ReviewPituitary2018
Can tissue biomarkers reliably predict the biological behavior of craniopharyngiomas? A comprehensive overview.
Review in Pituitary, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Association of histological subtype with risk of recurrence in craniopharyngioma patients: a systematic review and meta-analysis.Neurosurgical review · 2022Pooled it
- Comprehensive molecular characterization of craniopharyngiomas using whole transcriptome and spatial transcriptomics approaches.Brain tumor pathology · 2025Article
- Recent advances in craniopharyngioma pathophysiology and emerging therapeutic approaches.Frontiers in endocrinology · 2025Review
- Diagnostic support in pediatric craniopharyngioma using deep learning.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024Article
- Predictive Factors for Pediatric Craniopharyngioma Recurrence: An Extensive Narrative Review.Diagnostics (Basel, Switzerland) · 2023Review
- The molecular pathogenesis of craniopharyngiomas.Archives of endocrinology and metabolism · 2023Review
- Evaluation of B7-H3 Targeted Immunotherapy in a 3D Organoid Model of Craniopharyngioma.Biomolecules · 2022Article
- Duct-like diverticulum at the base of third ventricle tumors: a morphological signature diagnostic of papillary craniopharyngioma.Neurosurgical review · 2022Article
- Strictly third ventricle craniopharyngiomas: pathological verification, anatomo-clinical characterization and surgical results from a comprehensive overview of 245 cases.Neurosurgical review · 2022Review
- Sex Hormone Receptor Expression in Craniopharyngiomas and Association with Tumor Aggressiveness Characteristics.Journal of clinical medicine · 2022Article
- Craniopharyngioma and the Third Ventricle: This Inescapable Topographical Relationship.Frontiers in oncology · 2022Article
- Pathological and Prognostic Characterization of Craniopharyngioma Based on the Expression of TrkA, β-Catenin, Cell Cycle Markers, and BRAF V600E Mutation.Frontiers in endocrinology · 2022Article
- Bioinformatics analysis and validation of the critical genes associated with adamantinomatous craniopharyngioma.Frontiers in oncology · 2022Article
- Aggressive Childhood-onset Papillary Craniopharyngioma Managed With Vemurafenib, a BRAF Inhibitor.Journal of the Endocrine Society · 2021Article
- Craniopharyngioma adherence: a reappraisal of the evidence.Neurosurgical review · 2020Review
- Advances in the management of craniopharyngioma in children and adults.Radiology and oncology · 2019Review
- Sporadic adamantinomatous craniopharyngioma with double-hit somatic APC mutations.Neuro-oncology advancesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe growing interest in the molecular and genetic alterations of craniopharyngiomas (CPs) is embodied in recent studies revealing insights into the CP tumorigenesis and identifying novel molecular pathways amenable of targeted therapies. The actual impact of this new information, however, remains inconclusive.
methodsWe present a comprehensive review of the accumulated knowledge on molecular biology of CPs and a critical analysis on the strengths and weaknesses of the studies focused on CP molecular/genetic alterations published to date.
resultsA thorough analysis of the alterations of β-catenin/CTNNB1 and BRAF genes investigated in 1123 CP cases included in 27 studies, showed that, on average, CTNNB1 mutations were present in two-thirds of adamantinomatous CPs and BRAF mutations in 90% of papillary CPs. Their role as oncogenic drivers has not been well established. Although rare, coexistence of both mutations may occur. The involvement of pituitary stem cells in human CP tumorigenesis is still uncertain. Expression of stem markers in human CP samples predominantly occurred along the CP border in contact with brain tissue. Finally, none of the various molecular alterations which have been proposed as markers for CP recurrence can be used today as reliable predictors of the CP behavior.
conclusionsThe isolated evaluation of CPs' molecular or genetic profiles that do not take into consideration fundamental pathological and therapeutic factors, specifically the tumor topography and the degree of tumor removal, may actually generate confusion regarding the reliability of some biomarkers to predict the CP biological behavior.
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