ArticleNeuro-oncology2009
Epigenetic silencing of the kinase tumor suppressor WNK2 is tumor-type and tumor-grade specific.
Article in Neuro-oncology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 56 citations in OpenAlex.
- Epigenetic Alterations in Meningiomas-A Review.Biomedicines · 2026Review
- The Wnt signaling networks in higher-grade meningiomas: from molecular pathogenesis to therapeutic innovation.Cancer cell international · 2026Review
- WNK2 oncogenicity revealed by the discovery and functional characterization of novel gene isoforms in MYD88 mutated Waldenström's Macroglobulinemia.Blood cancer journal · 2026Article
- Article
- DNA methylation meningioma biomarkers: attributes and limitations.Frontiers in molecular neuroscience · 2023Review
- Correlation between DNA Methylation and Cell Proliferation Identifies New Candidate Predictive Markers in Meningioma.Cancers · 2022Article
- An update regarding the role of WNK kinases in cancer.Cell death & disease · 2022Review
- Oncogenic Role of miR-217 During Clear Cell Renal Carcinoma Progression.Frontiers in oncology · 2022Article
- Receptor Tyrosine Kinases as Candidate Prognostic Biomarkers and Therapeutic Targets in Meningioma.International journal of molecular sciences · 2021Review
- Adult-type granulosa cell tumor of the ovary: a FOXL2-centric disease.The journal of pathology. Clinical research · 2021Article
- In vitro and in silico assessment of the effect of WWOX expression on invasiveness pathways associated with AP-2 transcription factors in bladder cancer.BMC urology · 2021Article
- LINC00858 knockdown inhibits gastric cancer cell growth and induces apoptosis through reducing WNK2 promoter methylation.Cellular oncology (Dordrecht, Netherlands) · 2020Article
- Long non-coding RNA LINC00858 exerts a tumor-promoting role in colon cancer via HNF4α and WNK2 regulation.Cellular oncology (Dordrecht, Netherlands) · 2020Article
- Article
- Is DNA Methylation a Ray of Sunshine in Predicting Meningioma Prognosis?Frontiers in oncology · 2020Article
- Molecular characteristics of meningiomas.Journal of pathology and translational medicine · 2020Review
- Recent Advances in Meningioma Immunogenetics.Frontiers in oncology · 2019Review
- WNK Kinases in Development and Disease.Current topics in developmental biology · 2017Review
- Blood DNA methylation markers in prospectively identified hepatocellular carcinoma cases and controls from Taiwan.World journal of hepatology · 2016Article
- Silencing of the tumor suppressor gene WNK2 is associated with upregulation of MMP2 and JNK in gliomas.Oncotarget · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Both genetic and epigenetic mechanisms contribute to meningioma development by altering gene expression and protein function. To determine the relative contribution of each mechanism to meningioma development, we used an integrative approach measuring copy number and DNA methylation changes genomewide. We found that genetic alterations affected 1.9%, 7.4%, and 13.3% of the 691 loci studied, whereas epigenetic mechanisms affected 5.4%, 9.9%, and 10.3% of these loci in grade I, II, and III meningiomas, respectively. Genetic and epigenetic mechanisms rarely involved the same locus in any given tumor. The predilection for epigenetic rather than genetic silencing was exemplified at the 5' CpG island of WNK2, a serine-threonine kinase gene on chromosome 9q22.31. WNK2 is known to negatively regulate epidermal growth factor receptor signaling via inhibition of MEK1 (mitogen-activated protein kinase kinase 1), and point mutations have been reported in WNK1, WNK2, WNK3, and WNK4. In meningiomas, WNK2 was aberrantly methylated in 83% and 71% of grade II and III meningiomas, respectively, but rarely in a total of 209 tumors from 13 other tumor types. Aberrant methylation of the CpG island was associated with decreased expression in primary tumors. WNK2 could be reactivated with a methylation inhibitor in IOMM-Lee, a meningioma cell line with a densely methylated WNK2 CpG island and lack of WNK2 expression. Expression of exogenous WNK2 inhibited colony formation, implicating it as a potential cell growth suppressor. These findings indicate that epigenetic mechanisms are common across meningiomas of all grades and that for specific genes such as WNK2, epigenetic alteration may be the dominant, grade-specific mechanism of gene inactivation.
Indexed as
Identifiers
What OpenQuestion holds
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.