Cited by 78

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Wnt Signalling in Acute Myeloid Leukaemia

Gruszka, Alicja M., Valli, Debora, Alcalay, Myriam·2019·Cells

Abstract

Acute myeloid leukaemia (AML) is a group of malignant diseases of the haematopoietic system. AML occurs as the result of mutations in haematopoietic stem/progenitor cells, which upregulate Wnt signalling through a variety of mechanisms. Other mechanisms of Wnt activation in AML have been described such as Wnt antagonist inactivation through promoter methylation. Wnt signalling is necessary for the maintenance of leukaemic stem cells. Several molecules involved in or modulating Wnt signalling have a prognostic value in AML. These include: β-catenin, LEF-1, phosphorylated-GSK3β, PSMD2, PPARD, XPNPEP, sFRP2, RUNX1, AXIN2, PCDH17, CXXC5, LLGL1 and PTK7. Targeting Wnt signalling for tumour eradication is an approach that is being explored in haematological and solid tumours. A number of preclinical studies confirms its feasibility, albeit, so far no reliable clinical trial data are available to prove its utility and efficacy.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3390/cells8111403

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Figures

Figure 1 Canonical and non-canonical Wnt signalling.
Figure 1 Canonical and non-canonical Wnt signalling.CC BY · PubMed Central
Figure 2 Mechanisms activating Wnt signalling in acute myeloid leukaemia (AML) and their consequences for the disease outcome.
Figure 2 Mechanisms activating Wnt signalling in acute myeloid leukaemia (AML) and their consequences for the disease outcome.CC BY · PubMed Central
Figure 3 Wnt signalling in AML. The proteins in coral red have been specifically implicated in AML. Thin red bar-headed arrows indicate where investigational inhibitors act, while thick red bar-headed arrows show the targets of agents used in clinical trials. ER—endoplasmic reticulum.
Figure 3 Wnt signalling in AML. The proteins in coral red have been specifically implicated in AML. Thin red bar-headed arrows indicate where investigational inhibitors act, while thick red bar-headed arrows show the targets of agents used in clinical trials. ER—endoplasmic reticulum.CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Research works printed but not linked: 76

  1. Saultz, J.N., and Garzon, R. (2016). Acute Myeloid Leukemia: A Concise Review. J. Clin. Med., 5. · DOI
  2. Dohner, 2015, Acute Myeloid Leukemia, N. Engl. J. Med., 373, 1136, 10.1056/NEJMra1406184 · DOI
  3. Gaidzik, 2008, Prognostic implications of gene mutations in acute myeloid leukemia with normal cytogenetics, Semin. Oncol., 35, 346, 10.1053/j.seminoncol.2008.04.005 · DOI
  4. Bullinger, 2017, Genomics of Acute Myeloid Leukemia Diagnosis and Pathways, J. Clin. Oncol., 35, 934, 10.1200/JCO.2016.71.2208 · DOI
  5. Heidel, 2015, Evolutionarily conserved signaling pathways: Acting in the shadows of acute myelogenous leukemia’s genetic diversity, Clin. Cancer Res., 21, 240, 10.1158/1078-0432.CCR-14-1436 · DOI
  6. Dick, 2005, Acute myeloid leukemia stem cells, Ann. N Y Acad. Sci., 1044, 1, 10.1196/annals.1349.001 · DOI
  7. Nusse, 2012, Three decades of Wnts: A personal perspective on how a scientific field developed, EMBO J., 31, 2670, 10.1038/emboj.2012.146 · DOI
  8. Anastas, 2013, WNT signalling pathways as therapeutic targets in cancer, Nat. Rev. Cancer, 13, 11, 10.1038/nrc3419 · DOI
  9. Ono, M., Lai, K.K.Y., Wu, K., Nguyen, C., Lin, D.P., Murali, R., and Kahn, M. (2018). Nuclear receptor/Wnt beta-catenin interactions are regulated via differential CBP/p300 coactivator usage. PLoS ONE, 13. · DOI
  10. Daulat, 2017, Wnt/Planar Cell Polarity Signaling: New Opportunities for Cancer Treatment, Trends. Cancer, 3, 113, 10.1016/j.trecan.2017.01.001 · DOI
  11. De, 2011, Wnt/Ca2+ signaling pathway: A brief overview, Acta. Biochim. Biophys. Sin. (Shanghai), 43, 745, 10.1093/abbs/gmr079 · DOI
  12. Cruciat, 2013, Secreted and transmembrane wnt inhibitors and activators, Cold Spring Harb Perspect Biol., 5, a015081, 10.1101/cshperspect.a015081 · DOI · Paper page
  13. Simon, 2005, Constitutive activation of the Wnt/beta-catenin signalling pathway in acute myeloid leukaemia, Oncogene, 24, 2410, 10.1038/sj.onc.1208431 · DOI
  14. Steffen, 2004, Translocation products in acute myeloid leukemia activate the Wnt signaling pathway in hematopoietic cells, Mol. Cell Biol., 24, 2890, 10.1128/MCB.24.7.2890-2904.2004 · DOI
  15. Zheng, 2004, Gamma-catenin contributes to leukemogenesis induced by AML-associated translocation products by increasing the self-renewal of very primitive progenitor cells, Blood, 103, 3535, 10.1182/blood-2003-09-3335 · DOI
  16. Morgan, 2013, gamma-Catenin is overexpressed in acute myeloid leukemia and promotes the stabilization and nuclear localization of beta-catenin, Leukemia, 27, 336, 10.1038/leu.2012.221 · DOI
  17. Ugarte, 2015, Wnt signaling induces transcription, spatial proximity, and translocation of fusion gene partners in human hematopoietic cells, Blood, 126, 1785, 10.1182/blood-2015-04-638494 · DOI
  18. Fu, 2014, Clinical significance of lymphoid enhancer-binding factor 1 expression in acute myeloid leukemia, Leuk Lymphoma, 55, 371, 10.3109/10428194.2013.805759 · DOI
  19. Metzeler, 2012, High expression of lymphoid enhancer-binding factor-1 (LEF1) is a novel favorable prognostic factor in cytogenetically normal acute myeloid leukemia, Blood, 120, 2118, 10.1182/blood-2012-02-411827 · DOI
  20. Morgan, 2019, LEF-1 drives aberrant beta-catenin nuclear localization in myeloid leukemia cells, Haematologica, 104, 1365, 10.3324/haematol.2018.202846 · DOI
  21. Petropoulos, 2008, A novel role for Lef-1, a central transcription mediator of Wnt signaling, in leukemogenesis, J. Exp. Med., 205, 515, 10.1084/jem.20071875 · DOI
  22. Wang, 2010, The Wnt/beta-catenin pathway is required for the development of leukemia stem cells in AML, Science, 327, 1650, 10.1126/science.1186624 · DOI
  23. Majeti, 2009, Dysregulated gene expression networks in human acute myelogenous leukemia stem cells, Proc. Natl. Acad. Sci. USA, 106, 3396, 10.1073/pnas.0900089106 · DOI · Paper page
  24. Barbieri, 2016, Nucleophosmin leukemogenic mutant activates Wnt signaling during zebrafish development, Oncotarget, 7, 55302, 10.18632/oncotarget.10878 · DOI
  25. Cocciardi, 2019, Clonal evolution patterns in acute myeloid leukemia with NPM1 mutation, Nat. Commun., 10, 2031, 10.1038/s41467-019-09745-2 · DOI
  26. Reikvam, H., Aasebo, E., Brenner, A.K., Bartaula-Brevik, S., Gronningsaeter, I.S., Forthun, R.B., Hovland, R., and Bruserud, O. (2019). High Constitutive Cytokine Release by Primary Human Acute Myeloid Leukemia Cells Is Associated with a Specific Intercellular Communication Phenotype. J. Clin. Med., 8. · DOI
  27. Tsykunova, 2012, The surface molecule signature of primary human acute myeloid leukemia (AML) cells is highly associated with NPM1 mutation status, Leukemia, 26, 557, 10.1038/leu.2011.243 · DOI
  28. Tickenbrock, 2005, Flt3 tandem duplication mutations cooperate with Wnt signaling in leukemic signal transduction, Blood, 105, 3699, 10.1182/blood-2004-07-2924 · DOI
  29. Valencia, 2009, Wnt signaling pathway is epigenetically regulated by methylation of Wnt antagonists in acute myeloid leukemia, Leukemia, 23, 1658, 10.1038/leu.2009.86 · DOI
  30. Cheng, 2011, Secreted-frizzled related protein 1 is a transcriptional repression target of the t(8;21) fusion protein in acute myeloid leukemia, Blood, 118, 6638, 10.1182/blood-2011-05-354712 · DOI
  31. Guezguez, 2016, GSK3 Deficiencies in Hematopoietic Stem Cells Initiate Pre-neoplastic State that Is Predictive of Clinical Outcomes of Human Acute Leukemia, Cancer Cell, 29, 61, 10.1016/j.ccell.2015.11.012 · DOI
  32. Lazzaroni, 2016, Intronless WNT10B-short variant underlies new recurrent allele-specific rearrangement in acute myeloid leukaemia, Sci. Rep., 6, 37201, 10.1038/srep37201 · DOI
  33. Beghini, 2012, Regeneration-associated WNT signaling is activated in long-term reconstituting AC133bright acute myeloid leukemia cells, Neoplasia, 14, 1236, 10.1593/neo.121480 · DOI
  34. Xin, 2018, DIXDC1 promotes the growth of acute myeloid leukemia cells by upregulating the Wnt/beta-catenin signaling pathway, Biomed. Pharmacother, 107, 1548, 10.1016/j.biopha.2018.08.144 · DOI
  35. Najafi, 2019, Cyclooxygenase-2 in cancer: A review, J. Cell Physiol., 234, 5683, 10.1002/jcp.27411 · DOI
  36. Lilly, 2004, Expression of Cyclooxygenase-2 (COX-2) in Human Leukemias and Hematopoietic Cells, Blood, 104, 4336, 10.1182/blood.V104.11.4336.4336 · DOI
  37. Duciel, L., Monraz Gomez, L.C., Kondratova, M., Kuperstein, I., and Saule, S. (2019). The Phosphatase PRL-3 Is Involved in Key Steps of Cancer Metastasis. J. Mol. Biol. · DOI
  38. Zhou, J., Bi, C., Chng, W.J., Cheong, L.L., Liu, S.C., Mahara, S., Tay, K.G., Zeng, Q., Li, J., and Guo, K. (2011). PRL-3, a metastasis associated tyrosine phosphatase, is involved in FLT3-ITD signaling and implicated in anti-AML therapy. PLoS ONE, 6. · DOI
  39. Zhou, 2017, LIN28B Activation by PRL-3 Promotes Leukemogenesis and a Stem Cell-like Transcriptional Program in AML, Mol. Cancer Res., 15, 294, 10.1158/1541-7786.MCR-16-0275-T · DOI
  40. Chong, 2019, Non-canonical activation of beta-catenin by PRL-3 phosphatase in acute myeloid leukemia, Oncogene, 38, 1508, 10.1038/s41388-018-0526-3 · DOI
  41. Behrmann, 2018, Acute Myeloid Leukemia and the Bone Marrow Niche-Take a Closer Look, Front. Oncol., 8, 444, 10.3389/fonc.2018.00444 · DOI
  42. Yamane, 2001, Wnt signaling regulates hemopoiesis through stromal cells, J. Immunol., 167, 765, 10.4049/jimmunol.167.2.765 · DOI
  43. Lane, 2011, Differential niche and Wnt requirements during acute myeloid leukemia progression, Blood, 118, 2849, 10.1182/blood-2011-03-345165 · DOI
  44. Kode, 2014, Leukaemogenesis induced by an activating beta-catenin mutation in osteoblasts, Nature, 506, 240, 10.1038/nature12883 · DOI
  45. Kode, 2016, FoxO1-dependent induction of acute myeloid leukemia by osteoblasts in mice, Leukemia, 30, 1, 10.1038/leu.2015.161 · DOI
  46. Hu, 2015, Galectin-3 mediates bone marrow microenvironment-induced drug resistance in acute leukemia cells via Wnt/beta-catenin signaling pathway, J. Hematol. Oncol., 8, 1, 10.1186/s13045-014-0099-8 · DOI
  47. Chien, 2013, Adhesion of Acute Myeloid Leukemia Blasts to E-Selectin In The Vascular Niche Enhances Their Survival By Mechanisms Such As Wnt Activation, Blood, 122, 61, 10.1182/blood.V122.21.61.61 · DOI
  48. Esposito, 2019, Bone vascular niche E-selectin induces mesenchymal-epithelial transition and Wnt activation in cancer cells to promote bone metastasis, Nat. Cell Biol., 21, 627, 10.1038/s41556-019-0309-2 · DOI
  49. Liang, 2003, Wnt5a inhibits B cell proliferation and functions as a tumor suppressor in hematopoietic tissue, Cancer Cell, 4, 349, 10.1016/S1535-6108(03)00268-X · DOI
  50. Heidel, 2013, The cell fate determinant Llgl1 influences HSC fitness and prognosis in AML, J. Exp. Med., 210, 15, 10.1084/jem.20120596 · DOI
  51. Beekman, 2012, Sequential gain of mutations in severe congenital neutropenia progressing to acute myeloid leukemia, Blood, 119, 5071, 10.1182/blood-2012-01-406116 · DOI
  52. Prebet, 2010, The cell polarity PTK7 receptor acts as a modulator of the chemotherapeutic response in acute myeloid leukemia and impairs clinical outcome, Blood, 116, 2315, 10.1182/blood-2010-01-262352 · DOI · Paper page
  53. Lhoumeau, 2016, Ptk7-Deficient Mice Have Decreased Hematopoietic Stem Cell Pools as a Result of Deregulated Proliferation and Migration, J. Immunol., 196, 4367, 10.4049/jimmunol.1500680 · DOI
  54. Zang, S., Liu, N., Wang, H., Wald, D.N., Shao, N., Zhang, J., Ma, D., Ji, C., and Tse, W. (2014). Wnt signaling is involved in 6-benzylthioinosine-induced AML cell differentiation. BMC Cancer, 14. · DOI
  55. Ysebaert, 2006, Expression of beta-catenin by acute myeloid leukemia cells predicts enhanced clonogenic capacities and poor prognosis, Leukemia, 20, 1211, 10.1038/sj.leu.2404239 · DOI
  56. Xu, 2008, Clinical significance of nuclear non-phosphorylated beta-catenin in acute myeloid leukaemia and myelodysplastic syndrome, Br. J. Haematol., 140, 394, 10.1111/j.1365-2141.2007.06914.x · DOI
  57. Chen, 2009, Prognostic significance of beta-catenin and topoisomerase IIalpha in de novo acute myeloid leukemia, Am. J. Hematol., 84, 87, 10.1002/ajh.21334 · DOI
  58. Griffiths, 2015, Pharmacological targeting of beta-catenin in normal karyotype acute myeloid leukemia blasts, Haematologica, 100, e49, 10.3324/haematol.2014.113118 · DOI
  59. Xu, 2016, The clinical significance of gamma-catenin in acute myeloid leukemia, Onco. Targets Ther., 9, 3861, 10.2147/OTT.S105514 · DOI
  60. Skokowa, 2006, LEF-1 is crucial for neutrophil granulocytopoiesis and its expression is severely reduced in congenital neutropenia, Nat. Med., 12, 1191, 10.1038/nm1474 · DOI
  61. Ruvolo, 2015, Phosphorylation of GSK3alpha/beta correlates with activation of AKT and is prognostic for poor overall survival in acute myeloid leukemia patients, BBA Clin., 4, 59, 10.1016/j.bbacli.2015.07.001 · DOI
  62. Taskesen, E., Staal, F.J., and Reinders, M.J. (2015). An integrated approach of gene expression and DNA-methylation profiles of WNT signaling genes uncovers novel prognostic markers in acute myeloid leukemia. BMC Bioinformatics, 16. · DOI
  63. Martin, 2010, Epigenetic regulation of the non-canonical Wnt pathway in acute myeloid leukemia, Cancer Sci., 101, 425, 10.1111/j.1349-7006.2009.01413.x · DOI
  64. Yin, 2016, Protocadherin 17 functions as a tumor suppressor suppressing Wnt/beta-catenin signaling and cell metastasis and is frequently methylated in breast cancer, Oncotarget, 7, 51720, 10.18632/oncotarget.10102 · DOI
  65. Xu, 2019, Reduced protocadherin17 expression in leukemia stem cells: The clinical and biological effect in acute myeloid leukemia, J. Transl. Med., 17, 102, 10.1186/s12967-019-1851-1 · DOI
  66. Astori, 2013, CXXC5 (retinoid-inducible nuclear factor, RINF) is a potential therapeutic target in high-risk human acute myeloid leukemia, Oncotarget, 4, 1438, 10.18632/oncotarget.1195 · DOI
  67. Bruserud, 2015, Expression of the potential therapeutic target CXXC5 in primary acute myeloid leukemia cells - high expression is associated with adverse prognosis as well as altered intracellular signaling and transcriptional regulation, Oncotarget, 6, 2794, 10.18632/oncotarget.3056 · DOI
  68. Kuhnl, 2015, Downregulation of the Wnt inhibitor CXXC5 predicts a better prognosis in acute myeloid leukemia, Blood, 125, 2985, 10.1182/blood-2014-12-613703 · DOI
  69. Minke, 2009, Small molecule inhibitors of WNT signaling effectively induce apoptosis in acute myeloid leukemia cells, Eur. J. Haematol., 82, 165, 10.1111/j.1600-0609.2008.01188.x · DOI
  70. Li, 2014, Sequential combination of decitabine and idarubicin synergistically enhances anti-leukemia effect followed by demethylating Wnt pathway inhibitor promoters and downregulating Wnt pathway nuclear target, J. Transl. Med., 12, 167, 10.1186/1479-5876-12-167 · DOI
  71. Fiskus, 2015, Pre-clinical efficacy of combined therapy with novel beta-catenin antagonist BC2059 and histone deacetylase inhibitor against AML cells, Leukemia, 29, 1267, 10.1038/leu.2014.340 · DOI
  72. Ma, 2015, SKLB-677, an FLT3 and Wnt/beta-catenin signaling inhibitor, displays potent activity in models of FLT3-driven AML, Sci. Rep., 5, 15646, 10.1038/srep15646 · DOI
  73. Jiang, 2018, Disruption of Wnt/beta-Catenin Exerts Antileukemia Activity and Synergizes with FLT3 Inhibition in FLT3-Mutant Acute Myeloid Leukemia, Clin. Cancer Res., 24, 2417, 10.1158/1078-0432.CCR-17-1556 · DOI
  74. Chen, 2013, Combination of celecoxib and doxorubicin increases growth inhibition and apoptosis in acute myeloid leukemia cells, Leuk Lymphoma, 54, 2517, 10.3109/10428194.2013.781170 · DOI
  75. Casanova, 2008, A celecoxib derivative inhibits focal adhesion signaling and induces caspase-8-dependent apoptosis in human acute myeloid leukemia cells, Int. J. Cancer, 123, 217, 10.1002/ijc.23516 · DOI
  76. Winer, 2019, Novel therapy in Acute myeloid leukemia (AML): Moving toward targeted approaches, Ther. Adv. Hematol., 10, 2040620719860645, 10.1177/2040620719860645 · DOI

Cited by

See all 78

Metadata

Authors
Gruszka, A. M., Valli, D., & Alcalay, M.
Affiliations
Department of Experimental Oncology, Istituto Europeo di Oncologia IRCCS, Via Adamello 16, 20 139 Milan, Italy
Venue
Cells
Publisher
MDPI AG
Published
2019-11-07
Volume
8
Issue
11
Pages
1403
ISSN
2073-4409
Cited by
78
References
2
Language
en

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review