ReviewLeukemia2019
Aberrant Wnt signaling in multiple myeloma: molecular mechanisms and targeting options.
Review in Leukemia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
125 citing papers in PubMed, 184 citations in OpenAlex.
- Phase II trial of single-agent panobinostat consolidation improves responses after sub-optimal transplant outcomes in multiple myeloma.British journal of haematology · 2021Trial
- A single-cell atlas of multiple myeloma defines malignant archetypes and proliferative states.Nature genetics · 2026Article
- Comprehensive Analyses of SOX7 Provide Novel Insights on Its Tumor Suppressor Role and Its Target Genes with Therapeutic Implications in Multiple Myeloma.International journal of molecular sciences · 2026Article
- CD70/CD27 signaling promotes the pathogenesis of multiple myeloma and represents a promising therapeutic target.Leukemia · 2026Article
- Regulatory mechanisms of LGR4 on cancer and cancer stem cell properties.Discover oncology · 2026Review
- Deciphering epigenetic crosstalk in multiple myeloma pathogenesis and treatment.Clinical epigenetics · 2026Review
- Spatial multi-omics of multiple myeloma uncovers niche-dependent pro-myeloma and immunosuppressive signaling in the bone marrow and extramedullary lesions.bioRxiv : the preprint server for biology · 2026Article
- Genomic profiling enables personalized strategies to overcome drug resistance in multiple myeloma.Discover oncology · 2026Review
- The role of KPNA3 in multiple myeloma: implications for targeting nuclear import.Apoptosis : an international journal on programmed cell death · 2026Article
- An odyssey of monoclonal gammopathies: focusing on precursors and the progression from MGUS and SMM to multiple Myeloma, with a brief overview of novel therapeutic strategies.Clinical and experimental medicine · 2026Review
- FTO-Mediated m6A Demethylation of SERPINF1 Attenuates Multiple Myeloma Progression via the Wnt/β-Catenin Pathway.Journal of microbiology and biotechnology · 2026Article
- Increase in serum DKK1 levels attenuates the anabolic response to romosozumab in postmenopausal osteoporosis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026Observational
- CYLD Limits Neutrophil-Driven Psoriatic Inflammation.Inflammation · 2026Article
- MMSA-1 is regulated by Wnt/TCF4 and involved in multiple myeloma progression and invasion via RAS/RAF signaling pathway.Annals of hematology · 2026Article
- The role of epigenetic modifications in hematological cancers.Frontiers in oncology · 2026Review
- Non-coding RNAs as predictive factors of oncological outcomes in plasma cell myeloma.Oncology reviews · 2026Review
- Targeting Wnt/β-catenin signaling enhances the efficacy of anti-CD38 immunotherapy in multiple myeloma.Neoplasia (New York, N.Y.) · 2025Article
- Sex-specific dysregulation of exosomal non-coding RNAs drives multiple myeloma progression.Blood cancer journal · 2025Article
- Immunophenotypic changes in the tumor and tumor microenvironment during progression to multiple myeloma.PLoS genetics · 2025Article
- PMEPA1 Binds NEDD4L to Inhibit the Malignant Progression of Multiple Myeloma by Inactivating Wnt/β-Catenin Signaling.Cell biochemistry and biophysics · 2025Article
65 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant activation of Wnt/β-catenin signaling plays a central role in the pathogenesis of a wide variety of malignancies and is typically caused by mutations in core Wnt pathway components driving constitutive, ligand-independent signaling. In multiple myelomas (MMs), however, these pathway intrinsic mutations are rare despite the fact that most tumors display aberrant Wnt pathway activity. Recent studies indicate that this activation is caused by genetic and epigenetic lesions of Wnt regulatory components, sensitizing MM cells to autocrine Wnt ligands and paracrine Wnts emanating from the bone marrow niche. These include deletion of the tumor suppressor CYLD, promotor methylation of the Wnt antagonists WIF1, DKK1, DKK3, and sFRP1, sFRP2, sFRP4, sFRP5, as well as overexpression of the co-transcriptional activator BCL9 and the R-spondin receptor LGR4. Furthermore, Wnt activity in MM is strongly promoted by interaction of both Wnts and R-spondins with syndecan-1 (CD138) on the MM cell-surface. Functionally, aberrant canonical Wnt signaling plays a dual role in the pathogenesis of MM: (I) it mediates proliferation, migration, and drug resistance of MM cells; (II) MM cells secrete Wnt antagonists that contribute to the development of osteolytic lesions by impairing osteoblast differentiation. As discussed in this review, these insights into the causes and consequences of aberrant Wnt signaling in MM will help to guide the development of targeting strategies. Importantly, since Wnt signaling in MM cells is largely ligand dependent, it can be targeted by drugs/antibodies that act upstream in the pathway, interfering with Wnt secretion, sequestering Wnts, or blocking Wnt (co)receptors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.