ReviewOncogene2022
Neurofibromin and suppression of tumorigenesis: beyond the GAP.
Review in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 90 citations in OpenAlex.
- Durable responses to long-term selumetinib in Chinese pediatric NF1 patients with inoperable plexiform neurofibromas.Frontiers in pharmacology · 2026Trial
- Effect of NFX-179 MEK inhibitor on cutaneous neurofibromas in persons with neurofibromatosis type 1.Science advances · 2024Trial
- Precision therapeutic strategies for advanced gastrointestinal stromal tumors.Cancer metastasis reviews · 2026Review
- Neurofibromin in bone disease: Mechanisms and therapeutic implications (Review).International journal of molecular medicine · 2026Review
- Article
- Epilepsy, Cognitive, and Behavioral Outcomes in Neurocutaneous Syndromes: A Comparative Review of NF1, TSC, and Sturge-Weber Syndrome.Children (Basel, Switzerland) · 2026Review
- Resolving variants of uncertain significance in neurofibromatosis: An integrated approach combining deep learning and minigene assays.Functional & integrative genomics · 2026Article
- Article
- Progressive cervicothoracic meningocele with neurovascular compression and spinal deformity in neurofibromatosis type 1: a decade-long radiological and clinical evolution with operative repair. Illustrative case.Journal of neurosurgery. Case lessons · 2026Article
- Pathogenic Neurofibromatosis type 1 gene variants in tumors of non-NF1 patients and role of R1276.FEBS open bio · 2026Article
- An intercostal artery aneurysm rupture in a patient with neurofibromatosis type 1-associated gastrointestinal stromal tumor during sunitinib therapy.Clinical journal of gastroenterology · 2026Article
- ERKed by too much signaling: from oncogenic driver to therapeutic vulnerability.Cellular and molecular life sciences : CMLS · 2026Review
- The Role of CRISPR and Its Therapeutic Applications in Glioblastoma.International journal of molecular sciences · 2026Review
- Pharmacogenomic Synthetic Lethal Screens Reveal Hidden Vulnerabilities and New Therapeutic Approaches for Treatment of NF1-Associated Tumors.Molecular cancer therapeutics · 2026Article
- Preimplantation genetic testing for neurofibromatosis type 1: molecular genetic aspects and impact on reproductive counseling.Human reproduction (Oxford, England) · 2026Observational
- Neurofibromin 1 (International journal of molecular sciences · 2026Article
- Cribriform Tumor of the Skin: Identification of 6q and 9q Loss as a Recurrent Cytogenomic Alteration.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2026Article
- Integrative Genomic and Functional Analysis Reveals NF1 Loss as a Modifier of DNA Damage and Replication Stress Responses in Ovarian Cancer.Human mutation · 2026Article
- Article
- Clinical characteristics and healthcare burden of neurofibromatosis type 1 in Saudi Arabia: a single centre experience.Hereditary cancer in clinical practice · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Neurofibromatosis type 1 (NF1) is an autosomal dominant genetic disease and one of the most common inherited tumor predisposition syndromes, affecting 1 in 3000 individuals worldwide. The NF1 gene encodes neurofibromin, a large protein with RAS GTP-ase activating (RAS-GAP) activity, and loss of NF1 results in increased RAS signaling. Neurofibromin contains many other domains, and there is considerable evidence that these domains play a role in some manifestations of NF1. Investigating the role of these domains as well as the various signaling pathways that neurofibromin regulates and interacts with will provide a better understanding of how neurofibromin acts to suppress tumor development and potentially open new therapeutic avenues. In this review, we discuss what is known about the structure of neurofibromin, its interactions with other proteins and signaling pathways, its role in development and differentiation, and its function as a tumor suppressor. Finally, we discuss the latest research on potential therapeutics for neurofibromin-deficient neoplasms.
Indexed as
Identifiers
What Socratic 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 Socratic graph.