ArticleBlood2013
Adult T-cell leukemia cells overexpress Wnt5a and promote osteoclast differentiation.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Estrogen related receptor alpha in castration-resistant prostate cancer cells promotes tumor progression in bone.Oncotarget · 2016Pooled it
- Targeting Wnt Signaling in Acute Lymphoblastic Leukemia.Cancers · 2025Review
- PNPO-Mediated Oxidation of DVL3 Promotes Multiple Myeloma Malignancy and Osteoclastogenesis by Activating the Wnt/β-Catenin Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The HTLV-I oncoprotein Tax inactivates the tumor suppressor FBXW7.Journal of virology · 2024Article
- Illuminating (HTLV-1)-induced adult T-cell leukemia/lymphoma transcriptomic signature: A systems virology approach.Virus research · 2023Article
- SETD2-mediated epigenetic regulation of noncanonical Wnt5A during osteoclastogenesis.Clinical epigenetics · 2021Article
- Article
- Multiple osteolytic primary peripheral T-cell bone lymphoma: the first case report.The Journal of international medical research · 2021Article
- High stroma-derived WNT5A is an indicator for low-risk prostate cancer.FEBS open bio · 2021Article
- Overexpression of aberrant Wnt5a and its effect on acquisition of malignant phenotypes in adult T-cell leukemia/lymphoma (ATL) cells.Scientific reports · 2021Article
- Novel Mutations in a Lethal Case of Lymphomatous Adult T Cell Lymphoma with Cryptic Myocardial Involvement.Current oncology (Toronto, Ont.) · 2021Article
- Loss of FBXW7-mediated degradation of BRAF elicits resistance to BET inhibitors in adult T cell leukemia cells.Molecular cancer · 2020Article
- The Regulation of Bone Metabolism and Disorders by Wnt Signaling.International journal of molecular sciences · 2019Review
- Article
- Aberrant Wnt Signaling Pathway in the Hematopoietic Stem/Progenitor Compartment in Experimental Leukemic Animal.Journal of cell communication and signaling · 2019Article
- WNT5A induces castration-resistant prostate cancer via CCL2 and tumour-infiltrating macrophages.British journal of cancer · 2018Article
- Genetic deficiency of Wnt5a diminishes disease severity in a murine model of rheumatoid arthritis.Arthritis research & therapy · 2017Article
- Wnt5a and CCL25 promote adult T-cell acute lymphoblastic leukemia cell migration, invasion and metastasis.Oncotarget · 2017Article
- NOTCH1 Activation Depletes the Pool of Side Population Stem Cells in ATL.Journal of cancer sciences · 2017Article
- Adult T-cell leukemia: molecular basis for clonal expansion and transformation of HTLV-1-infected T cells.Blood · 2017Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Adult T-cell leukemia/lymphoma (ATL) is etiologically linked to infection with the human T-cell leukemia/lymphoma virus type 1 (HTLV-I). ATL is classified into 4 distinct clinical diseases: acute, lymphoma, chronic, and smoldering. Acute ATL is the most aggressive form, representing 60% of cases and has a 4-year survival of < 5%. A frequent complication and cause of death in acute ATL patients is the presence of lytic bone lesions and hypercalcemia. We analyzed the Wnt/β-catenin pathway because of its common role in cancer and bone remodeling. Our study demonstrated that ATL cells do not express high levels of β-catenin but displayed high levels of LEF-1/TCF genes along with elevated levels of β-catenin (LEF-1/TCF target genes) responsive genes. By profiling Wnt gene expression, we discovered that ATL patient leukemia cells shifted expression toward the noncanonical Wnt pathway. Interestingly, ATL cells overexpressed the osteolytic-associated genes-Wnt5a, PTHLH, and RANKL. We further show that Wnt5a secreted by ATL cells favors osteoclast differentiation and expression of RANK. Our results suggest that Wnt5a is a major contributing factor to the increase in osteolytic bone lesions and hypercalcemia found in ATL patients. Anti-Wnt5a therapy may prevent or reduce osteolytic lesions found in ATL patients and improve therapy outcome.
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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.