Relevant bibliographies by topics / Acute myeloid leukemia, Wnt/β-catenin, MSC / Journal articles
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Journal articles on the topic 'Acute myeloid leukemia, Wnt/β-catenin, MSC'

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Published: 11 March 2023

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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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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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11

Chai-Ho, Wanxing, Martina M. Roos, Michelle Li, et al. "Grb10 Is a Tumor Suppressor in Human Acute Myeloid Leukemia." Blood 132, Supplement 1 (2018): 1344. http://dx.doi.org/10.1182/blood-2018-99-110844.

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Abstract Acute myeloid leukemia (AML) is a common and potentially fatal hematologic malignancy. Allogeneic stem cell transplantation is the only curative therapy for most subtypes of AML, but carries a significant risk of transplant-related mortality. The development of novel therapies to eradicate AML remains a substantial area of unmet medical need. Growth factor receptor bound protein 10 (Grb10) is a member of the family of imprinted genes. Our laboratory demonstrated that in normal hematopoietic system, deletion of the maternal allele of Grb10 significantly increased hematopoietic stem cel
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12

Hassan, Nunki, Hangyu Yi, Lucie Gaspard-Boulinc, et al. "GADD45a Controls Self-Renewal in Acute Myeloid Leukemia Stem Cells." Blood 136, Supplement 1 (2020): 31. http://dx.doi.org/10.1182/blood-2020-142389.

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Acute myeloid leukemia (AML) is a heterogenous malignancy, where the persistence of chemo-resistant leukemia stem cells (LSCs) contributes to disease relapse. We have previously demonstrated the clinical significance of WNT/β-catenin signaling in driving AML LSCs (Science, 327:1650-1653, 2010; Cancer Cell, 38:1-16, 2020). In this study, we uncover that GADD45a (growth arrest and DNA-damage inducible protein) is an essential regulator of β-catenin signaling pathway and its loss promotes LSC function and leukemia progression. Transgenic knockout of Gadd45a led to a progressive increase in aberra
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13

Hassan, Nunki, Basit Salik, Alastair Duly, and Jenny Yingzi Wang. "Rspo-LGR4 Cooperates with HOXA9 to Sustain Self-Renewal in Acute Myeloid Leukemia." Blood 134, Supplement_1 (2019): 2669. http://dx.doi.org/10.1182/blood-2019-129704.

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Acute myeloid leukemia (AML) is associated with high relapse rates and poor survival, with limited response to conventional cancer therapy and lacking effective targeting of highly self-renewing leukemic stem cells (LSCs). The mechanism underlying the high self-renewal activity of LSCs that determines the aggressiveness of disease remains poorly understood. Although we and others have previously demonstrated the clinical significance of aberrant WNT/β-catenin signaling in AML (Science, 327:1650-1653, 2010; Cancer Cell, 18:606-618, 2010), its pharmacologically tractable components essential for
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14

Almars, Amany, Panagiota S. Chondrou, Emenike K. Onyido та ін. "Increased FLYWCH1 Expression is Negatively Correlated with Wnt/β-catenin Target Gene Expression in Acute Myeloid Leukemia Cells". International Journal of Molecular Sciences 20, № 11 (2019): 2739. http://dx.doi.org/10.3390/ijms20112739.

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Acute myeloid leukaemia (AML) is a heterogeneous clonal malignancy of hematopoietic progenitor cells. The Wnt pathway and its downstream targets are tightly regulated by β-catenin. We recently discovered a new protein, FLYWCH1, which can directly bind nuclear β-catenin. Herein, we studied the FLYWCH1/β-catenin pathway in AML cells using qRT-PCR, Western blot, and immunofluorescence assays. In addition, the stemness activity and cell cycle were analysed by the colony-forming unit (CFU) using methylcellulose-based and Propidium iodide/flow cytometry assays. We found that FLYWCH1 mRNA and protein
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15

Chai, Li, Wei Cui, Jianchang Chang, Chunhui Di, Hesham Amin та Yupo Ma. "SALL4, a Novel Oncogene Induces Myelodysplastic Syndrome and Acute Myeloid Leukemia Via Wnt/β-Catenin Pathway." Blood 106, № 11 (2005): 1371. http://dx.doi.org/10.1182/blood.v106.11.1371.1371.

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Abstract SALL4, a gene homologous to the Drosophila homeotic spalt, is a zinc finger transcriptional factor essential for human development. In Drosophila, spalt is regulated by the Wnt signaling pathway, a pathway critical for hematopoietic self-renewal of stem cells. We cloned SALL4 and its isoforms (SALL4A and SALL4B). We used immunohistochemistry, to demonstrate that SALL4 was constitutively expressed in primary acute myeloid leukemia cells (French American British, FAB: M1 to M5, N=81). The SALL4 in RNA was quantitative in bone marrow cells derived from acute myeloid leukemia (AML) and co
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16

Wang, Lei, and Jie Jin. "The Mechanisms of Synergistically Cytotoxicity Induced by Homoharringtonine and Aclarubicin in Acute Myeloid Leukemia Cells." Blood 120, no. 21 (2012): 4313. http://dx.doi.org/10.1182/blood.v120.21.4313.4313.

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Abstract Abstract 4313 Previous studies showed HAA regime [HHT (homoharringtonine), cytarabine and ACR (aclarubicin)] resulted in a high complete remission (CR) rate and a better overall survival (OS) rate in patients with primary acute myeloid leukemia. To confirm if a synergistically cytotoxicity was found in AML cells, we investigated the antitumor effect relationship of HHT and ACR against AML cells. Using in vitro system, we demonstrated that simultaneous exposure to HHT and ACR resulted in strong synergistic anti-proliferative effect and apoptosis inducing in AML cells. In vivo, combinat
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17

Tong, Hongyan, Kongfei Li, Chen Mei, Chao Hu, and Jie Jin. "Synergistic Effect of Sequential Combination of Decitabine and Idarubicin in Mouse Model of Human Acute Myeloid Leukemia." Blood 120, no. 21 (2012): 1515. http://dx.doi.org/10.1182/blood.v120.21.1515.1515.

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Abstract Abstract 1515 Background: Decitabine is a prototype for epigenetic therapy in cancer which targets DNA methyltransferase. While it was known that decitabine monotherapy has been associated with a relative low rate of complete remission rates in acute myeloid leukemia and myelodysplastic syndrome. Several groups have attempted to increase the response rate with decitabine-based therapy by developing combinations. In the preliminary experiments, we investigated the effect of anti-leukemia drugs (idarubicin, daunorubicin, cytarabine, thalidomide and homoharringtonine) in combination simu
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18

Jimbo, Koji, Takaaki Konuma, Takahiro Ito, Yaeko Nakajima-Takagi, Atsushi Iwama та Arinobu Tojo. "Immunoglobulin Superfamily Member 8 Is Indispensable for Myeloid Leukemia Via Wnt/β-Catenin Signaling Pathway". Blood 136, Supplement 1 (2020): 23–24. http://dx.doi.org/10.1182/blood-2020-136045.

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Immunoglobulin superfamily member 8 (IGSF8, also known as EWI-2, PGRL, and CD316), is a cell surface protein containing 4 immunoglobulin domains. IGSF8 directly binds to the tetraspanin molecules, CD9 and CD81, and modulates cell adhesion, migration, and growth. Previous studies demonstrated that IGSF8 was associated with prognosis and metastasis in several solid tumors. However, the role of IGSF8 in normal hematopoiesis and myeloid leukemia is still unclear. First, we examined the expression levels of Igsf8 in various hematopoietic fraction of wild-type murine bone marrow cells, and found tha
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19

Griffiths, Elizabeth A., Craig M. Hooker, Michael A. McDevitt, Judith E. Karp, James G. Herman, and Hetty E. Carraway. "Acute Myeloid Leukemia Is Characterized by Wnt Pathway Inhibitor Promoter Methylation." Blood 112, no. 11 (2008): 2253. http://dx.doi.org/10.1182/blood.v112.11.2253.2253.

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Abstract The Wnt pathway contributes to a stem-cell like phenotype in a variety of cancer subtypes. Nuclear localization of non-phosphorylated, active β-catenin is a surrogate marker for Wnt pathway activation and has been associated with adverse outcome in patients with acute myeloid leukemia (AML). Wnt pathway inhibitors including APC, DKK1, DKK3, LKB1/STK11, RASSF1A, RUNX3, SFRP1, SFRP2, SFRP4, SFRP5, SOX17, and WIF1 contain extensive promoter region CpG islands. Wnt pathway inhibitors are silenced by promoter methylation in many malignancies including lung cancer, colon cancer and acute ly
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20

Moore, Amy C., Joseph M. Amann, Christopher S. Williams, et al. "Myeloid Translocation Gene Family Members Associate with T-Cell Factors (TCFs) and Influence TCF-Dependent Transcription." Molecular and Cellular Biology 28, no. 3 (2007): 977–87. http://dx.doi.org/10.1128/mcb.01242-07.

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ABSTRACT Canonical Wnt signaling is mediated by a molecular “switch” that regulates the transcriptional properties of the T-cell factor (TCF) family of DNA-binding proteins. Members of the myeloid translocation gene (MTG) family of transcriptional corepressors are frequently disrupted by chromosomal translocations in acute myeloid leukemia, whereas MTG16 may be inactivated in up to 40% of breast cancer and MTG8 is a candidate cancer gene in colorectal carcinoma. Genetic studies imply that this corepressor family may function in stem cells. Given that mice lacking Myeloid Translocation Gene Rel
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21

Sayitoglu, Muge, Ozden Hatirnaz, Yucel Erbilgin, Fatmahan Atalar, and Ugur Ozbek. "Different Activation of WNT Signaling Pathway in B-Cell and T-Cell Acute Leukemias." Blood 108, no. 11 (2006): 4317. http://dx.doi.org/10.1182/blood.v108.11.4317.4317.

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Abstract WNT signaling pathway proteins function as hematopoietic growth factors and regulate proliferation in normal T-cell and B-cell development. Recent experimental evidence demonstrated that oncogenic transformation in leukemias of both lymphoid and myeloid lineages is dependent on WNT signaling. Not much is known about activation of WNT signaling pathway, its ligands and receptors in hematopoiesis and leukemia pathogenesis. To define its role in leukemia, we aimed to determine mRNA levels of the critical members of WNT pathway (WNT5A, WNT10B, FZ5, β catenin, APC, TCF-1 and LEF-1) by usin
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22

Kode, Aruna, Sanil Manavalan, Ioanna Mossialou, et al. "Leukemogenic Transformation of Hematopoietic Cells by Constitutive Activation of Canonical Wnt Signaling in Osteoblast Precursors." Blood 120, no. 21 (2012): 509. http://dx.doi.org/10.1182/blood.v120.21.509.509.

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Abstract Abstract 509 Osteoblasts, the bone forming cells, are implicated in the fate of healthy and malignant stem cells. They affect self-renewal and expansion of hematopoietic stem cells (HSCs) and homing of tumor cells into the bone marrow. Here we show that constitutive activation of canonical Wnt signaling in osteoblast precursors disrupts hematopoiesis in mice by shifting the differentiation potential of HSC progenitors to the myeloid lineage which results in accumulation of granulocyte/monocyte progenitors and concomitant development of acute myeloid leukemia (AML). B-lymphopoiesis is
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23

Hu, Kaimin, Lizhen Liu, Binsheng Wang та ін. "Bone Marrow Mesenchymal Stromal Cells Protect Acute Lymphocytic Leukemia Cells From Cytotoxic Agents Via MAPK/Erk and Wnt/β-Catenin Signal Pathways". Blood 120, № 21 (2012): 4736. http://dx.doi.org/10.1182/blood.v120.21.4736.4736.

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Abstract Abstract 4736 Acute lymphoblastic leukemia (ALL) remains one of the greatest challenges in oncology. Relapsed ALL is a leading cause of death in young people, and further improvements in outcome will required the development of therapeutic approaches directed against rational therapeutic targets. Increasing evidence indicated that the bone marrow microenvironment plays a crucial role in the pathogenesis of leukemia by promoting tumor cell growth and survival as well as drug resistance. As a pivotal component of the bone marrow microenvironment, how bone marrow derived mesenchymal stro
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Tickenbrock, Lara, Joachim Schwäble, Markus Wiedehage, et al. "Flt3 tandem duplication mutations cooperate with Wnt signaling in leukemic signal transduction." Blood 105, no. 9 (2005): 3699–706. http://dx.doi.org/10.1182/blood-2004-07-2924.

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AbstractActivating Flt3 mutations occur in about 30% of patients with acute myeloid leukemia (AML), often as in-frame internal tandem duplication (ITD) at the juxtamembrane domain of the receptor. These mutations transform hematopoietic cell lines and primary mouse bone marrow. Here, we analyzed the interaction between oncogenic Flt3-ITD mutations and the Wingless-type (Wnt) signaling pathway in the myeloid progenitor cell line 32D. Microarray analyses revealed higher mRNA expression of Frizzled-4, a receptor for Wnt ligands in 32D/Flt3-ITD cells. Findings were verified by quantitative realtim
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25

Müller-Tidow, Carsten, Björn Steffen, Thomas Cauvet, et al. "Translocation Products in Acute Myeloid Leukemia Activate the Wnt Signaling Pathway in Hematopoietic Cells." Molecular and Cellular Biology 24, no. 7 (2004): 2890–904. http://dx.doi.org/10.1128/mcb.24.7.2890-2904.2004.

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ABSTRACT The acute myeloid leukemia (AML)-associated translocation products AML1-ETO, PML-retinoic acid receptor alpha (RARα), and PLZF-RARα encode aberrant transcription factors. Several lines of evidence suggest similar pathogenetic mechanisms for these fusion proteins. We used high-density oligonucleotide arrays to identify shared target genes in inducibly transfected U937 cells expressing AML1-ETO, PML-RARα, or PLZF-RARα. All three fusion proteins significantly repressed the expression of 38 genes and induced the expression of 14 genes. Several of the regulated genes were associated with W
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26

Cheng, Chi Keung, Libby Li, Suk Hang Cheng, et al. "Secreted-frizzled related protein 1 is a transcriptional repression target of the t(8;21) fusion protein in acute myeloid leukemia." Blood 118, no. 25 (2011): 6638–48. http://dx.doi.org/10.1182/blood-2011-05-354712.

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Abstract Secreted-frizzled related proteins (SFRPs) are modulators of the Wnt signaling pathway that is closely involved in normal and malignant hematopoiesis. Epigenetic deregulation of Wnt modulators leading to aberrant signaling has been reported in adult patients with acute myeloid leukemia (AML), but its occurrence in childhood patients with AML and the role of individual modulators are unclear. In this study, we examined SFRP1, SFRP2, SFRP4, and SFRP5 promoter methylation in 83 patients with AML (59 children and 24 adults) and found preferential SFRP1 methylation and mRNA down-regulation
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27

Liu, Lin, Keyan Chen, Hua Fan та Feng Jin. "MiR-599 regulates the activity of acute myeloid leukemia cells through MYC-mediated Wnt/β-catenin signaling". Annals of Translational Medicine 10, № 3 (2022): 149. http://dx.doi.org/10.21037/atm-21-6852.

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28

Ji, Hongyan, Li Chen, Yuqian Xing та ін. "CD82 supports survival of childhood acute myeloid leukemia cells via activation of Wnt/β-catenin signaling pathway". Pediatric Research 85, № 7 (2019): 1024–31. http://dx.doi.org/10.1038/s41390-019-0370-3.

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Liu, Ye, Wei Wang, Yuan Li та Yao Huang. "SOX30 confers a tumor suppressive effect in acute myeloid leukemia through inactivation of Wnt/β-catenin signaling". Molecular and Cellular Probes 52 (серпень 2020): 101578. http://dx.doi.org/10.1016/j.mcp.2020.101578.

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Xin, Hong, Chengliang Li та Minjuan Wang. "DIXDC1 promotes the growth of acute myeloid leukemia cells by upregulating the Wnt/β-catenin signaling pathway". Biomedicine & Pharmacotherapy 107 (листопад 2018): 1548–55. http://dx.doi.org/10.1016/j.biopha.2018.08.144.

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31

Golding, Michelle, Pragya Srivastava, Golda Collamat та ін. "SGI-110, a Novel Hypomethylating Agent, Induces the WNT Inhibitor Secreted Frizzled Related Protein-2 (SFRP2), and Down Regulates β-Catenin in Acute Myeloid Leukemia (AML) Cells". Blood 120, № 21 (2012): 1290. http://dx.doi.org/10.1182/blood.v120.21.1290.1290.

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Abstract Abstract 1290 Introduction: SGI-110 (Astex Pharmaceuticals, Inc.) is a dinucleotide hypomethylating agent whose active metabolite is decitabine (DAC). This drug demonstrates superior pharmacokinetics relative to the parent drug as a result of resistance to modification by cytidine deaminase, and is being investigated in myeloid malignancy in the phase I/II setting. We and others have demonstrated that WNT inhibitory genes including SFRP2 are epigenetically silenced in AML and that exposure to DNA methyltransferase inhibitors such as 5-Azacitidine (AZA) and DAC can re-express these gen
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32

Braggio, Danielle Almeida, Fernanda Costas C. de Faria, David Koller та ін. "Preclinical efficacy of the Wnt/β-catenin pathway inhibitor BC2059 for the treatment of desmoid tumors". PLOS ONE 17, № 10 (2022): e0276047. http://dx.doi.org/10.1371/journal.pone.0276047.

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Mutation in the CTNNB1 gene, leading to a deregulation of the WTN/β-catenin pathway, is a common feature of desmoid tumors (DTs). Many β-catenin inhibitors have recently been tested in clinical studies; however, BC2059 (also referred as Tegavivint), a selective inhibitor of nuclear β-catenin that works through binding TBL-1, is the only one being evaluated in a clinical study, specifically for treatment of desmoid tumor patients. Preclinical studies on BC2059 have shown activity in multiple myeloma, acute myeloid leukemia and osteosarcoma. Our preclinical studies provide data on the efficacy o
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Sun, Clare, Christopher S. Seet, Jun Zhang, Yechen Xiao, Dewen You, and Jiwang Zhang. "FLT3 Signaling Enhances Stemness in Murine MLL-AF9 Acute Myeloid Leukemia." Blood 120, no. 21 (2012): 2980. http://dx.doi.org/10.1182/blood.v120.21.2980.2980.

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Abstract Abstract 2980 Acute myeloid leukemia (AML) is developmentally similar to normal hematopoiesis and driven by a subpopulation of leukemia stem cells (LSCs). LSCs are defined by their ability to self-renew and differentiate into more mature leukemia cells. These properties are influenced by the stem cell niche in which they reside. A number of key cytokines within this microenvironment have been identified, including CXCL12 and stem cell factor (SCF), while others have altered the lineage fate of leukemia by in vitro manipulation of growth factor conditions. Activating mutations in fms-l
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Li, C., H. Xin, Y. Shi та J. Mu. "Knockdown of TRIM24 suppresses growth and induces apoptosis in acute myeloid leukemia through downregulation of Wnt/GSK-3β/β-catenin signaling". Human & Experimental Toxicology 39, № 12 (2020): 1725–36. http://dx.doi.org/10.1177/0960327120938845.

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Tripartite motif-containing protein 24 (TRIM24) has currently emerged as a crucial cancer-related gene present in a wide range of human cancer types. However, the involvement of TRIM24 in acute myeloid leukemia (AML) has not been well investigated. The present study aims to investigate the significance, cellular function, and potential regulatory mechanism of TRIM24 in AML. We found that TRIM24 expression was significantly upregulated in AML compared with normal tissues. AML patients with low expression of TRIM24 had higher survival rates than those expressing TRIM24 at higher levels. High exp
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35

Wu, Jun, Yingying Xie, and Limei Han. "miR-144-3p Derived from Bone Marrow Mesenchymal Stem Cells (BMSCs) Restrains the Drug Resistance of Acute Myeloid Leukemia (AML)." Journal of Biomaterials and Tissue Engineering 12, no. 8 (2022): 1525–29. http://dx.doi.org/10.1166/jbt.2022.3065.

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This study assessed whether miR-144-3p derived from BMSCs restrains the drug resistance of AML. Our study intends to assess miR-144-3p’s role in AML drug resistance. Drug resistance AML cells were transfected with miR-144-3p mimic or NC followed by measuring miR-144-3p level, relation of miR-144-3p with Wnt, cell activity and apoptosis by flow cytometry and the expression of signal proteins by Western Blot. The action of miR-144-3p in inducting drug resistance of K562/AND was more effective. Cell apoptosis and proliferative index was increased by overexpression of miR-144-3p along with signifi
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Golding, Michelle, Benjamin E. Paluch, Pragya Srivastava та ін. "Patients Treated With Decitabine Demonstrate Changes In β-Catenin Localization From The Nucleus To The Cytoplasm In Circulating Blasts". Blood 122, № 21 (2013): 3956. http://dx.doi.org/10.1182/blood.v122.21.3956.3956.

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Abstract Background The DNA methyltransferase inhibitors (DNMTi) 5-azacitidine (Aza) and decitabine (Dac) are a standard of care for patients with myelodysplatic syndrome (MDS) and acute myeloid leukemia (AML). Many hypotheses exist for the mechanism of these agents, including re-expression of epigenetically silenced tumor suppressor genes and direct cytotoxicity. We and others have shown hypermethylation of WNT/β-catenin inhibitory genes in primary MDS and AML samples. Activation of WNT/β-catenin signaling has furthermore been shown to play a role in the development and relapse of AML. Inhibi
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Agarwal, Puneet, Bin Zhang, Yinwei Ho, et al. "Inhibition of CML Stem Cell Renewal By the Porcupine Inhibitor WNT974." Blood 126, no. 23 (2015): 54. http://dx.doi.org/10.1182/blood.v126.23.54.54.

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Abstract Treatment of chronic myeloid leukemia (CML) with BCR-ABL tyrosine kinase inhibitors (TKIs) fails to eradicate the leukemia stem cells (LSCs) from which the disease arises. Others and we have shown that extrinsic signals from the bone marrow (BM) microenvironment play an important role in the resistance of CML LSC to TKI treatment. Our studies indicate that microenvironmental Wnt signaling may play a role for in protecting CML LSC from TKI treatment (Blood. 2013; 121(10):1824-38). Wnt secretion and activity requires their palmitoylation by the Porcupine acyltransferase (PORCN). WNT974
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Sakoda, Teppei, Yoshikane Kikushige, Toshihiro Miyamoto, and Koichi Akashi. "TIM-3/Gal-9 Signaling Enhances Self-Renewal Capacity of AML-LSCs through Mimicking Canonical Wnt Signaling." Blood 128, no. 22 (2016): 1673. http://dx.doi.org/10.1182/blood.v128.22.1673.1673.

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Abstract (Introduction) Acute myeloid leukemia (AML) originates from self-renewing leukemic stem cells (LSCs). Self-renewal capacity is one of the most important biological features of LSCs, and therefore, targeting self-renewal machineries of LSCs should be necessary for the eradication of LSCs. We have recently identified the autocrine loop consisted of LSCs-specific surface molecule TIM-3 and its ligand galectin-9 (Gal-9) in human myeloid malignancies. TIM-3/Gal-9 autocrine loop constitutively activates the nucleus accumulation of β-catenin in primary AML LSCs. However, the precise mechanis
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Dietrich, Philipp A., Murray D. Norris та Jenny Yingzi Wang. "GPR84, a Proinflammatory Receptor, Sustains Wnt/β-Catenin Signaling In Leukemic Stem Cells For Maintenance Of MLL-AF9-Induced Leukemogenesis". Blood 122, № 21 (2013): 3781. http://dx.doi.org/10.1182/blood.v122.21.3781.3781.

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Abstract Inappropriate activation of Wnt/β-catenin signaling confers hematopoietic progenitors the property of self-renewal that promotes malignant transformation in MLL-rearranged acute myeloid leukemia (AML). However, it has been noted that activation of β-catenin is observed in tumors without clear mutations in the major components of the pathway or increase in Wnt signaling. This suggests that other developmental signaling pathways may be capable of inducing activation or downstream signaling of β-catenin. Recently, a number of G protein-coupled receptors (GPCRs) have been shown to activat
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40

Shahid, Akbar Muhammed, In Hwa Um, Mustafa Elshani, Ying Zhang та David James Harrison. "NUC-7738 regulates β-catenin signalling resulting in reduced proliferation and self-renewal of AML cells". PLOS ONE 17, № 12 (2022): e0278209. http://dx.doi.org/10.1371/journal.pone.0278209.

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Acute myeloid leukemia (AML) stem cells are required for the initiation and maintenance of the disease. Activation of the Wnt/β-catenin pathway is required for the survival and development of AML leukaemia stem cells (LSCs) and therefore, targeting β-catenin is a potential therapeutic strategy. NUC-7738, a phosphoramidate transformation of 3’-deoxyadenosine (3’-dA) monophosphate, is specifically designed to generate the active anti-cancer metabolite 3’-deoxyadenosine triphosphate (3’-dATP) intracellularly, bypassing key limitations of breakdown, transport, and activation. NUC-7738 is currently
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Zhou, Hongsheng, Po Yee Mak, Hong Mu та ін. "Combination of Tyrosine Kinase Inhibitor with β-Catenin/CBP Modulator C82 Reverses TKI Resistance, Eradicates Quiescent CML Stem/Progenitors Cells, and Overcomes MSC-Associated Microenvironmental Protection". Blood 124, № 21 (2014): 401. http://dx.doi.org/10.1182/blood.v124.21.401.401.

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Abstract Bcr-Abl tyrosine kinase inhibitors (TKIs) are effective in inducing remissions and improving survival in patients with CML but do not eliminate CML leukemia stem cells (LSCs). Wnt/β-catenin pathway is established to be active in CML and essential for CML LSC, while adult HSCs do not require fully active β-catenin for maintenance. Furthermore, Wnt/β-catenin signaling pathway plays a critical role in TKI resistance and stromal-mediated microenvironmental protection for CML stem and progenitor cells. We propose that combinations of β-catenin inhibitors and TKIs represent a potentially ef
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42

Yi, Hangyu, Jianlong Wang, Maria Kavallaris та Jenny Yingzi Wang. "Lgr4-Mediated Potentiation Of Wnt/β-Catenin Signaling Promotes MLL Leukemogenesis Via An Rspo3/Wnt3a-Gnaq Pathway In Leukemic Stem Cells". Blood 122, № 21 (2013): 887. http://dx.doi.org/10.1182/blood.v122.21.887.887.

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Abstract Although the clinical importance of aberrant Wnt/β-catenin signaling has been recognized in various cancers, including MLL-rearranged acute myeloid leukemia (MLL AML), its key tractable pathway components have not yet been discovered in leukemic stem cells (LSC). Our studies have identified an Rspo3/Wnt3a-Lgr4-Gnaq pathway, which significantly potentiates β-catenin signaling in MLL LSC. Genetic and pharmacological targeting of this pathway impairs LSC self-renewal and survival, inhibiting MLL-AF9-induced leukemia progression in vivo. Gene expression analysis of AML patient samples (Nu
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Jiang, Xuejie, Po Yee Mak, Hong Mu та ін. "Disruption of Wnt/β-Catenin Exerts Antileukemia Activity and Synergizes with FLT3 Inhibition in FLT3-Mutant Acute Myeloid Leukemia". Clinical Cancer Research 24, № 10 (2018): 2417–29. http://dx.doi.org/10.1158/1078-0432.ccr-17-1556.

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44

Zhai, Hong, Junting Zhao, Juan Pu, Pan Zhao та Jin Wei. "LncRNA-DUXAP8 Regulation of the Wnt/β-Catenin Signaling Pathway to Inhibit Glycolysis and Induced Apoptosis in Acute Myeloid Leukemia". Turkish Journal of Hematology 38, № 4 (2021): 264–72. http://dx.doi.org/10.4274/tjh.galenos.2021.2020.0769.

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45

Wu, Shiwen, Dongqin Shen та Li Zhao. "AKAP9 Upregulation Predicts Unfavorable Prognosis in Pediatric Acute Myeloid Leukemia and Promotes Stemness Properties via the Wnt/β-Catenin Pathway". Cancer Management and Research Volume 14 (січень 2022): 157–67. http://dx.doi.org/10.2147/cmar.s343033.

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46

Li, Hongjiao, Chenglian Xie, Yurong Lu, Kaijing Chang, Feng Guan та Xiang Li. "Exosomal miR92a Promotes Cytarabine Resistance in Myelodysplastic Syndromes by Activating Wnt/β-catenin Signal Pathway". Biomolecules 12, № 10 (2022): 1448. http://dx.doi.org/10.3390/biom12101448.

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Cytarabine (Ara-C) has been one of the frontline therapies for clonal hematopoietic stem cell disorders, such as myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), but Ara-C resistance often occurs and leads to treatment failure. Exosomal microRNAs (miRNAs, miRs) as small noncoding RNA that play important roles in post-transcriptional gene regulation, can be delivered into recipient cells by exosomes and regulate target genes’ expression. miR92a has been reported to be dysregulated in many cancers, including MDS and AML. However, the effects of exosomal miR92a in hematologic mali
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Iasenza, Isabella Angela, Safia Safa, Frederic Barabe, Sonia Cellot, Brian T. Wilhelm, and Kolja Eppert. "High-Throughput Chemical Screen on Acute Myeloid Leukemia Stem Cells Identifies Novel Anti-LSC Compounds." Blood 138, Supplement 1 (2021): 1871. http://dx.doi.org/10.1182/blood-2021-145369.

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Abstract Acute myeloid leukemia (AML) is an aggressive form of blood cancer defined by the uncontrolled proliferation and clonal expansion of immature myeloblast cells in the blood and bone marrow, leading to hematopoietic failure. Despite the use of aggressive and cytotoxic standard-of-care drugs, patients often relapse and succumb to the disease partially due to the inability of medically unfit patients to withstand the cytotoxic treatments, regrowth from minimal residual disease and the chemo-resistant nature of leukemic stem cells (LSCs) which can remain in a quiescent state and reside in
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48

Daud, Siti Sarah, Alan K. Burnett, Richard L. Darley, and Alex Tonks. "Large-Scale Integration of Gene Profiling Identifies TCF7L2/TCF4 as the Most Frequently Dysregulated Wnt Signaling Component In AML." Blood 116, no. 21 (2010): 2480. http://dx.doi.org/10.1182/blood.v116.21.2480.2480.

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Abstract Abstract 2480 Acute myeloid leukemia (AML) represents one of the most genetically heterogeneous malignancies; however, some processes are commonly dysregulated. One of the most frequently dysregulated processes in AML is Wnt signaling. In solid cancers, aberrant Wnt signaling has been shown to promote cancer by increasing nuclear accumulation of β-catenin and with consequent activation of target genes. In AML, overexpression of β-catenin is also common; in addition however, patient studies and genetic models indicate that other components of the Wnt pathway are also commonly dysregula
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49

Beghini, Alessandro. "Core Binding Factor Leukemia: Chromatin Remodeling Moves Towards Oncogenic Transcription." Cancers 11, no. 12 (2019): 1973. http://dx.doi.org/10.3390/cancers11121973.

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Acute myeloid leukemia (AML), the most common acute leukemia in adults, is a heterogeneous malignant clonal disorder arising from multipotent hematopoietic progenitor cells characterized by genetic and concerted epigenetic aberrations. Core binding factor-Leukemia (CBFL) is characterized by the recurrent reciprocal translocations t(8;21)(q22;q22) or inv(16)(p13;q22) that, expressing the distinctive RUNX1-RUNX1T1 (also known as Acute myeloid leukemia1-eight twenty-one, AML1-ETO or RUNX1/ETO) or CBFB-MYH11 (also known as CBFβ-SMMHC) translocation product respectively, disrupt the essential hemat
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50

Agarwal, Puneet, Bin Zhang, YinWei Ho, et al. "Inhibition of CML Stem Cell Growth By Targeting WNT Signaling Using a Porcupine Inhibitor." Blood 124, no. 21 (2014): 3130. http://dx.doi.org/10.1182/blood.v124.21.3130.3130.

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Abstract BCR-ABL tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of chronic myeloid leukemia (CML). However, TKIs are unable to eradicate the leukemia stem cells (LSCs) from which CML arises, despite effective inhibition of BCR-ABL kinase activity in this population. There is evidence that extrinsic signals from the bone marrow (BM) microenvironment play an important role in the resistance of CML LSC to TKI treatment. Our previous studies have shown a role for Wnt signaling in protecting CML LSC from TKI treatment (Blood. 2013; 121(10):1824-38). Palmitoylation of Wnts by th
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