ArticleCancer research2018
Familial and Somatic
Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 29 citations in OpenAlex.
- Allostery is a widespread cause of loss-of-function variant pathogenicity.Nature communications · 2026Article
- Phenotype-Specific Recalibration of MAVE Data Enables Repurposing ofmedRxiv : the preprint server for health sciences · 2026Article
- CDK6/4 inactivates BAP1 deubiquitinase destabilizing VHL to promote metastatic colonization in liver.Molecular cancer · 2026Article
- Tumor suppressor BAP1 emerges as a key regulator of metabolism and cell death in tumors.Frontiers in cell and developmental biology · 2026Review
- Case report: complete response and long-term survival on third-line immunotherapy in patient with pleural mesothelioma.Frontiers in oncology · 2024Article
- Structural basis of histone H2A lysine 119 deubiquitination by Polycomb repressive deubiquitinase BAP1/ASXL1.Science advances · 2023Article
- Structural basis of histone H2A lysine 119 deubiquitination by Polycomb Repressive Deubiquitinase BAP1/ASXL1.bioRxiv : the preprint server for biology · 2023Article
- ASXL1/2 mutations and myeloid malignancies.Journal of hematology & oncology · 2022Review
- Oncogenic gene expression and epigenetic remodeling of cis-regulatory elements in ASXL1-mutant chronic myelomonocytic leukemia.Nature communications · 2022Article
- Kinetic Characterization of ASXL1/2-Mediated Allosteric Regulation of the BAP1 Deubiquitinase.Molecular cancer research : MCR · 2021Article
- Association between serum anti‑ASXL2 antibody levels and acute ischemic stroke, acute myocardial infarction, diabetes mellitus, chronic kidney disease and digestive organ cancer, and their possible association with atherosclerosis and hypertension.International journal of molecular medicine · 2020Article
- Selective Modulation of Dynamic Protein Complexes.Cell chemical biology · 2020Review
- BAP1 regulates epigenetic switch from pluripotency to differentiation in developmental lineages giving rise to BAP1-mutant cancers.Science advances · 2019Article
- Comprehensive Study of the Clinical Phenotype of Germline BAP1 Variant-Carrying Families Worldwide.Journal of the National Cancer Institute · 2018Review
- A bidentate Polycomb Repressive-Deubiquitinase complex is required for efficient activity on nucleosomes.Nature communications · 2018Article
- Genomics and Epigenetics of Malignant Mesothelioma.High-throughput · 2018Review
- Deubiquitinating Enzymes and Bone Remodeling.Stem cells international · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Deleterious mutations of the ubiquitin carboxy-terminal hydrolase BAP1 found in cancers are predicted to encode inactive truncated proteins, suggesting that loss of enzyme function is a primary tumorigenic mechanism. However, many tumors exhibit missense mutations or in-frame deletions or insertions, often outside the functionally critical UCH domain in this tumor suppressor protein. Thus, precisely how these mutations inactivate BAP1 is unknown. Here, we show how these mutations affect BAP1 interactions with the Polycomb group-like protein, ASXL2, using combinations of computational modeling technology, molecular biology, and
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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.