ArticleBlood2015
Downregulation of the Wnt inhibitor CXXC5 predicts a better prognosis in acute myeloid leukemia.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- CXXC5 is a ubiquitinated protein and is degraded by the ubiquitin-proteasome pathway.Protein science : a publication of the Protein Society · 2025Article
- Signal integrator function of CXXC5 in Cancer.Cell communication and signaling : CCS · 2025Review
- MiR-28-3p regulates high glucose-induced endothelial dysfunction by targeting CXXC5.Archives of medical science : AMS · 2025Article
- Zinc-finger protein CXXC5 promotes breast carcinogenesis by regulating the TSC1/mTOR signaling pathway.The Journal of biological chemistry · 2023Article
- The epigenetic regulator RINF (CXXC5) maintainsHaematologica · 2022Article
- Down-Regulation of CXXC5 De-Represses MYCL1 to Promote Hepatic Stellate Cell Activation.Frontiers in cell and developmental biology · 2021Article
- Deciphering the role of Wnt signaling in acute myeloid leukemia prognosis: how alterations in DNA methylation come into play in patients' prognosis.Journal of cancer research and clinical oncology · 2020Review
- Wnt Signalling in Acute Myeloid Leukaemia.Cells · 2019Review
- Increased FLYWCH1 Expression is Negatively Correlated with Wnt/β-catenin Target Gene Expression in Acute Myeloid Leukemia Cells.International journal of molecular sciences · 2019Article
- CXXC5: A novel regulator and coordinator of TGF-β, BMP and Wnt signaling.Journal of cellular and molecular medicine · 2019Review
- CXXC5 MediatesInternational journal of biological sciences · 2019Article
- Subclonal mutation selection in mouse lymphomagenesis identifies known cancer loci and suggests novel candidates.Nature communications · 2018Article
- Overexpression of CXXC5 is a strong poor prognostic factor in ER+ breast cancer.Oncology letters · 2018Article
- Downregulation of ROS1 enhances the therapeutic efficacy of arsenic trioxide in acute myeloid leukemia cell lines.Oncology letters · 2018Article
- Cancer subtype identification using somatic mutation data.British journal of cancer · 2018Article
- Impact of Specimen Heterogeneity on Biomarkers in Repository Samples from Patients with Acute Myeloid Leukemia: A SWOG Report.Biopreservation and biobanking · 2018Article
- Investigating the microRNA-mRNA regulatory network in acute myeloid leukemia.Oncology letters · 2017Article
- Molecular characterization of EZH2 mutant patients with myelodysplastic/myeloproliferative neoplasms.Leukemia · 2017Article
- Association of a cytarabine chemosensitivity related gene expression signature with survival in cytogenetically normal acute myeloid leukemia.Oncotarget · 2017Article
- DNA Methylation Events as Markers for Diagnosis and Management of Acute Myeloid Leukemia and Myelodysplastic Syndrome.Disease markers · 2017Review
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Authors and funding
21 authors at 8 institutions in 4 countries.
Funding
Abstract
The gene CXXC5 on 5q31 is frequently deleted in acute myeloid leukemia (AML) with del(5q), suggesting that inactivation of CXXC5 might play a role in leukemogenesis. Here, we investigated the functional and prognostic implications of CXXC5 expression in AML. CXXC5 mRNA was downregulated in AML with MLL rearrangements, t(8;21) and GATA2 mutations. As a mechanism of CXXC5 inactivation, we found evidence for epigenetic silencing by promoter methylation. Patients with CXXC5 expression below the median level had a lower relapse rate (45% vs 59%; P = .007) and a better overall survival (OS, 46% vs 28%; P < .001) and event-free survival (EFS, 36% vs 21%; P < .001) at 5 years, independent of cytogenetic risk groups and known molecular risk factors. In gene-expression profiling, lower CXXC5 expression was associated with upregulation of cell-cycling genes and co-downregulation of genes implicated in leukemogenesis (WT1, GATA2, MLL, DNMT3B, RUNX1). Functional analyses demonstrated CXXC5 to inhibit leukemic cell proliferation and Wnt signaling and to affect the p53-dependent DNA damage response. In conclusion, our data suggest a tumor suppressor function of CXXC5 in AML. Inactivation of CXXC5 is associated with different leukemic pathways and defines an AML subgroup with better 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.