ArticleScientific reports2020
Transcriptome and methylome analysis reveals three cellular origins of pituitary tumors.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Pituitary neuroendocrine tumors with PIT1/SF1 co-expression show distinct clinicopathological and molecular features.Acta neuropathologica · 2024Pooled it
- Genomic characterization of aggressiveness in pituitary neuroendocrine tumors.Neuro-oncology · 2026Article
- Single-cell epigenetic landscape, microenvironment interactions, and gene regulatory modules of non-functioning pituitary adenomas.Cell systems · 2026Article
- DNA methylation profiling predicts postsurgical regrowth in SF1-lineage nonfunctioning pituitary neuroendocrine tumors.Neuro-oncology · 2026Article
- Mixed gangliocytoma-pituitary neuroendocrine tumour: clinical, immunohistochemical, and molecular genetic profiles in a series of four patients.Acta neuropathologica communications · 2026Article
- New Insights from the Expression of the Mismatch Repair System in Pituitary Neuroendocrine Tumors.Endocrine pathology · 2026Article
- Mast cells act as pro-angiogenic and pro-tumorigenic players in pituitary gonadotroph tumors.Neuro-oncology · 2026Article
- Phenotypic and functional characteristics of pituitary adenoma stem cells.World journal of clinical cases · 2025Article
- SHP2 inhibition reduces somatotroph tumor growth in a pre-clinical model.Neuro-oncology · 2025Article
- Current understanding of the role of DNA methylation in pituitary neuroendocrine tumors.Neuro-oncology advances · 2025Article
- Review
- Article
- A case of familial partial lipodystrophy type 2 masquerading as Cushing syndrome: Explaining an atypical phenotype by whole-exome sequencing.Archives of endocrinology and metabolism · 2025Article
- DNA Methylation in Pituitary Adenomas: A Scoping Review.International journal of molecular sciences · 2025Article
- Grading and staging for pituitary neuroendocrine tumors.Brain pathology (Zurich, Switzerland) · 2025Review
- The 2022 WHO classification of tumors of the pituitary gland: An update on aggressive and metastatic pituitary neuroendocrine tumors.Brain pathology (Zurich, Switzerland) · 2025Review
- Article
- Longitudinal multiomics analysis of aggressive pituitary neuroendocrine tumors: comparing primary and recurrent tumors from the same patient, reveals genomic stability and heterogeneous transcriptomic profiles with alterations in metabolic pathways.Acta neuropathologica communications · 2024Article
- Genome-Wide DNA Methylation Profiling as a Prognostic Marker in Pituitary Adenomas-A Pilot Study.Cancers · 2024Article
- The Immune Microenvironment Landscape of Pituitary NeuroEndocrine Tumors, a Transcriptomic Approach.Genes · 2024Article
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pituitary adenomas (PA) are the second most common intracranial tumors. These neoplasms are classified according to the hormone they produce. The majority of PA occur sporadically, and their molecular pathogenesis is incompletely understood. The present transcriptomic and methylomic analysis of PA revealed that they segregate into three molecular clusters according to the transcription factor driving their terminal differentiation. First cluster, driven by NR5A1, consists of clinically non-functioning PA (CNFPA), comprising gonadotrophinomas and null cell; the second cluster consists of clinically evident ACTH adenomas and silent corticotroph adenomas, driven by TBX19; and the third, POU1F1-driven TSH-, PRL- and GH-adenomas, segregated together. Genes such as CACNA2D4, EPHA4 and SLIT1, were upregulated in each of these three clusters, respectively. Pathway enrichment analysis revealed specific alterations of these clusters: calcium signaling pathway in CNFPA; renin-angiotensin system for ACTH-adenomas and fatty acid metabolism for the TSH-, PRL-, GH-cluster. Non-tumoral pituitary scRNAseq data confirmed that this clustering also occurs in normal cytodifferentiation. Deconvolution analysis identify potential mononuclear cell infiltrate in PA consists of dendritic, NK and mast cells. Our results are consistent with a divergent origin of PA, which segregate into three clusters that depend on the specific transcription factors driving late pituitary cytodifferentiation.
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