibitory and apoptotic effects on osteosarcoma cells through the inhibition of STAT3 and activation of caspase-3/9.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/farmacologia
Apoptose/efeitos dos fármacos
Biflavonoides/farmacologia
Neoplasias Ósseas/patologia
Caspase 3/metabolismo
Caspase 9/metabolismo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Proteínas de Neoplasias/antagonistas & inibidores
Osteossarcoma/patologia
Fator de Transcrição STAT3/antagonistas & inibidores
[Mh] Termos MeSH secundário: Divisão Celular
Linhagem Celular Tumoral
Ciclina D1/biossíntese
Ativação Enzimática/efeitos dos fármacos
Genes bcl-1
Genes bcl-2
Seres Humanos
Proteínas Inibidoras de Apoptose/biossíntese
Proteínas Inibidoras de Apoptose/genética
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Poli(ADP-Ribose) Polimerases/biossíntese
Poli(ADP-Ribose) Polimerases/genética
Proteínas Proto-Oncogênicas c-bcl-2/biossíntese
Fator de Transcrição STAT3/genética
Proteína bcl-X/biossíntese
Proteína bcl-X/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (BCL2L1 protein, human); 0 (BIRC5 protein, human); 0 (Biflavonoids); 0 (CCND1 protein, human); 0 (Inhibitor of Apoptosis Proteins); 0 (Neoplasm Proteins); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (bcl-X Protein); 136601-57-5 (Cyclin D1); 481-46-9 (ginkgetin); EC 2.4.2.30 (Poly(ADP-ribose) Polymerases); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (CASP9 protein, human); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151118
[St] Status:MEDLINE
[do] DOI:10.3892/or.2015.4427


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[PMID]:26744872
[Au] Autor:Di Martino S; Catapano O; Siesto SR; Di Paolo M; Pugliese S; Morelli CD; Fiorica F; Varriale E; Di Francia R; Abbadessa A
[Ad] Endereço:Pathology Unit, A.O. Sant'Anna e San Sebastiano, Caserta, Italy. salvo-dimartino@libero.it.
[Ti] Título:Quantitative PCR detection of t(11;14) bcl-1/JH in mantle cell lymphoma patients: comparison of peripheral blood and bone marrow aspirate samples.
[So] Source:Eur Rev Med Pharmacol Sci;19(24):4801-10, 2015 Dec.
[Is] ISSN:2284-0729
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Mantle cell lymphoma (MCL) is a non-Hodgkin lymphoma (NHL) featured by participation of the lymph nodes, spleen, blood and bone marrow with a short remission period to standard therapies and a median overall survival of 4-5 years. PATIENTS AND METHODS: In this study, we compare the levels of bcl-1/JH fusion products detected by q-PCR in the concurrent peripheral blood (PB) and bone marrow (BM) aspirate samples from 7 patients with MCL. RESULTS: In patients with moderate to high levels of bcl-1/JH copies, the results of q-PCR analysis of PB and BM aspirate samples correlate well. In patients with high levels of bcl-1/JH copies, instead, PB levels are a good indication of tumor burden. Finally, in patients with low levels of bcl-1/JH copies, the t(11;14) may be detected by identification of neoplastic cells. CONCLUSIONS: Our data suggest that PB can be reliably used in place of BM aspirate both for detection of translocation status during minimal residual disease monitoring and for a possible molecular relapse, especially in those patients who have moderate to high levels of bcl-1/JH copies. If these results will be confirmed on a wider number of MCL patients, future study will be required to address the issue.
[Mh] Termos MeSH primário: Genes bcl-1
Linfoma de Célula do Manto/genética
[Mh] Termos MeSH secundário: Medula Óssea/patologia
Células da Medula Óssea
Transplante de Medula Óssea
Genes bcl-1/genética
Seres Humanos
Linfoma de Célula do Manto/sangue
Recidiva Local de Neoplasia
Reação em Cadeia da Polimerase em Tempo Real
Indução de Remissão
Translocação Genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[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:160109
[St] Status:MEDLINE


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[PMID]:26564741
[Au] Autor:Tan X; Ye H; Yang K; Chen D; Tang H
[Ad] Endereço:Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
[Ti] Título:[Circadian rhythm variation of the clock genes Per1 and cell cycle related genes in different stages of carcinogenesis of buccal mucosa in animal model].
[So] Source:Zhonghua Kou Qiang Yi Xue Za Zhi;50(7):392-8, 2015 Jul.
[Is] ISSN:1002-0098
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To investigate the expression and circadian rhythm variation of biological clock gene Per1 and cell cycle genes p53, CyclinD1, cyclin-dependent kinases (CDK1), CyclinB1 in different stages of carcinogenesis in buccal mucosa and its relationship with the development of buccal mucosa carcinoma. METHODS: Ninety golden hamsters were housed under 12 hours light-12 hours dark cycles, and the model of buccal squamous cell carcinoma was established by using the dimethylbenzanthracene (DMBA) to smear the golden hamster buccal mucosa. Before the DMBA was used and after DMBA was used 6 weeks and 14 weeks respectively, the golden hamsters were sacrificed at 6 different time points (5 rats per time point) within 24 hour, including 4, 8, 12, 16, 20 and 24 hour after lights onset (HALO), and the normal buccal mucosa, precancerous lesions and cancer tissue were obtained, respectively. HE stained sections were prepared to observe the canceration of each tissue. Real time RT-PCR was used to detect the mRNA expression of Per1, p53, CyclinD1, CDK1 and CyclinB1, and a cosine analysis method was applied to determine the circadian rhythm variation of Per1, p53, CyclinD1, CDK1 and CyclinB1 mRNA expression, which were characterized by median, amplitude and acrophase. RESULTS: The expression of Per1, p53, CDK1 and CyclinD1 mRNA in 6 different time points within 24 hours in the tissues of three different stages of carcinogenesis had circadian rhythm, respectively. However, the CyclinB1 mRNA was expressed with circadian rhythm just in normal and cancer tissue (P < 0.05), while in precancerous lesions the circadian rhythm was in disorder (P > 0.05). As the development of carcinoma, the median of Per1 and p53 mRNA expression were significantly decreased (P < 0.05), yet the median of CDK1, CyclinB1 and CyclinD1 mRNA expression were significantly increased (P < 0.05). The amplitude of Per1, p53 and CyclinD1 mRNA expression was significantly decreased as the development of carcinoma (P < 0.05), however the amplitude of CDK1 mRNA expression was significantly increased (P < 0.05). In addition, there was no significant difference in the amplitude of CyclinB1 mRNA expression. The time that the peak expression value of Per1 and CDK1 mRNA appeared (Acrophase) in precancerous lesions was remarkably earlier than that in normal tissues, but the acrophase of p53 and CyclinD1 mRNA expression was remarkably delayed. Moreover, the acrophase of CDK1 and CyclinB1 mRNA expression in cancer tissues was obviously earlier than that in normal tissues, yet there was no significant variation in acrophase of Per1, p53, CyclinD1 mRNA expression between normal tissues and cancer tissues. CONCLUSIONS: The circadian rhythm of clock gene Per1 and cell cycle genes p53, CyclinD1, CDK1, CyclinB1 expression remarkably varied with the occurrence and development of carcinoma. Further research into the interaction between circadian and cell cycle of two cycle activity and relationship with the carcinogenesis may providenew ideas and methods of individual treatment and the mechanism of carcinogenesis.
[Mh] Termos MeSH primário: Proteína Quinase CDC2/genética
Carcinoma de Células Escamosas/genética
Ritmo Circadiano/genética
Ciclina B1/genética
Genes bcl-1
Genes p53
Neoplasias Bucais/genética
Proteínas Circadianas Period/genética
[Mh] Termos MeSH secundário: 9,10-Dimetil-1,2-benzantraceno
Animais
Carcinogênese
Carcinógenos
Carcinoma de Células Escamosas/induzido quimicamente
Carcinoma de Células Escamosas/patologia
Ciclo Celular
Cricetinae
Modelos Animais de Doenças
Regulação Neoplásica da Expressão Gênica
Mesocricetus
Mucosa Bucal
Neoplasias Bucais/induzido quimicamente
Neoplasias Bucais/patologia
Lesões Pré-Cancerosas/genética
RNA Mensageiro/metabolismo
Ratos
Reação em Cadeia da Polimerase em Tempo Real
Fatores de Tempo
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens); 0 (Cyclin B1); 0 (Period Circadian Proteins); 0 (RNA, Messenger); 57-97-6 (9,10-Dimethyl-1,2-benzanthracene); EC 2.7.11.22 (CDC2 Protein Kinase)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:151113
[Lr] Data última revisão:
151113
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:151114
[St] Status:MEDLINE


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[PMID]:26491150
[Au] Autor:Lee HR; Mitra J; Lee S; Gao SJ; Oh TK; Kim MH; Ha T; Jung JU
[Ad] Endereço:Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California, USA hyelee@usc.edu jaeujung@med.usc.edu.
[Ti] Título:Kaposi's Sarcoma-Associated Herpesvirus Viral Interferon Regulatory Factor 4 (vIRF4) Perturbs the G1-S Cell Cycle Progression via Deregulation of the cyclin D1 Gene.
[So] Source:J Virol;90(2):1139-43, 2015 Oct 21.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kaposi's sarcoma-associated herpesvirus (KSHV) infection modulates the host cell cycle to create an environment optimal for its viral-DNA replication during the lytic life cycle. We report here that KSHV vIRF4 targets the ß-catenin/CBP cofactor and blocks its occupancy on the cyclin D1 promoter, suppressing the G1-S cell cycle progression and enhancing KSHV replication. This shows that KSHV vIRF4 suppresses host G1-S transition, possibly providing an intracellular milieu favorable for its replication.
[Mh] Termos MeSH primário: Pontos de Checagem do Ciclo Celular
Genes bcl-1
Herpesvirus Humano 8/fisiologia
Interações Hospedeiro-Patógeno
Fatores Reguladores de Interferon/metabolismo
Fragmentos de Peptídeos/antagonistas & inibidores
Sialoglicoproteínas/antagonistas & inibidores
Proteínas Virais/metabolismo
beta Catenina/antagonistas & inibidores
[Mh] Termos MeSH secundário: Regulação para Baixo
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CTNNB1 protein, human); 0 (Interferon Regulatory Factors); 0 (Peptide Fragments); 0 (Sialoglycoproteins); 0 (Viral Proteins); 0 (beta Catenin); 0 (bone sialoprotein (35-62), human); 0 (viral interferon regulatory factors)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151023
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.01897-15


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[PMID]:26431489
[Au] Autor:Anania M; Gasparri F; Cetti E; Fraietta I; Todoerti K; Miranda C; Mazzoni M; Re C; Colombo R; Ukmar G; Camisasca S; Pagliardini S; Pierotti M; Neri A; Galvani A; Greco A
[Ad] Endereço:Molecular Mechanisms Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
[Ti] Título:Identification of thyroid tumor cell vulnerabilities through a siRNA-based functional screening.
[So] Source:Oncotarget;6(33):34629-48, 2015 Oct 27.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The incidence of thyroid carcinoma is rapidly increasing. Although generally associated with good prognosis, a fraction of thyroid tumors are not cured by standard therapy and progress to aggressive forms for which no effective treatments are currently available. In order to identify novel therapeutic targets for thyroid carcinoma, we focused on the discovery of genes essential for sustaining the oncogenic phenotype of thyroid tumor cells, but not required to the same degree for the viability of normal cells (non-oncogene addiction paradigm). We screened a siRNA oligonucleotide library targeting the human druggable genome in thyroid cancer BCPAP cell line in comparison with immortalized normal human thyrocytes (Nthy-ori 3-1). We identified a panel of hit genes whose silencing interferes with the growth of tumor cells, while sparing that of normal ones. Further analysis of three selected hit genes, namely Cyclin D1, MASTL and COPZ1, showed that they represent common vulnerabilities for thyroid tumor cells, as their inhibition reduced the viability of several thyroid tumor cell lines, regardless the histotype or oncogenic lesion. This work identified non-oncogenes essential for sustaining the phenotype of thyroid tumor cells, but not of normal cells, thus suggesting that they might represent promising targets for new therapeutic strategies.
[Mh] Termos MeSH primário: Carcinoma/genética
Proteína Coatomer/genética
Genes bcl-1/genética
Sequenciamento de Nucleotídeos em Larga Escala/métodos
Proteínas Associadas aos Microtúbulos/genética
Proteínas Serina-Treonina Quinases/genética
Neoplasias da Glândula Tireoide/genética
[Mh] Termos MeSH secundário: Western Blotting
Carcinoma/patologia
Carcinoma Papilar
Linhagem Celular Tumoral
Proliferação Celular/genética
Imunofluorescência
Perfilação da Expressão Gênica/métodos
Seres Humanos
Reação em Cadeia da Polimerase
RNA Interferente Pequeno
Análise de Sequência de RNA/métodos
Neoplasias da Glândula Tireoide/patologia
Transcriptoma
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Coatomer Protein); 0 (Microtubule-Associated Proteins); 0 (RNA, Small Interfering); EC 2.7.11.1 (MASTL protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151003
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.5282


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[PMID]:26258271
[Au] Autor:Sarkozy C; Coiffier B
[Ad] Endereço:Hospices Civils de Lyon, Service d'Hématologie, Pierre Bénite, France.
[Ti] Título:Primary refractory diffuse large B cell lymphoma in the rituximab era.
[So] Source:Curr Opin Oncol;27(5):377-83, 2015 Sep.
[Is] ISSN:1531-703X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: The aim of this review is to describe the outcome of primary refractory diffuse large B cell lymphoma in the rituximab era and the different therapeutic options as well as new biological markers that could allow the pathologist to distinguish these cases at diagnosis. RECENT FINDINGS: Diffuse large B cell lymphoma outcome has been impressively improved since the introduction of rituximab in association with anthracycline-based chemotherapy; however, primary refractory patients still represent an unmet medical need. SUMMARY: If patients without relapse after 2 years from diagnosis have an outcome comparable to healthy individuals, primary refractory patients still represent 20% of the cases with a very poor overall survival. These cases are usually described as progressive patients during first line or patients reaching a nonadequate partial response or those relapsing within a year after reaching a response.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Murinos/administração & dosagem
Linfoma Difuso de Grandes Células B/tratamento farmacológico
Recidiva Local de Neoplasia/prevenção & controle
Proteínas Proto-Oncogênicas c-myc/sangue
Rituximab/administração & dosagem
Terapia de Salvação/métodos
[Mh] Termos MeSH secundário: Protocolos de Quimioterapia Combinada Antineoplásica
Biomarcadores Tumorais/sangue
Intervalo Livre de Doença
Genes bcl-1/efeitos dos fármacos
Genes bcl-2/efeitos dos fármacos
Seres Humanos
Linfoma Difuso de Grandes Células B/mortalidade
Linfoma Difuso de Grandes Células B/patologia
Recidiva Local de Neoplasia/mortalidade
Prognóstico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Murine-Derived); 0 (Biomarkers, Tumor); 0 (MYC protein, human); 0 (Proto-Oncogene Proteins c-myc); 4F4X42SYQ6 (Rituximab)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:150811
[Lr] Data última revisão:
150811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150811
[St] Status:MEDLINE
[do] DOI:10.1097/CCO.0000000000000209


  9 / 263 MEDLINE  
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[PMID]:26112963
[Au] Autor:Anghel N; Cotoraci C; Ivan A; Suciu M; Herman H; Balta C; Nicolescu L; Olariu T; Galajda Z; Ardelean A; Hermenean A
[Ad] Endereço:Department of Histology, Faculty of Medicine, Pharmacy and Dentistry, Vasile Goldis Western University of Arad, Romania.
[Ti] Título:Chrysin attenuates cardiomyocyte apoptosis and loss of intermediate filaments in a mouse model of mitoxantrone cardiotoxicity.
[So] Source:Histol Histopathol;30(12):1465-75, 2015 Dec.
[Is] ISSN:1699-5848
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Chrysin (CHR) is a natural flavonoid and is present in high concentration in honey, propolis and many plant extracts. The aim of the present study was to evaluate the effects of CHR to reduce cardiomyocyte apoptosis and loss of intermediate filaments in a mouse model of mitoxantrone cardiotoxicity. Morphology of the cardiomyocytes was determined by optic and transmission electron microscopy and biochemistry methods. The expression of Bcl-2, Bax and Caspase-3 were assessed by immunofluorecence. Tunel assay was used to assess apoptosis in cardiomyocytes. In addition, the distribution of desmin protein was evaluated using immunohistochemistry. Our results show that MTX treatment significantly increased serum levels of creatine kinase isoenzyme (CK-MB), indicator of cardiac injury and withdrawn under CHR protection. Expression levels of Bcl-2 decreased, while those of Bax and caspase-3 increased following MTX treatment. 50 mg/kg of daily CHR intake reduced Bax and caspase-3 immunopositivity and restored Bcl-2 levels to a value comparable to the control. TUNEL (+) cardiomyocyte nuclei of MTX group showed typical signs of apoptosis which almost completely disappeared in response to 50 mg/kg CHR treatment. In parallel, an irregular distribution and a weak expression of desmin is associated with MTX induced cardiotoxic effects which was also restored by CHR treatment. In conclusion chrysin inhibits MTX-triggered cardiomyocyte apoptosis via multiple pathways, including decrease of the Bax/Bcl-2 ratio and caspase-3 expression along with preservation of the desmin disarray.
[Mh] Termos MeSH primário: Antineoplásicos/toxicidade
Apoptose/efeitos dos fármacos
Flavonoides/farmacologia
Cardiopatias/induzido quimicamente
Cardiopatias/patologia
Filamentos Intermediários/efeitos dos fármacos
Mitoxantrona/toxicidade
Miócitos Cardíacos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Caspase 3/biossíntese
Creatina Quinase Forma MB/biossíntese
Fragmentação do DNA/efeitos dos fármacos
Desmina/metabolismo
Genes bcl-1/genética
Camundongos
Proteína X Associada a bcl-2/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Bax protein, mouse); 0 (Desmin); 0 (Flavonoids); 0 (bcl-2-Associated X Protein); 3CN01F5ZJ5 (chrysin); BZ114NVM5P (Mitoxantrone); EC 2.7.3.2 (Creatine Kinase, MB Form); EC 3.4.22.- (Casp3 protein, mouse); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:151112
[Lr] Data última revisão:
151112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150627
[St] Status:MEDLINE
[do] DOI:10.14670/HH-11-641


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[PMID]:25940700
[Au] Autor:Casimiro MC; Di Sante G; Crosariol M; Loro E; Dampier W; Ertel A; Yu Z; Saria EA; Papanikolaou A; Li Z; Wang C; Addya S; Lisanti MP; Fortina P; Cardiff RD; Tozeren A; Knudsen ES; Arnold A; Pestell RG
[Ad] Endereço:Departments of Cancer Biology, Thomas Jefferson University & Hospital, Philadelphia, PA 19107, USA.
[Ti] Título:Kinase-independent role of cyclin D1 in chromosomal instability and mammary tumorigenesis.
[So] Source:Oncotarget;6(11):8525-38, 2015 Apr 20.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cyclin D1 is an important molecular driver of human breast cancer but better understanding of its oncogenic mechanisms is needed, especially to enhance efforts in targeted therapeutics. Currently, pharmaceutical initiatives to inhibit cyclin D1 are focused on the catalytic component since the transforming capacity is thought to reside in the cyclin D1/CDK activity. We initiated the following study to directly test the oncogenic potential of catalytically inactive cyclin D1 in an in vivo mouse model that is relevant to breast cancer. Herein, transduction of cyclin D1(-/-) mouse embryonic fibroblasts (MEFs) with the kinase dead KE mutant of cyclin D1 led to aneuploidy, abnormalities in mitotic spindle formation, autosome amplification, and chromosomal instability (CIN) by gene expression profiling. Acute transgenic expression of either cyclin D1(WT) or cyclin D1(KE) in the mammary gland was sufficient to induce a high CIN score within 7 days. Sustained expression of cyclin D1(KE) induced mammary adenocarcinoma with similar kinetics to that of the wild-type cyclin D1. ChIP-Seq studies demonstrated recruitment of cyclin D1(WT) and cyclin D1(KE) to the genes governing CIN. We conclude that the CDK-activating function of cyclin D1 is not necessary to induce either chromosomal instability or mammary tumorigenesis.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Ciclina D1/fisiologia
Neoplasias Mamárias Experimentais/genética
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Aneuploidia
Animais
Domínio Catalítico/genética
Transformação Celular Neoplásica/genética
Células Cultivadas
Centrossomo/ultraestrutura
Instabilidade Cromossômica/genética
Ciclina D1/deficiência
Ciclina D1/genética
Feminino
Fibroblastos
Genes bcl-1
Seres Humanos
Vírus do Tumor Mamário do Camundongo/fisiologia
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Mutação
Piperazinas/farmacologia
Piridinas/farmacologia
Proteínas Recombinantes de Fusão/metabolismo
Fuso Acromático/ultraestrutura
Transdução Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CCND1 protein, human); 0 (Ccnd1 protein, mouse); 0 (Piperazines); 0 (Pyridines); 0 (Recombinant Fusion Proteins); 136601-57-5 (Cyclin D1); G9ZF61LE7G (palbociclib)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150506
[St] Status:MEDLINE



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