Добірка наукової літератури з теми "Acute myeloid leukemia, Wnt/β-catenin, MSC"

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Статті в журналах з теми "Acute myeloid leukemia, Wnt/β-catenin, MSC"

1

Davis, Richard E., Vivian R. Ruvolo, Zhiqiang Wang, et al. "GCS-100 Induces Apoptosis of Acute Myeloid Leukemia Cells By Disrupting Galectin-Mediated Survival Signaling." Blood 124, no. 21 (2014): 904. http://dx.doi.org/10.1182/blood.v124.21.904.904.

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Abstract Galectins are a family of b-galactoside binding proteins with effects on cell adhesion, apoptosis, cell cycle, and mRNA processing. Galectin-3 (LGALS3) is unique among galectins by having an N terminal region of roughly 130 amino acids that allows for multimerization and binding to other proteins independent of carbohydrate binding. In addition to promoting BCL2 gene expression and mitochondrial integrity, LGALS3 (along with LGALS1) positively regulates RAS signaling and thus stabilizes survival proteins dependent on ERK phosphorylation such as MCL-1. The pro-survival functions of LGA
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2

Takam Kamga, Paul, Giada Dal Collo, Adriana Cassaro, et al. "Inhibition of GSK-3 Signalling Enhances Sensitivity of Non-Promyelocitic Acute Myeloid Leukemia (AML) Cell to Chemotherapy." Blood 128, no. 22 (2016): 1582. http://dx.doi.org/10.1182/blood.v128.22.1582.1582.

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Abstract Background: GSK-3 is a serine-threonine kinase involved in metabolic regulation as well as in the control of many pathways associated to cancer development, including Notch Wnt/β-catenin, Hedgehog, and AKT. It has been demonstrated that association of GSK-3 inhibitors with All-trans-retinoic acid (ATRA) significantly improves ATRA-mediated differentiation and cell death of acute promyelocytic (APL) leukaemia cells. However, little is currently known about the contribution of GSK-3 role to non-promyelocytic AML cell response to treatment with chemotherapeutic agents. Aims: In this stud
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3

Roversi, Fernanda Marconi, Maura Lima Pereira Bueno, Rafael Gonçalves Barbosa Gomes, et al. "A Novel WNT5A-Mimicking Peptide Affects Leukemia Cell Survival in the Bone Marrow Microenvironment." Blood 138, Supplement 1 (2021): 2949. http://dx.doi.org/10.1182/blood-2021-148744.

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Abstract Background: The crosstalk between hematopoietic cells and bone marrow (BM) microenvironment in hematological malignancies is related to disease initiation, maintenance and relapse. BM niche sustains a protective response against currently available treatments that have shown unwanted adverse effects and high levels of toxicity for patients. WNT5a is a glycoprotein secreted by mesenchymal stromal cells (MSC) that activates the WNT non-canonical pathway in hematopoietic cells, modulating important biological processes related to neoplasia development. Aims: To investigate WNT5a mRNA exp
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4

Takam Kamga, Paul, Adriana Cassaro, Giada Dal Collo та ін. "Role of Wnt/β-Catenin Signalling in Acute Myeloid Leukemia (AML) Cell Response to Chemotherapy". Blood 128, № 22 (2016): 2753. http://dx.doi.org/10.1182/blood.v128.22.2753.2753.

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Abstract Background: Growing evidences from both preclinical and clinical investigations reveal the critical role of Wnt signalling for the development of many cancers and for their response to chemotherapy. Although recent studies suggest that aberrant Wnt signalling can be involved in the neoplastic myeloid cell growth, the contribution of the Wnt/β-catenin pathway to AML survival and chemoresistance is still unclear. Aims: In this study, we investigated the contribution of WNT/β-CATENIN signalling to AML survival and chemoresistance. For this purpose we tested different modulators of Wnt/β-
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5

Elyamany, Ghaleb, Hassan Rizwan, Ariz Akhter, et al. "“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 (2023): 604–13. http://dx.doi.org/10.3390/cimb45010040.

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Dysregulated Wnt/β-catenin signal transduction is implicated in initiation, propagation, and poor prognosis in AML. Epigenetic inactivation is central to Wnt/β-catenin hyperactivity, and Wnt/β-catenin inhibitors are being investigated as targeted therapy. Dysregulated Wnt/β-catenin signaling has also been linked to accelerated aging. Since AML is a disease of old age (>60 yrs), we hypothesized age-related differential activity of Wnt/β-catenin signaling in AML patients. We probed Wnt/β-catenin expression in a series of AML in the elderly (>60 yrs) and compared it to a cohort of pediatric
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6

Takam Kamga, Paul, Giada Dal Collo, Adriana Cassaro та ін. "Small Molecule Inhibitors of Microenvironmental Wnt/β-Catenin Signaling Enhance the Chemosensitivity of Acute Myeloid Leukemia". Cancers 12, № 9 (2020): 2696. http://dx.doi.org/10.3390/cancers12092696.

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Wnt/β-catenin signaling has been reported in Acute Myeloid leukemia, but little is known about its significance as a prognostic biomarker and drug target. In this study, we first evaluated the correlation between expression levels of Wnt molecules and clinical outcome. Then, we studied—in vitro and in vivo—the anti-leukemic value of combinatorial treatment between Wnt inhibitors and classic anti-leukemia drugs. Higher levels of β-catenin, Ser675-phospho-β-catenin and GSK-3α (total and Ser 9) were found in AML cells from intermediate or poor risk patients; nevertheless, patients presenting high
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7

Man, Cheuk Him, Tsz Kan Fung, Haixia Wan, et al. "Suppression of SOX7 by DNA methylation and its tumor suppressor function in acute myeloid leukemia." Blood 125, no. 25 (2015): 3928–36. http://dx.doi.org/10.1182/blood-2014-06-580993.

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8

Zhuang, Lihui, Richard Darley, Oliver G. Ottmann, Joanna Zabkiewicz та 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 (2018): 2776. http://dx.doi.org/10.1182/blood-2018-99-113811.

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Abstract Eradication of minimal residual disease is a key goal in AML treatment. It has been found that interaction between leukaemic blasts and different cells of the bone marrow niche contributes to AML drug resistance. Previously we have demonstrated that β-catenin may mediate drug resistance in both short and long-term stromal co-culture assays. β-catenin is known to correlate with poor prognosis in AML. β-catenin has dual roles as both a central effector molecule of the canonical Wnt signalling pathway and a component of adherens junction. The role of Wnt/β-catenin in AML has been well es
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9

Zhang, Bin, Tinisha McDonald, Tessa L. Holyoake, et al. "Microenvironmental Protection of CML Stem and Progenitor Cells From Tyrosine Kinase Inhibitors Through N-Cadherin and Wnt Signaling." Blood 120, no. 21 (2012): 912. http://dx.doi.org/10.1182/blood.v120.21.912.912.

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Abstract Abstract 912 BCR-ABL tyrosine kinase inhibitors (TKI) do not eliminate leukemia stem cells (LSC) in chronic myeloid leukemia (CML), which remain a potential source of relapse. TKI treatment effectively inhibits BCR-ABL kinase activity in CML LSC, indicating that additional kinase-independent mechanisms contribute to LSC preservation. We investigated the role of signals from the bone marrow (BM) microenvironment in protecting chronic phase (CP) CML stem/progenitor cells from TKI treatment. Culture with human BM mesenchymal stromal cells (MSC), immortalized by ectopic expression of telo
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10

Morgan, Rhys Gareth, Lorna Pearn, Kate Liddiard та ін. "Distinct Regulation of β- and γ-Catenin throughout Hematopoietic Development Contrasts with Their Cooperative Roles In Acute Myeloid Leukemia." Blood 116, № 21 (2010): 1573. http://dx.doi.org/10.1182/blood.v116.21.1573.1573.

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Abstract Abstract 1573 Wnt proteins are important developmental regulators and are known to play a role in maintenance of hematopoietic stem cells (HSC). Wnt signaling has also been identified as one of the most frequently dysregulated processes associated with acute myeloid leukemia (AML), though the significance of this observation is as yet poorly understood. Here we investigate the role of two Wnt signaling proteins; β-catenin and γ-catenin and their respective roles in both normal human hematopoiesis and in AML. These proteins have dual and overlapping roles as transcriptional activators
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