ReviewTrends in genetics : TIG2014
A rationale to target the SWI/SNF complex for cancer therapy.
Review in Trends in genetics : TIG, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 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
115 citing papers in PubMed, 179 citations in OpenAlex.
- G3BP1 is a SWI/SNF-bound regulator of transcription that modulates activation of STATs.Bioscience reports · 2026Article
- BRG1 (SMARCA4) Status Dictates the Response to EGFR Inhibitors in Wild-Type EGFR Non-Small Cell Lung Cancer.Cancers · 2025Article
- Multidimensional OMICs reveal ARID1A orchestrated control of DNA damage, splicing, and cell cycle in normal-like and malignant urothelial cells.Molecular oncology · 2025Article
- MYC Regulates a DNA Repair Gene Expression Program in Small Cell Carcinoma of the Ovary, Hypercalcemic Type.Cancers · 2025Article
- Structural and functional characterisation and regulatory mechanisms of SWI/SNF and RSC chromatin remodelling complexes in fungi.Mycology · 2025Review
- Chromatin remodeling in lymphocytic function and fate: the multifaceted roles of SWI/SNF complex.Frontiers in immunology · 2025Review
- BRD9 promotes the progression of gallbladder cancer via CST1 upregulation and interaction with FOXP1 through the PI3K/AKT pathway and represents a therapeutic target.Gene therapy · 2024Article
- New strategies in soft tissue sarcoma treatment.Journal of hematology & oncology · 2024Review
- Unveil Intrahepatic Cholangiocarcinoma Heterogeneity through the Lens of Omics and Multi-Omics Approaches.Cancers · 2024Review
- A SWI/SNF-dependent transcriptional regulation mediated by POU2AF2/C11orf53 at enhancer.Nature communications · 2024Article
- Therapeutic Role of Synthetic Lethality inJournal of immunotherapy and precision oncology · 2024Review
- Degraders in epigenetic therapy: PROTACs and beyond.Theranostics · 2024Review
- Dual blockade of BRD4 and ATR/WEE1 pathways exploitsResearch square · 2023Article
- Genetic and chemical targeting of the ATPase complex TIP48 and 49 impairs acute myeloid leukemia.Leukemia · 2023Article
- BRD9 Degradation Disrupts Ribosome Biogenesis in Multiple Myeloma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Mutual Regulation of ncRNAs and Chromatin Remodeling Complexes in Normal and Pathological Conditions.International journal of molecular sciences · 2023Review
- ARID1A in cancer: Friend or foe?Frontiers in oncology · 2023Review
- INO80 function is required for mouse mammary gland development, but mutation alone may be insufficient for breast cancer.Frontiers in cell and developmental biology · 2023Article
- BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.The EMBO journal · 2022Article
- Sirt2 promotes white matter oligodendrogenesis during development and in models of neonatal hypoxia.Nature communications · 2022Article
55 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
2 authors at 1 institution in 1 country.
Funding
Abstract
SWI/SNF is a multisubunit chromatin-remodeling complex that performs fundamental roles in gene regulation, cell lineage specification, and organismal development. Mutations that inactivate SWI/SNF subunits are found in nearly 20% of human cancers, which indicates that the proper functioning of this complex is necessary to prevent tumor formation in diverse tissues. Recent studies show that SWI/SNF-mutant cancers depend on residual SWI/SNF complexes for their aberrant growth, thus revealing synthetic lethal interactions that could be exploited for therapeutic purposes. Other studies reveal that certain acute leukemias and small cell lung cancers, which lack SWI/SNF mutations, can be vulnerable to inhibition of the SWI/SNF ATPase subunit BRG1, whereas several normal and malignant cell types do not show this sensitivity. Here, we review the emerging evidence that implicates SWI/SNF as a tumor-dependency and candidate drug target in human cancer.
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.