ArticleThe American journal of pathology2007
Epigenetic silencing through DNA and histone methylation of fibroblast growth factor receptor 2 in neoplastic pituitary cells.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- The role of epigenetic modification in tumorigenesis and progression of pituitary adenomas: a systematic review of the literature.PloS one · 2013Pooled it
- The role of methylation in pituitary neuroendocrine tumors current insights and emerging perspectives.Molecular biology reports · 2026Review
- Current understanding of the role of DNA methylation in pituitary neuroendocrine tumors.Neuro-oncology advances · 2025Article
- DNA Methylation in Pituitary Adenomas: A Scoping Review.International journal of molecular sciences · 2025Article
- The evolution and application of multi-omic analysis for pituitary neuroendocrine tumors.Frontiers in medicine · 2025Review
- Targeting FGFR for cancer therapy.Journal of hematology & oncology · 2024Review
- Potential roles of FGF5 as a candidate therapeutic target in prostate cancer.American journal of clinical and experimental urology · 2023Review
- DNA methylation patterns in juvenile systemic sclerosis and localized scleroderma.Clinical immunology (Orlando, Fla.) · 2021Article
- Genomics and Epigenomics of Pituitary Tumors: What Do Pathologists Need to Know?Endocrine pathology · 2021Review
- Identification of potential and novel target genes in pituitary prolactinoma by bioinformatics analysis.AIMS neuroscience · 2021Article
- 2b or Not 2b: How Opposing FGF Receptor Splice Variants Are Blocking Progress in Precision Oncology.Journal of oncology · 2021Review
- Global DNA methylation pattern involved in the modulation of differentiation potential of adipogenic and myogenic precursors in skeletal muscle of pigs.Stem cell research & therapy · 2020Article
- FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020Review
- Exploring the Role of Novel Medical Therapies for Aggressive Pituitary Tumors: A Review of the Literature-"Are We There Yet?"Cancers · 2020Review
- Genetic and Epigenetic Causes of Pituitary Adenomas.Frontiers in endocrinology · 2020Review
- The Genetics of Pituitary Adenomas.Journal of clinical medicine · 2019Review
- The Epigenomics of Pituitary Adenoma.Frontiers in endocrinology · 2019Review
- Overexpression of DNA (Cytosine-5)-Methyltransferase 1 (DNMT1) And DNA (Cytosine-5)-Methyltransferase 3A (DNMT3A) Is Associated with Aggressive Behavior and Hypermethylation of Tumor Suppressor Genes in Human Pituitary Adenomas.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Validation of epigenetic mechanisms regulating gene expression in canine B-cell lymphoma: An in vitro and in vivo approach.PloS one · 2018Article
- Animal models of pituitary neoplasia.Molecular and cellular endocrinology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Four members of the fibroblast growth factor receptor (FGFR) family of tyrosine kinases transduce signals of a diverse group of more than 23 fibroblast growth factor (FGF) ligands. Each prototypic receptor is composed of three immunoglobulin-like extracellular domains, two of which are involved in ligand binding. Alternative RNA splicing of one of two exons results in two different forms of the second half of the third immunoglobulin-like domain, the IIIb or IIIc isoforms. The contribution of each receptor and their isoforms in tumorigenesis remains unknown. In the pituitary, FGFR2 is expressed primarily as the IIIb isoform in normal adenohypophysial cells. In contrast, FGFR2 is significantly down-regulated in mouse corticotroph AtT20 tumor cells where the 5' promoter is methylated. Treatment of AtT20 cells with 5'-azacytidine resulted in FGFR2 re-expression, mainly as the FGFR2-IIIb isoform. Chromatin immunoprecipitation revealed evidence of histone methylation, but not of deacetylation, in the silencing of FGFR2 in AtT20 cells. Exposure of these cells to the cognate FGFR2-IIIb ligand FGF-7 resulted in diminished Rb phosphorylation and accumulation of p21 and p27, indicating diminished cell cycle progression. Examination of primary human pituitary adenomas revealed FGFR2 down-regulation in 52% (11 of 21) of samples and FGFR2 promoter DNA methylation in 45% (10 of 22) of samples. These data highlight the contribution from DNA and histone methylation as epigenetic mechanisms responsible for FGFR2 silencing in pituitary neoplasia.
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Registered trials
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