ReviewCancer cell2014
Vulnerabilities of mutant SWI/SNF complexes in cancer.
Review in Cancer cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 1 of them a synthesis that pooled it.
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
170 citing papers in PubMed, 1 synthesis or guideline pooled it.
- High expression of SMARCA4 or SMARCA2 is frequently associated with an opposite prognosis in cancer.Scientific reports · 2018Pooled it
- A phase 2 study of dasatinib in recurrent clear cell carcinoma of the ovary, fallopian tube, peritoneum or endometrium: NRG oncology/gynecologic oncology group study 0283.Gynecologic oncology · 2023Trial
- SMARCA4, STK11, and KEAP1 co-inactivation associates with poor prognosis and upregulation of the TGF-β pathway in lung adenocarcinoma.Translational oncology · 2026Article
- Delineating SWI/SNF gene and subtype expression in cancer.Epigenetics & chromatin · 2026Article
- Comprehensive molecular characterization of cutaneous squamous cell carcinoma reveals determinants of metastatic progression.medRxiv : the preprint server for health sciences · 2026Article
- SMARCA4 activation engages FOSL1 to drive enhancer reprogramming and tumorigenic phenotypes in SMARCA4-deficient LUAD cells.Cell death discovery · 2026Article
- A SWI/SNF-specific Ig-like domain, SWIFT, is a transcription factor binding platform.Science (New York, N.Y.) · 2026Article
- Chromatin Accessibility in Cancer: Biological Functions, Mechanisms, Therapeutic Potential, and Future Directions.MedComm · 2026Review
- ARID1A deficiency activates OSM-STAT3 axis in endometrial cancer, creating vulnerability to JAK/STAT3 inhibition.International journal of biological sciences · 2026Article
- A New WHO Entity of SMARCB1/INI1-Deficient Undifferentiated Thoracic Tumors: Rare, Aggressive, and Overlooked.Cureus · 2025Article
- Clinicopathological and molecular perspectives on thoracic SMARCA4-deficient undifferentiated tumors and SMARCA4-deficient non-small cell lung carcinomas.Pathologica · 2025Review
- ARID1A loss enhances sensitivity to c-MET inhibition by dual targeting of GPX4 and iron homeostasis, inducing ferroptosis.Cell death and differentiation · 2025Article
- BRG1 Loss Is Frequent in Lung Cancer and Transforms Lung Epithelial Cells via Transcriptional and Epigenetic Reprograming.Cancers · 2025Article
- ACTL6A depletion induces KLF4-mediated anti-tumorigenic effects in colorectal cancer.Cell death & disease · 2025Article
- Epigenetic control in thyroid cancer: mechanisms and clinical perspective.Cell death discovery · 2025Review
- The role and mechanism of ARID1A in immunotherapy of gastric cancer.Clinical and experimental medicine · 2025Article
- Article
- Brain metastases lung adenocarcinoma patients with BRG1 loss have a grim prognosis, featuring unique morphological and methylation characteristics.Clinical & experimental metastasis · 2025Article
- Identification of selective SWI/SNF dependencies in enzalutamide-resistant prostate cancer.Communications biology · 2025Article
- SMARCA4 regulates the NK-mediated killing of senescent cells.Science advances · 2025Article
110 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
3 authors.
Funding
Abstract
Cancer genome sequencing efforts have revealed the novel theme that chromatin modifiers are frequently mutated across a wide spectrum of cancers. Mutations in genes encoding subunits of SWI/SNF (BAF) chromatin remodeling complexes are particularly prevalent, occurring in 20% of all human cancers. As these are typically loss-of-function mutations and not directly therapeutically targetable, central goals have been to elucidate mechanism and identify vulnerabilities created by these mutations. Here, we discuss emerging data that these mutations lead to the formation of aberrant residual SWI/SNF complexes that constitute a specific vulnerability and discuss the potential for exploiting these dependencies in SWI/SNF mutant cancers.
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.