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Pesquisa : G05.308.370.500 [Categoria DeCS]
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[PMID]:28465412
[Au] Autor:Severson E; Arnett KL; Wang H; Zang C; Taing L; Liu H; Pear WS; Shirley Liu X; Blacklow SC; Aster JC
[Ad] Endereço:Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
[Ti] Título:Genome-wide identification and characterization of Notch transcription complex-binding sequence-paired sites in leukemia cells.
[So] Source:Sci Signal;10(477), 2017 May 02.
[Is] ISSN:1937-9145
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Notch transcription complexes (NTCs) drive target gene expression by binding to two distinct types of genomic response elements, NTC monomer-binding sites and sequence-paired sites (SPSs) that bind NTC dimers. SPSs are conserved and have been linked to the Notch responsiveness of a few genes. To assess the overall contribution of SPSs to Notch-dependent gene regulation, we determined the DNA sequence requirements for NTC dimerization using a fluorescence resonance energy transfer (FRET) assay and applied insights from these in vitro studies to Notch-"addicted" T cell acute lymphoblastic leukemia (T-ALL) cells. We found that SPSs contributed to the regulation of about a third of direct Notch target genes. Although originally described in promoters, SPSs are present mainly in long-range enhancers, including an enhancer containing a newly described SPS that regulates expression. Our work provides a general method for identifying SPSs in genome-wide data sets and highlights the widespread role of NTC dimerization in Notch-transformed leukemia cells.
[Mh] Termos MeSH primário: Elementos Facilitadores Genéticos
Regulação Leucêmica da Expressão Gênica
Genoma Humano
Leucemia-Linfoma Linfoblástico de Células T Precursoras/genética
Receptores Notch/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Perfilação da Expressão Gênica
Seres Humanos
Camundongos
Leucemia-Linfoma Linfoblástico de Células T Precursoras/metabolismo
Regiões Promotoras Genéticas
Ligação Proteica
Receptores Notch/genética
Transdução de Sinais
Fatores de Transcrição/genética
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Notch); 0 (Transcription Factors)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180303
[Lr] Data última revisão:
180303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:28457753
[Au] Autor:Sadovnik I; Herrmann H; Eisenwort G; Blatt K; Hoermann G; Mueller N; Sperr WR; Valent P
[Ad] Endereço:Department of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, Vienna, Austria.
[Ti] Título:Expression of CD25 on leukemic stem cells in BCR-ABL1 CML: Potential diagnostic value and functional implications.
[So] Source:Exp Hematol;51:17-24, 2017 07.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Chronic myeloid leukemia (CML) is a stem cell-derived leukemia in which neoplastic cells exhibit the Philadelphia chromosome and the related oncoprotein BCR-ABL1. The disease is characterized by an accumulation of myeloid precursor cells in the peripheral blood and bone marrow (BM). A small fraction of neoplastic cells in the CML clone supposedly exhibits self-renewal and thus long-term disease-propagating ability. However, so far, little is known about the phenotype, function, and target expression profiles of these leukemic stem cells (LSCs). Recent data suggest that CML LSCs aberrantly express the interleukin-2 receptor alpha chain CD25. Whereas normal CD34 /CD38 BM stem cells display only low amounts of CD25 or lack CD25 altogether, CD34 /CD38 LSCs express CD25 strongly in more than 90% of all patients with untreated CML. As a result, CD25 can be used to identify and quantify CML LSCs. In addition, it has been shown that CD25 serves as a negative growth regulator of CML LSCs. Here, we review the value of CD25 as a novel marker and potential drug target in CML LSCs.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/biossíntese
Proteínas de Fusão bcr-abl/metabolismo
Regulação Leucêmica da Expressão Gênica
Subunidade alfa de Receptor de Interleucina-2/biossíntese
Leucemia Mielogênica Crônica BCR-ABL Positiva/diagnóstico
Leucemia Mielogênica Crônica BCR-ABL Positiva/metabolismo
Proteínas de Neoplasias/metabolismo
Células-Tronco Neoplásicas/metabolismo
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/metabolismo
Antígenos CD34/metabolismo
Células da Medula Óssea/metabolismo
Seres Humanos
Glicoproteínas de Membrana/metabolismo
Células-Tronco Neoplásicas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (BCR-ABL1 fusion protein, human); 0 (Biomarkers, Tumor); 0 (IL2RA protein, human); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Membrane Glycoproteins); 0 (Neoplasm Proteins); EC 2.7.10.2 (Fusion Proteins, bcr-abl); EC 3.2.2.5 (CD38 protein, human); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180224
[Lr] Data última revisão:
180224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:28456748
[Au] Autor:van Gils N; Verhagen HJMP; Smit L
[Ad] Endereço:Department of Hematology, VU University Medical Center, Cancer Center Amsterdam, Amsterdam, The Netherlands.
[Ti] Título:Reprogramming acute myeloid leukemia into sensitivity for retinoic-acid-driven differentiation.
[So] Source:Exp Hematol;52:12-23, 2017 08.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The success of all-trans retinoic acid (ATRA) therapy for acute promyelocytic leukemia (APL) provides a rationale for using retinoic acid (RA)-based therapy for other subtypes of acute myeloid leukemia (AML). Recently, several studies showed that ATRA may drive leukemic cells efficiently into differentiation and/or apoptosis in a subset of AML patients with an NPM1 mutation, a FLT3-ITD, an IDH1 mutation, and patients overexpressing EVI-1. Because not all patients within these molecular subgroups respond to ATRA and clinical trials that tested ATRA response in non-APL AML patients have had disappointing results, the identification of additional biomarkers may help to identify patients who strongly respond to ATRA-based therapy. Searching for response biomarkers might also reveal novel RA-based combination therapies with an efficient differentiation/apoptosis-inducing effect in non-APL AML patients. Preliminary studies suggest that the epigenetic or transcriptional state of leukemia cells determines their susceptibility to ATRA. We hypothesize that reprogramming by inhibitors of epigenetic-modifying enzymes or by modulation of microRNA expression might sensitize non-APL AML cells for RA-based therapy. AML relapse is caused by a subpopulation of leukemia cells, named leukemic stem cells (LSCs), which are in a different epigenetic state than the total bulk of the AML. The survival of LSCs after therapy is the main cause of the poor prognosis of AML patients, and novel differentiation therapies should drive these LSCs into maturity. In this review, we summarize the current knowledge on the epigenetic aspects of susceptibility to RA-induced differentiation in APL and non-APL AML.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Leucemia Mieloide/tratamento farmacológico
Tretinoína/uso terapêutico
[Mh] Termos MeSH secundário: Acetilação/efeitos dos fármacos
Doença Aguda
Antineoplásicos/uso terapêutico
Apoptose/genética
Diferenciação Celular/genética
Regulação Leucêmica da Expressão Gênica/efeitos dos fármacos
Histonas/metabolismo
Seres Humanos
Leucemia Mieloide/genética
Leucemia Mieloide/patologia
MicroRNAs/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Histones); 0 (MicroRNAs); 5688UTC01R (Tretinoin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180224
[Lr] Data última revisão:
180224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:29254309
[Au] Autor:Tahir IM; Iqbal T; Jamil A; Saqib M
[Ad] Endereço:Pharmaceutical Research Lab, Department of Biochemistry, University of Agriculture, Faisalabad-Pakistan.
[Ti] Título:Association of BCL-2 with oxidative stress and total antioxidant status in pediatric acute lymphoblastic leukemia.
[So] Source:J Biol Regul Homeost Agents;31(4):1023-1027, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:B-Cell Lymphoma protein-2 (BCL-2) is one of the most studied proteins with substantial regulatory potential for both apoptosis and autophagy. BCL-2 confer chemoresistance through influencing cancer pathophysiology. Serum level of lactate dehydrogenase (LDH) predicts increased anaerobic glycolysis and is associated with metabolic modulation in cancer cells. In the present research, the interplay of BCL-2, total oxidative status (TOS) and LDH was investigated in patients with acute lymphoblastic leukemia (ALL). The studied parameters, BCL-2 protein (p less than 0.001), TOS (p less than 0.001) and LDH (p less than 0.001) were significantly elevated in the ALL group compared to the normal group (N-group). However, the total antioxidant status (TAS) was reduced significantly (p less than 0.01) in ALL patients. In the ALL group, the TOS had significant negative correlation with TAS (p less than 0.01). Furthermore, non-significant positive correlations were found between BCL-2 and LDH, BCL-2 and TAS and LDH and TAS (each with; p>0.05). However, a negative non-significant correlation was observed between BCL-2 and TOS and LDH and TOS (each with; p>0.05).
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Regulação Leucêmica da Expressão Gênica
L-Lactato Desidrogenase/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
Proteínas Proto-Oncogênicas c-bcl-2/genética
[Mh] Termos MeSH secundário: Adolescente
Criança
Pré-Escolar
Feminino
Seres Humanos
Lactente
L-Lactato Desidrogenase/sangue
Masculino
Oxirredução
Estresse Oxidativo
Leucemia-Linfoma Linfoblástico de Células Precursoras/sangue
Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamento farmacológico
Leucemia-Linfoma Linfoblástico de Células Precursoras/patologia
Proteínas Proto-Oncogênicas c-bcl-2/sangue
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BCL2 protein, human); 0 (Proto-Oncogene Proteins c-bcl-2); EC 1.1.1.27 (L-Lactate Dehydrogenase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


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[PMID]:29220122
[Au] Autor:Feng Y; Shen Y; Chen H; Wang X; Zhang R; Peng Y; Lei X; Liu T; Liu J; Gu L; Wang F; Yang Y; Bai J; Wang J; Zhao W; He A
[Ad] Endereço:Department of Hematology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
[Ti] Título:Expression profile analysis of long non-coding RNA in acute myeloid leukemia by microarray and bioinformatics.
[So] Source:Cancer Sci;109(2):340-353, 2018 Feb.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nt that are involved in tumorigenesis and play a key role in cancer progression. To determine whether lncRNAs are involved in acute myeloid leukemia (AML), we analyzed the expression profile of lncRNAs and mRNAs in AML. Five pairs of AML patients and iron deficiency anemia (IDA) controls were screened by microarray. Through coexpression analysis, differently expressed transcripts were divided into modules, and lncRNAs were functionally annotated. We further analyzed the clinical significance of crucial lncRNAs from modules in public data. Finally, the expression of three lncRNAs, RP11-222K16.2, AC092580.4, and RP11-305O.6, were validated in newly diagnosed AML, AML relapse, and IDA patient groups by quantitative RT-PCR, which may be associated with AML patients' overall survival. Further analysis showed that RP11-222K16.2 might affect the differentiation of natural killer cells, and promote the immunized evasion of AML by regulating Eomesodermin expression. Analysis of this study revealed that dysregulated lncRNAs and mRNAs in AML vs IDA controls could affect the immune system and hematopoietic cell differentiation. The biological functions of those lncRNAs need to be further validated.
[Mh] Termos MeSH primário: Anemia Ferropriva/genética
Leucemia Mieloide Aguda/genética
Análise de Sequência com Séries de Oligonucleotídeos/métodos
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Biologia Computacional/métodos
Feminino
Perfilação da Expressão Gênica/métodos
Regulação Leucêmica da Expressão Gênica
Redes Reguladoras de Genes
Seres Humanos
Masculino
Prognóstico
Mapas de Interação de Proteínas
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Long Noncoding)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13465


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[PMID]:28921505
[Au] Autor:Wolf C; Garding A; Filarsky K; Bahlo J; Robrecht S; Becker N; Zucknick M; Rouhi A; Weigel A; Claus R; Weichenhan D; Eichhorst B; Fischer K; Hallek M; Kuchenbauer F; Plass C; Döhner H; Stilgenbauer S; Lichter P; Mertens D
[Ad] Endereço:Mechanisms of Leukemogenesis, German Cancer Research Center (DKFZ), Heidelberg, Germany.
[Ti] Título:NFATC1 activation by DNA hypomethylation in chronic lymphocytic leukemia correlates with clinical staging and can be inhibited by ibrutinib.
[So] Source:Int J Cancer;142(2):322-333, 2018 Jan 15.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:B cell receptor (BCR) signaling is a key for survival of chronic lymphocytic leukemia (CLL) cells, and BCR signaling inhibitors are clinically active. However, relapse and resistance to treatment require novel treatment options. To detect novel candidate therapeutic targets, we performed a genome-wide DNA methylation screen with custom arrays and identified aberrant promoter DNA methylation in 2,192 genes. The transcription factor NFATC1 that is a downstream effector of BCR signaling was among the top hypomethylated genes and was concomitantly transcriptionally upregulated in CLL. Intriguingly, NFATC1 promoter DNA hypomethylation levels were significantly variant in clinical trial cohorts from different disease progression stages and furthermore correlated with Binet disease staging and thymidine kinase levels, strongly suggesting a central role of NFATC1 in CLL development. Functionally, DNA hypomethylation at NFATC1 promoter inversely correlated with RNA levels of NFATC1 and dysregulation correlated with expression of target genes BCL-2, CCND1 and CCR7. The inhibition of the NFAT regulator calcineurin with tacrolimus and cyclosporin A and the BCR signaling inhibitor ibrutinib significantly reduced NFAT activity in leukemic cell lines, and NFAT inhibition resulted in increased apoptosis of primary CLL cells. In summary, our results indicate that the aberrant activation of NFATC1 by DNA hypomethylation and BCR signaling plays a major role in the pathomechanism of CLL.
[Mh] Termos MeSH primário: Metilação de DNA
Regulação Leucêmica da Expressão Gênica
Leucemia Linfocítica Crônica de Células B/genética
Fatores de Transcrição NFATC/genética
Recidiva Local de Neoplasia/genética
Pirazóis/farmacologia
Pirimidinas/farmacologia
[Mh] Termos MeSH secundário: Idoso
Biomarcadores Tumorais
Feminino
Seres Humanos
Leucemia Linfocítica Crônica de Células B/tratamento farmacológico
Leucemia Linfocítica Crônica de Células B/patologia
Masculino
Fatores de Transcrição NFATC/antagonistas & inibidores
Fatores de Transcrição NFATC/metabolismo
Recidiva Local de Neoplasia/tratamento farmacológico
Recidiva Local de Neoplasia/patologia
Estadiamento de Neoplasias
Regiões Promotoras Genéticas
Inibidores de Proteínas Quinases/farmacologia
Transdução de Sinais
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (NFATC Transcription Factors); 0 (PCI 32765); 0 (Protein Kinase Inhibitors); 0 (Pyrazoles); 0 (Pyrimidines)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171214
[Lr] Data última revisão:
171214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.31057


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[PMID]:29032147
[Au] Autor:Zhang TJ; Lin J; Zhou JD; Li XX; Zhang W; Guo H; Xu ZJ; Yan Y; Ma JC; Qian J
[Ad] Endereço:Department of Hematology, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, People's Republic of China; The Key Lab of Precision Diagnosis and Treatment of Zhenjiang City, Zhenjiang, Jiangsu, People's Republic of China; School of Medicine, Jiangsu University, Zhenjiang, Jiangsu
[Ti] Título:High bone marrow miR-19b level predicts poor prognosis and disease recurrence in de novo acute myeloid leukemia.
[So] Source:Gene;640:79-85, 2018 Jan 15.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Oncogenic role of miR-19 family has been identified in human cancers especially in lymphoid malignancies. However, to date, little studies investigated the role of miR-19 family in myeloid malignancies. Herein, we examined miR-19a/b expression and explored its clinical significance in de novo acute myeloid leukemia (AML). The detection of miR-19a/b expression was performed by real-time quantitative PCR in bone marrow mononuclear cells of 113 patients and 42 healthy donors. Both miR-19a/b levels were significantly increased in AML patients in contrast to controls. Patients with miR-19a/b overexpression were more frequently occurred in female, and had an older age. Moreover, cases with miR-19a overexpression had a higher frequency of U2AF1, C-KIT and CEBPA mutations, whereas miR-19b overexpressed cases harbored U2AF1 and IDH1/2 mutations. There was no significant association of miR-19a overexpression with complete remission (CR) rate and overall survival (OS) among whole-cohort AML, non-M3 AML, and cytogenetically normal AML (CN-AML). However, although miR-19b overexpression was not correlated with CR rate, patients with miR-19b overexpression presented significantly shorter OS in whole-cohort AML and a trend in non-M3 AML and CN-AML patients. Importantly, our data also showed that miR-19a/b expression level at CR phase was lower than diagnosis time, and was returned to primary level even higher when at relapse phase. Our findings revealed that miR-19a/b overexpression were frequent events in de novo AML patients. Moreover, up-regulation of miR-19b expression was associated with poor prognosis and disease recurrence in AML.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Medula Óssea/metabolismo
Regulação Leucêmica da Expressão Gênica
Leucemia Mieloide Aguda/genética
MicroRNAs/genética
Recidiva Local de Neoplasia/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais/metabolismo
Medula Óssea/patologia
Estudos de Casos e Controles
Criança
Feminino
Seguimentos
Perfilação da Expressão Gênica
Seres Humanos
Leucemia Mieloide Aguda/metabolismo
Leucemia Mieloide Aguda/patologia
Masculino
Meia-Idade
Mutação
Recidiva Local de Neoplasia/metabolismo
Recidiva Local de Neoplasia/patologia
Estadiamento de Neoplasias
Prognóstico
Curva ROC
Taxa de Sobrevida
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (MIRN19 microRNA, human); 0 (MicroRNAs)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171017
[St] Status:MEDLINE


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[PMID]:28084621
[Au] Autor:Mirzaei H; Fathullahzadeh S; Khanmohammadi R; Darijani M; Momeni F; Masoudifar A; Goodarzi M; Mardanshah O; Stenvang J; Jaafari MR; Mirzaei HR
[Ad] Endereço:Department of Medical Biotechnology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
[Ti] Título:State of the art in microRNA as diagnostic and therapeutic biomarkers in chronic lymphocytic leukemia.
[So] Source:J Cell Physiol;233(2):888-900, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Early diagnostic is one of the most important steps in cancer therapy which helps to design and choose a better therapeutic approach. The finding of biomarkers in various levels including genomics, transcriptomics, and proteomics levels could provide better treatment for various cancers such as chronic lymphocytic leukemia (CLL). The CLL is the one of main lymphoid malignancies which is specified by aggregation of mature B lymphocytes. Among different biomarkers (e.g., CD38, chromosomes abnormalities, ZAP-70, TP53, and microRNA [miRNA]), miRNAs have appeared as new diagnostic and therapeutic biomarkers in patients with the CLL disease. Multiple lines of evidence indicated that deregulation of miRNAs could be associated with pathological events which are present in the CLL. These molecules have an effect on a variety of targets such as Bcl2, c-fos, c-Myc, TP53, TCL1, and STAT3 which play critical roles in the CLL pathogenesis. It has been shown that expression of miRNAs could lead to the activation of B cells and B cell antigen receptor (BCR). Moreover, exosomes containing miRNAs are one of the other molecules which could contribute to BCR stimulation and progression of CLL cells. Hence, miRNAs and exosomes released from CLL cells could be used as potential diagnostic and therapeutic biomarkers for CLL. This critical review focuses on a very important aspect of CLL based on biomarker discovery covers the pros and cons of using miRNAs as important diagnostics and therapeutics biomarkers for this deadly disease.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Leucemia Linfocítica Crônica de Células B/genética
MicroRNAs/genética
[Mh] Termos MeSH secundário: Animais
Regulação Leucêmica da Expressão Gênica
Seres Humanos
Leucemia Linfocítica Crônica de Células B/diagnóstico
Leucemia Linfocítica Crônica de Células B/metabolismo
Leucemia Linfocítica Crônica de Células B/terapia
Técnicas de Diagnóstico Molecular
Valor Preditivo dos Testes
Prognóstico
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (MicroRNAs)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25799


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[PMID]:29068867
[Au] Autor:Mosakhani N; Missiry ME; Vakkila E; Knuutila S; Vakkila J
[Ad] Endereço:*Department of Pathology, Haartman Institute and HUSLAB, University of Helsinki †Hematology Research Unit, University of Helsinki, Helsinki, Finland ‡Department of Women's and Children's Health, Karolinska University Hospital, Stockholm, Sweden.
[Ti] Título:Low Expression of miR-18a as a Characteristic of Pediatric Acute Lymphoblastic Leukemia.
[So] Source:J Pediatr Hematol Oncol;39(8):585-588, 2017 Nov.
[Is] ISSN:1536-3678
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Acute lymphoblastic leukemia (ALL) occurs in both adults and children but the response to chemotherapy and survival is significantly worse in the adults. We aimed to study whether the expression of immune system-associated miRNAs would differ between adult and pediatric patients with ALL at the time of diagnosis. MATERIALS AND METHODS: Inflammation-associated miRNA analysis was performed in 19 adults and 79 pediatric patients with ALL and involved miR-10, miR-15, miR-16, miR-17-92 cluster, miR-33, miR-146a, miR-150, miR-155, miR-181a, miR-222, miR-223, and miR-339. MiRNAs were first analyzed by miRNA microarray and thereafter validated by qRT-PCR. Sufficient RNA for qRT-PCR was available for 42 pediatric and 19 adult patients. RESULTS: Of the studied miRNAs, only miR-18a differed significantly in microarray analysis between adult and pediatric ALL, being lower in children (FC, -3.74; P, 0.0037). Results were confirmed by qRT-PCR (down-regulated in pediatric patients, P 0.003161). The other members of the miR-17-92 cluster did not differ significantly. CONCLUSIONS: Pediatric and adult patients with ALL have remarkably similar patterns of immune-cell-associated miRNAs in their bone marrow at diagnosis. However, the low expression of miR-18a in pediatric ALL is interesting and demands further study.
[Mh] Termos MeSH primário: Expressão Gênica
MicroRNAs/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Medula Óssea/patologia
Estudos de Casos e Controles
Criança
Pré-Escolar
Aberrações Cromossômicas
Biologia Computacional/métodos
Feminino
Perfilação da Expressão Gênica
Regulação Leucêmica da Expressão Gênica
Seres Humanos
Lactente
Masculino
Meia-Idade
Leucemia-Linfoma Linfoblástico de Células Precursoras/diagnóstico
Leucemia-Linfoma Linfoblástico de Células Precursoras/imunologia
Interferência de RNA
RNA Mensageiro/genética
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN18 microRNA, human); 0 (MicroRNAs); 0 (RNA, Messenger)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171026
[St] Status:MEDLINE
[do] DOI:10.1097/MPH.0000000000000921


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[PMID]:29037126
[Au] Autor:Zhu K; Jiang B; Yang Y; Hu R; Liu Z
[Ad] Endereço:1 Department of Hematology, Shengjing Hospital of China Medical University, Shenyang, China.
[Ti] Título:DACT1 overexpression inhibits proliferation, enhances apoptosis, and increases daunorubicin chemosensitivity in KG-1α cells.
[So] Source:Tumour Biol;39(10):1010428317711089, 2017 Oct.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DACT1 has been shown to participate in the development of many types of tumors; however, its role and precise molecular mechanisms in leukemia are unclear. In this study, we investigated the effect of DACT1 on KG-1α leukemia cells to further understand the mechanisms of DACT1-mediated tumor suppression. We transfected a DACT1 expression plasmid to upregulate DACT1 in KG-1α cells and analyzed the resulting phenotypic changes. The results demonstrated that DACT1 overexpression inhibited KG-1α proliferation, increased apoptosis, and arrested cells in the G0/G1 phase. Mechanistically, DACT1 overexpression inhibited Wnt/ß-catenin signaling by reducing nuclear ß-catenin levels in KG-1α cells. Furthermore, the viability of KG-1α cells transfected with DACT1 was significantly reduced when treated with daunorubicin. We also found that DACT1 reduced P-glycoprotein expression in KG-1α cells. These findings revealed an inhibitory role for DACT1 in leukemogenesis and provided evidence that DACT1 is an attractive target for the development of novel anti-leukemia therapies.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/genética
Apoptose/genética
Proliferação Celular/genética
Daunorrubicina/farmacologia
Regulação Leucêmica da Expressão Gênica/genética
Leucemia/tratamento farmacológico
Leucemia/genética
Proteínas Nucleares/genética
[Mh] Termos MeSH secundário: Membro 1 da Subfamília B de Cassetes de Ligação de ATP/genética
Carcinogênese/genética
Linhagem Celular Tumoral
Fase G1/genética
Seres Humanos
Fase de Repouso do Ciclo Celular/genética
Transfecção/métodos
Regulação para Cima/genética
Via de Sinalização Wnt/genética
beta Catenina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATP-Binding Cassette, Sub-Family B, Member 1); 0 (Adaptor Proteins, Signal Transducing); 0 (DACT1 protein, human); 0 (Nuclear Proteins); 0 (beta Catenin); ZS7284E0ZP (Daunorubicin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317711089



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