ReviewNature reviews. Cancer2020
The duality of human oncoproteins: drivers of cancer and congenital disorders.
Review in Nature reviews. Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 79 citations in OpenAlex.
- Hydrophobic Tag Protein Degraders: An Emerging Therapeutic Strategy for Cancer.Pharmaceuticals (Basel, Switzerland) · 2026Review
- K-Ras controls asymmetric cell divisions from the primary cilium.Cell death & disease · 2026Article
- The exosomal miRNA/FOXN3 axis empowers fibroblasts with tumor-promoting functions via enhanced migration and altered secretome.Journal of nanobiotechnology · 2026Article
- Oncogenic PIK3CA mutations shape an immunoregulatory microenvironment in mosaic overgrowth disorders.PNAS nexus · 2026Article
- Identification of Raptor and GLI1 as USP37 substrates highlight its context-specific function in medulloblastoma cells.Oncogene · 2026Article
- Expanding the Genetic Landscape of Craniofacial Anomalies Through Transcriptome-Wide Association Studies.Research square · 2025Article
- Development of a Genetically Encoded and Potent PDE6D Inhibitor.Chembiochem : a European journal of chemical biology · 2025Article
- The impact of RAS on cell differentiation in health and disease.The Biochemical journal · 2025Review
- Expanding the Genetic Landscape of Craniofacial Anomalies Through Transcriptome-Wide Association Studies.Research square · 2025Article
- Perspectives in MicroRNA Therapeutics for Cystic Fibrosis.Non-coding RNA · 2025Review
- Leveraging cancer mutation data to inform the pathogenicity classification of germline missense variants.PLoS genetics · 2025Article
- An evaluation of genetic predisposition to congenital anomalies and pediatric cancer supportsGenetics in medicine open · 2025Article
- Cerebral Cavernous Malformation: From Genetics to Pharmacotherapy.Brain and behavior · 2025Review
- Prediction of viral oncoproteins through the combination of generative adversarial networks and machine learning techniques.Scientific reports · 2024Article
- RASopathies - what they reveal about RAS/MAPK signaling in skeletal muscle development.Disease models & mechanisms · 2024Review
- RAS-dependent RAF-MAPK hyperactivation by pathogenic RIT1 is a therapeutic target in Noonan syndrome-associated cardiac hypertrophy.Science advances · 2023Article
- K-Ras Binds Calmodulin-Related Centrin1 with Potential Implications for K-Ras Driven Cancer Cell Stemness.Cancers · 2023Article
- The homeostatic regulation of ribosome biogenesis.Seminars in cell & developmental biology · 2023Review
- ERK-mediated NELF-A phosphorylation promotes transcription elongation of immediate-early genes by releasing promoter-proximal pausing of RNA polymerase II.Nature communications · 2022Article
- Boosting Antitumor Immunity with an Expanded Neoepitope Landscape.Cancer research · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Human oncoproteins promote transformation of cells into tumours by dysregulating the signalling pathways that are involved in cell growth, proliferation and death. Although oncoproteins were discovered many years ago and have been widely studied in the context of cancer, the recent use of high-throughput sequencing techniques has led to the identification of cancer-associated mutations in other conditions, including many congenital disorders. These syndromes offer an opportunity to study oncoprotein signalling and its biology in the absence of additional driver or passenger mutations, as a result of their monogenic nature. Moreover, their expression in multiple tissue lineages provides insight into the biology of the proto-oncoprotein at the physiological level, in both transformed and unaffected tissues. Given the recent paradigm shift in regard to how oncoproteins promote transformation, we review the fundamentals of genetics, signalling and pathogenesis underlying oncoprotein duality.
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.