ArticleNature communications2017
SMARCA4-inactivating mutations increase sensitivity to Aurora kinase A inhibitor VX-680 in non-small cell lung cancers.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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
78 citing papers in PubMed, 115 citations in OpenAlex.
- Bibliometric analysis and knowledge mapping of thoracic SMARCA4-deficient undifferentiated tumor.Discover oncology · 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
- Dual PD-1/IL-2Rα targeting restores CD8Cell reports. Medicine · 2026Article
- Intrathoracic Rhabdoid Tumors Showing Rapid Progress in Patients with a History of Immune-suppressive Therapies for Hematological Diseases.Internal medicine (Tokyo, Japan) · 2026Article
- Challenges and opportunities for oncology drug repurposing informed by synthetic lethality.NPJ systems biology and applications · 2025Article
- Clinical characteristics and prognostic analysis of 22 cases of SMARCA4-deficient thoracic tumors: a retrospective observational study.Journal of thoracic disease · 2025Article
- BRG1 Loss Is Frequent in Lung Cancer and Transforms Lung Epithelial Cells via Transcriptional and Epigenetic Reprograming.Cancers · 2025Article
- The role of SMARCA4 in lung cancer.Scientific reports · 2025Review
- Concurrent SMARCA4-deficient and poorly differentiated adenocarcinomas in separate lung lobes: a case report and literature review.World journal of surgical oncology · 2025Review
- Discovery of Novel, Potent, and Orally Bioavailable SMARCA2 Proteolysis-Targeting Chimeras with Synergistic Antitumor Activity in Combination with Kirsten Rat Sarcoma Viral Oncogene Homologue G12C Inhibitors.Journal of medicinal chemistry · 2025Article
- Article
- Review
- Small cell lung carcinoma with YAP1 expression and SMARCA4-deficient undifferentiated tumors.Translational cancer research · 2025Article
- SMARCA4 deficiency in small cell lung cancer: A case report and narrative review of the literature.Biomolecules & biomedicine · 2025Review
- When rarity meets thoracic cancers: a narrative review from ITMIG 2024.Mediastinum (Hong Kong, China) · 2025Review
- Enhancer reprogramming underlies therapeutic utility of a SMARCA2 degrader in SMARCA4 mutant cancer.Cell chemical biology · 2024Article
- Application of integrin subunit genes in pancreatic cancer and the construction of a prognosis model.Journal of gastrointestinal oncology · 2024Article
- [Research Progress on SMARCA4 Mutation Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Review
- Therapeutic modulation of ROCK overcomes metabolic adaptation of cancer cells to OXPHOS inhibition and drives synergistic anti-tumor activity.bioRxiv : the preprint server for biology · 2024Article
- Chromatin remodellers as therapeutic targets.Nature reviews. Drug discovery · 2024Review
18 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
Abstract
Mutations in the SMARCA4/BRG1 gene resulting in complete loss of its protein (BRG1) occur frequently in non-small cell lung cancer (NSCLC) cells. Currently, no single therapeutic agent has been identified as synthetically lethal with SMARCA4/BRG1 loss. We identify AURKA activity as essential in NSCLC cells lacking SMARCA4/BRG1. In these cells, RNAi-mediated depletion or chemical inhibition of AURKA induces apoptosis and cell death in vitro and in xenograft mouse models. Disc large homologue-associated protein 5 (HURP/DLGAP5), required for AURKA-dependent, centrosome-independent mitotic spindle assembly is essential for the survival and proliferation of SMARCA4/BRG1 mutant but not of SMARCA4/BRG1 wild-type cells. AURKA inhibitors may provide a therapeutic strategy for biomarker-driven clinical studies to treat the NSCLCs harbouring SMARCA4/BRG1-inactivating mutations.
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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.