ArticleEndocrine pathology2013
The role of mediators of cell invasiveness, motility, and migration in the pathogenesis of silent corticotroph adenomas.
Article in Endocrine pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
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
16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.
- Predictors of silent corticotroph adenoma recurrence; a large retrospective single center study and systematic literature review.Pituitary · 2018Pooled it
- Silent corticotroph adenomas.Pituitary · 2015Pooled it
- Collagen in pituitary adenomas: A comprehensive review of biological roles and clinical implications.Journal of clinical & translational endocrinology · 2025Review
- Article
- Cystic versus non-cystic silent corticotrophic adenomas: clinical and histological analysis of 62 cases after microscopic transsphenoidal surgery-a retrospective, single-center study.Scientific reports · 2023Article
- Aggressive nonfunctioning pituitary neuroendocrine tumors.Brain tumor pathology · 2022Review
- Silent Corticotroph and Somatotroph Double Pituitary Adenoma: A Case Report and Review of Literature.Journal of neurological surgery reports · 2022Article
- Pituitary neuroendocrine tumors: a model for neuroendocrine tumor classification.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Review
- Genomics and Epigenomics of Pituitary Tumors: What Do Pathologists Need to Know?Endocrine pathology · 2021Review
- Aggressive Cushing's Disease: Molecular Pathology and Its Therapeutic Approach.Frontiers in endocrinology · 2021Review
- Article
- Clinical and Pathological Aspects of Silent Pituitary Adenomas.The Journal of clinical endocrinology and metabolism · 2019Review
- Distinct Expression Patterns of Osteopontin and Dentin Matrix Protein 1 Genes in Pituitary Gonadotrophs.Frontiers in endocrinology · 2019Article
- Epidemiology and biomarker profile of pituitary adenohypophysial tumors.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018Article
- Emerging Histopathological and Genetic Parameters of Pituitary Adenomas: Clinical Impact and Recommendation for Future WHO Classification.Endocrine pathology · 2016Review
- Aggressive pituitary adenomas--diagnosis and emerging treatments.Nature reviews. Endocrinology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Silent corticotroph adenomas (SCAs) represent a distinct subset of clinically non-functioning pituitary adenomas. There are two variants of SCA; type I are densely granulated basophilic tumors and type II are sparsely granulated and chromophobic tumors. SCAs are known to be aggressive than the more common non-functioning gonadotroph adenomas (NFGAs). Cell-matrix interactions play an important role in the pathogenesis of pituitary adenomas. In this study, we compared 19 SCAs and 50 NFGAs with known fibroblast growth factor receptor-4 (FGFR4) status using semi-quantitative immunohistochemistry to localize β1-integrin, osteopontin, and matrix metalloproteinase-1 (MMP-1) as cytoplasmic, membranous, or mixed cytoplasmic-membranous staining to achieve scores of 1-4. Staining for β1-integrin was significantly higher in SCAs (100 %, score 3.3) than in NFGAs (96 %; score 2.6) (p = 0.0482); there was no statistical difference within subgroups of SCA (type II score 3.4; type I score 2.8) (p = 0.2663). Osteopontin immunoreactivity was also higher in SCAs (100 %, score 3.7) than in NFGAs (42 %, score 0.8) (p = 0.0001); there was no statistical difference within subgroups of SCA (type II score 3.6; type I score 3.9) (p = 0.2787). In contrast, MMP-1 immunoreactivity was lower in SCAs (89 %; score 2.5) than in NFGAs (98 %; score 3.6) (p = 0.0005); there was no statistical difference within subgroups of SCA (type II score 2.7; type I score 2.0) (p = 0.30704). The MMP-1 results correlated with FGFR4 expression (NFGA 96 %, type II SCA 71 %, type I SCA 40 %). Our data indicate that the biological aggressivity of SCAs compared with NFGA may be due to high osteopontin expression; in contrast, high MMP-1 is characteristic of NFGAs that also express more FGFR4. Further investigations are warranted to clarify the underlying regulatory mechanisms of these markers. The high osteopontin or FGFR4/MMP-1 expression levels in SCAs and NFGAs, respectively, indicate the potential for therapeutic strategies targeting osteopontin or FGFR4/MMP-1 for inoperable tumors of these types.
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.