Littérature scientifique sur le sujet « Acute myeloid leukemia, Wnt/β-catenin, MSC »
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Articles de revues sur le sujet "Acute myeloid leukemia, Wnt/β-catenin, MSC"
Davis, Richard E., Vivian R. Ruvolo, Zhiqiang Wang, Wencai Ma, Wendy D. Schober, James Rolke, George Tidmarsh, Michael Andreeff et Peter P. Ruvolo. « GCS-100 Induces Apoptosis of Acute Myeloid Leukemia Cells By Disrupting Galectin-Mediated Survival Signaling ». Blood 124, no 21 (6 décembre 2014) : 904. http://dx.doi.org/10.1182/blood.v124.21.904.904.
Texte intégralTakam Kamga, Paul, Giada Dal Collo, Adriana Cassaro, Annalisa Adamo, Alessandro Gatti, Roberta Carusone, Mariano Di Trapani et al. « Inhibition of GSK-3 Signalling Enhances Sensitivity of Non-Promyelocitic Acute Myeloid Leukemia (AML) Cell to Chemotherapy ». Blood 128, no 22 (2 décembre 2016) : 1582. http://dx.doi.org/10.1182/blood.v128.22.1582.1582.
Texte intégralRoversi, Fernanda Marconi, Maura Lima Pereira Bueno, Rafael Gonçalves Barbosa Gomes, Guilherme Rossi Assis-Mendonça, Paulo Latuf Filho, Adriana Silva Santos Duarte et Sara T. Olalla Saad. « A Novel WNT5A-Mimicking Peptide Affects Leukemia Cell Survival in the Bone Marrow Microenvironment ». Blood 138, Supplement 1 (5 novembre 2021) : 2949. http://dx.doi.org/10.1182/blood-2021-148744.
Texte intégralTakam Kamga, Paul, Adriana Cassaro, Giada Dal Collo, Annalisa Adamo, Alessandro Gatti, Roberta Carusone, Martina Midolo et al. « Role of Wnt/β-Catenin Signalling in Acute Myeloid Leukemia (AML) Cell Response to Chemotherapy ». Blood 128, no 22 (2 décembre 2016) : 2753. http://dx.doi.org/10.1182/blood.v128.22.2753.2753.
Texte intégralElyamany, Ghaleb, Hassan Rizwan, Ariz Akhter, Mansour S. Aljabry, Sultan Alotaibi, Mohammad A. Hameed Albalawi, Meer-Taher Shabani-Rad, Tariq Mahmood Roshan et Adnan Mansoor. « “Losing the Brakes”—Suppressed Inhibitors Triggering Uncontrolled Wnt/ß-Catenin Signaling May Provide a Potential Therapeutic Target in Elderly Acute Myeloid Leukemia ». Current Issues in Molecular Biology 45, no 1 (9 janvier 2023) : 604–13. http://dx.doi.org/10.3390/cimb45010040.
Texte intégralTakam Kamga, Paul, Giada Dal Collo, Adriana Cassaro, Riccardo Bazzoni, Pietro Delfino, Annalisa Adamo, Alice Bonato et al. « Small Molecule Inhibitors of Microenvironmental Wnt/β-Catenin Signaling Enhance the Chemosensitivity of Acute Myeloid Leukemia ». Cancers 12, no 9 (21 septembre 2020) : 2696. http://dx.doi.org/10.3390/cancers12092696.
Texte intégralMan, Cheuk Him, Tsz Kan Fung, Haixia Wan, Chae Yin Cher, August Fan, Nelson Ng, Christa Ho et al. « Suppression of SOX7 by DNA methylation and its tumor suppressor function in acute myeloid leukemia ». Blood 125, no 25 (18 juin 2015) : 3928–36. http://dx.doi.org/10.1182/blood-2014-06-580993.
Texte intégralZhuang, Lihui, Richard Darley, Oliver G. Ottmann, Joanna Zabkiewicz et Caroline Alvares. « Bone Marrow Stromal Cells Mediate Adhesion Based Drug Resistance in Acute Myeloid Leukaemia through Reciprocal Feedback of the β-Catenin/CD44 Signalling Axis ». Blood 132, Supplement 1 (29 novembre 2018) : 2776. http://dx.doi.org/10.1182/blood-2018-99-113811.
Texte intégralZhang, Bin, Tinisha McDonald, Tessa L. Holyoake, Randall T. Moon, Dario Campana, Leonard Shultz et Ravi Bhatia. « Microenvironmental Protection of CML Stem and Progenitor Cells From Tyrosine Kinase Inhibitors Through N-Cadherin and Wnt Signaling ». Blood 120, no 21 (16 novembre 2012) : 912. http://dx.doi.org/10.1182/blood.v120.21.912.912.
Texte intégralMorgan, Rhys Gareth, Lorna Pearn, Kate Liddiard, Robert Hills, Alan Burnett, Alex Tonks et Richard L. Darley. « Distinct Regulation of β- and γ-Catenin throughout Hematopoietic Development Contrasts with Their Cooperative Roles In Acute Myeloid Leukemia. » Blood 116, no 21 (19 novembre 2010) : 1573. http://dx.doi.org/10.1182/blood.v116.21.1573.1573.
Texte intégralThèses sur le sujet "Acute myeloid leukemia, Wnt/β-catenin, MSC"
Bazzoni, Riccardo. « The Wnt/β-catenin Signaling : A Microenvironmental Support To Chemoresistance In Acute Myeloid Leukemia ». Doctoral thesis, 2021. http://hdl.handle.net/11562/1043500.
Texte intégralAlves, Tânia Patrícia Vasques. « The WNT/β-catenin signaling pathway as a potential therapeutic target in Acute Myeloid Leukemia ». Master's thesis, 2018. http://hdl.handle.net/10316/81893.
Texte intégralA Leucemia Mielóide Aguda (LMA) é a leucemia aguda mais comum nos adultos. Os avanços recentes nas terapias dirigidas a alvos moleculares específicos permitiram uma melhoria substancial nas taxas de remissão desta doença. Contudo, foram reportados vários casos de resistência às terapias atuais, o que conduz à necessidade de investigar novos alvos terapêuticos. A ativação constitutiva da via WNT/β-catenina foi observada em amostras de pacientes com LMA, tendo sido associada a um pior prognóstico.Neste contexto, o objetivo deste estudo foi avaliar o potencial terapêutico do IWR-1, um inibidor da via WNT/β-catenina, em dois modelos in vitro da LMA, com diferentes perfis genéticos.Para atingir esse objetivo, utilizámos dois modelos de LMA: as linhas celulares NB-4 e HL-60. A expressão de AXIN2 (o alvo específico de IWR-1) foi determinada por PCR em tempo real (qPCR). As células foram cultivadas na ausência e na presença de diferentes concentrações de IWR-1, que variaram de 10μM a 50μM. O efeito do IWR-1 na viabilidade celular foi determinado através do ensaio da resazurina. A avaliação da morte celular e do ciclo celular foram determinadas pela citometria de fluxo, utilizando a dupla marcação de anexina V/iodeto de propídeo, e pelo protocolo com iodeto de propídeo/RNAse, respetivamente. A análise morfológica foi realizada por microscopia ótica, utilizando a coloração de May-Grünwald-Giemsa. Os dados foram analisados recorrendo ao software Graphpad Prism.Ambas as linhas celulares expressaram o alvo do IWR-1, AXIN2. Contudo, as células HL-60 apresentaram níveis superiores de expressão em relação às células NB-4. Os resultados demonstraram que o IWR-1 induz uma diminuição da atividade metabólica de uma forma dependente da concentração do fármaco, do tempo de exposição e da linha celular, com valores de IC50 de 32,8µM para as células HL-60 e de 23,0µM para as células NB-4, após 48 horas de tratamento. A apoptose foi o principal mecanismo de morte celular ativado pelo IWR-1 em ambas as linhas celulares, o que foi confirmado por citometria de fluxo e análise morfológica. Nas células NB-4, o IWR-1 também induziu paragem do ciclo celular na fase G0/G1.Os resultados sugerem que a via WNT/β-catenina poderá constituir um potencial alvo terapêutico na LMA. Além disso, a eficácia do inibidor IWR-1 parece não depender dos níveis de expressão do alvo, AXIN2. As diferenças entre os efeitos observados nas duas linhas celulares poder-se-ão dever às diferenças entres os seus perfis genéticos.
Acute Myeloid Leukemia (AML) is the most common acute leukemia in adults. Recent advances in therapies directed to specific molecular targets allowed a substantial improvement in the rates of remission in this disease. However, several cases of resistance have been reported, which leads to a necessity to investigate new therapeutic targets. Constitutive activation of the WNT/β-catenin pathway has been observed in samples from patients with AML, being associated with worse prognosis. Therefore, the aim of this study was to evaluate the therapeutic potential of IWR-1, a WNT/β-catenin pathway inhibitor, in two in vitro models of AML with different genetic profiles. To achieve this purpose, we used two AML models: the NB-4 and HL-60 cell lines. The expression of AXIN2 (a specific target of IWR-1) was determined by real time PCR (qPCR). Cells were cultured in absence and presence of different concentrations of IWR-1 that ranged from 10μM to 50μM. The effect of IWR-1 on cell viability was determined using the resazurin assay. Cell death and cell cycle analysis were determined by flow cytometry, using the annexin V/propidium iodide double staining, and propidium iodide/RNase protocol, respectively. Morphological analysis was performed by optical microscopy after May-Grünwald-Giemsa staining. The data were analyzed using the Graphpad Prism software.Both cell lines expressed the IWR-1 target, AXIN2. However, HL-60 cells had higher expression levels than NB-4 cells. Our results showed that IWR-1 reduces metabolic activity in a time, dose and cell line dependent manner, with IC50 values of 32.8µM for HL-60 cells and 23.0µM for NB-4 cells, after 48h of treatment. Apoptosis was the main mechanism of cell death activated by IWR-1 in both cell lines, which was confirmed by flow cytometry and morphological analysis. In NB-4 cells, IWR-1 also induced cell cycle arrest in G0/G1 phase.The results suggest that the WNT pathway could constitute a potential therapeutic target in AML. Furthermore, the efficacy of the inhibitor IWR-1 seems not dependent on the expression levels of the target, AXIN2. The differences between the effects observed in both cell lines may be due to the differences between their genetic profiles.