ArticleNature communications2020
Functional characterization of SMARCA4 variants identified by targeted exome-sequencing of 131,668 cancer patients.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 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
93 citing papers in PubMed, 147 citations in OpenAlex.
- Clinicopathological characteristics and therapeutic outcomes in patients with non-small cell lung cancer harboringAnnals of medicine · 2026Article
- Interpreting human genetic variation at atomic resolution.Nature genetics · 2026Review
- Skeletal Muscle Metastasis in Patients With SMARCA4-Deficient Thoracic Tumors: A Retrospective Cohort Study.International journal of cancer · 2026Article
- SMARCA4, STK11, and KEAP1 co-inactivation associates with poor prognosis and upregulation of the TGF-β pathway in lung adenocarcinoma.Translational oncology · 2026Article
- Genetic analysis of primary lung interdigitating dendritic cell sarcomas.The Journal of pathology · 2026Article
- Discovery of SMD-6346: A Potent, Selective, and Orally Active SMARCA2 Degrader for Targeting SMARCA4-Deficient Human Cancers.Journal of medicinal chemistry · 2026Article
- BRG1-mediated suppression of ferroptosis underlies BTK inhibitor resistance.Nature communications · 2026Article
- Osimertinib Resistance in EGFR-Mutated Non-Small Cell Lung Cancer: Mechanisms and Therapeutic Strategies.MedComm · 2026Review
- BAF chromatin remodeling complexes inhibit immediate-early and early, but not late, transcription of herpes simplex virus 1.bioRxiv : the preprint server for biology · 2026Article
- Bibliometric analysis and knowledge mapping of thoracic SMARCA4-deficient undifferentiated tumor.Discover oncology · 2026Article
- SMARCA4-Directed Treatment in Oncology Clinical Trials: A Review.Journal of immunotherapy and precision oncology · 2026Review
- Two distinct SWI/SNF complexes direct chromatin-linked transcriptional programs in Toxoplasma.Nature communications · 2026Article
- SMARCA4 mutations drive metastatic progression and predict poor survival in breast cancer based on a real-world cohort study.Discover oncology · 2026Article
- Article
- An update on the role of SMARCA4 deficiency in gynecological neoplasms: how and where.Virchows Archiv : an international journal of pathology · 2026Review
- Analysis of SWI Complex Subunits in 69 Cases of TTF-1 Negative Non-Small Cell Lung Carcinoma.Diagnostic cytopathology · 2026Article
- [Clinicopathological, Genomic Characteristics and Prognostic Analysis in 18 Cases of SMARCA4-deficient or SMARCA4-mutated Pulmonary Tumors].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Article
- Dissecting the Binding Interactions of the Chromatin Remodeler SMARCA4 with G-Quadruplex DNA.Biochemistry · 2026Article
- Long non-coding RNA UCA1 modulates SMARCA2-containing SWI/SNF chromatin remodeling complexes in human colorectal cancer.iScience · 2026Article
- Ex vivo drug sensitivity profiling to complement molecular profiling in pediatric precision oncology.NPJ precision oncology · 2026Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genomic studies performed in cancer patients and tumor-derived cell lines have identified a high frequency of alterations in components of the mammalian switch/sucrose non-fermentable (mSWI/SNF or BAF) chromatin remodeling complex, including its core catalytic subunit, SMARCA4. Cells exhibiting loss of SMARCA4 rely on its paralog, SMARCA2, making SMARCA2 an attractive therapeutic target. Here we report the genomic profiling of solid tumors from 131,668 cancer patients, identifying 9434 patients with one or more SMARCA4 gene alterations. Homozygous SMARCA4 mutations were highly prevalent in certain tumor types, notably non-small cell lung cancer (NSCLC), and associated with reduced survival. The large sample size revealed previously uncharacterized hotspot missense mutations within the SMARCA4 helicase domain. Functional characterization of these mutations demonstrated markedly reduced remodeling activity. Surprisingly, a few SMARCA4 missense variants partially or fully rescued paralog dependency, underscoring that careful selection criteria must be employed to identify patients with inactivating, homozygous SMARCA4 missense mutations who may benefit from SMARCA2-targeted therapy.
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.