# ARID1A

Source: https://onco.cc/targets/arid1a/  
OnCo record `arid1a` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

ARID1A (AT-rich interactive domain-containing protein 1A) is a protein that switches other genes on and off. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Bladder & urothelial cancer, Colorectal cancer, Endometrial cancer and 5 more.

## Summary

Involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Component of SWI/SNF chromatin remodeling complexes that carry out key enzymatic activities, changing chromatin structure by altering DNA-histone contacts within a nucleosome in an ATP-dependent manner. Binds DNA non-specifically.

CIViC holds 14 clinical evidence items and 0 assertions across 7 variants, naming Dasatinib, Sorafenib, Nivolumab and Pembrolizumab and others. Open Targets scores its association with cancer at 0.85 (direct and indirect evidence; datatypes literature 1.00, affected pathway 0.89, genetic association 0.57, somatic mutation 0.98). IntOGen calls it a driver in 90 cohorts (1 activating, 89 loss-of-function), covering Burkitt Lymphoma, Bladder Urothelial Carcinoma, Invasive Breast Carcinoma, Renal Clear Cell Carcinoma, Cervical Squamous Cell Carcinoma, Cholangiocarcinoma and others.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: AT-rich interaction domain 1A; AT-rich interactive domain-containing protein 1A; B120; P270; C10rf4; BAF250; BAF250a; C1orf4; SMARCF1
- Tags: cancer-genes-wave
- Symbol: ARID1A
- Class: transcription
- Biology: Involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Component of SWI/SNF chromatin remodeling complexes that carry out key enzymatic activities, changing chromatin structure by altering DNA-histone contacts within a nucleosome in an ATP-dependent manner. Binds DNA non-specifically. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a postmitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to postmitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. Location: Nucleus (UniProt). Locus 1p36.11 (HGNC).
- Where found: Bladder & urothelial cancer: Open Targets association 0.76 with urinary bladder cancer (MONDO_0001187); IntOGen driver in 9 cohorts (BLCA, UTUC); Colorectal cancer: Open Targets association 0.74 with colorectal cancer (MONDO_0005575); CIViC evidence names this disease; Endometrial cancer: Open Targets association 0.72 with endometrial cancer (MONDO_0011962); IntOGen driver in 4 cohorts (UCEC); Gastric & gastro-oesophageal junction cancer: Open Targets association 0.69 with gastric cancer (MONDO_0001056); CIViC evidence names this disease; Breast cancer: Open Targets association 0.68 with breast cancer (MONDO_0007254); IntOGen driver in 8 cohorts (BRCA); Lung cancer: Open Targets association 0.68 with lung cancer (MONDO_0008903); IntOGen driver in 1 cohort (LUNG); Pancreatic ductal adenocarcinoma: inactivating mutation (swi/snf and chromatin genes) 5-9%; Colorectal cancer: inactivating mutation 9-13%; Gallbladder cancer: mutation (loss of function) 13-25%

## Notes

- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: CIViC lists 6 therapies; IntOGen calls it an activating (Act) driver in 1 cohort; IntOGen calls it a loss-of-function (LoF) driver in 89 cohorts; CIViC holds 14 clinical evidence items on its variants. Evidence tier "clinical-evidence" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.
- Diseases the sources name that have no OnCo cancer page yet, so they are not linked: Ovarian Clear Cell Carcinoma; Ovarian Clear Cell Adenocarcinoma; Low-Grade Glioma, NOS.
- Pancreatic ductal adenocarcinoma: inactivating mutations in 5 to 9%, alongside KMT2C, KMT2D, SMARCA4, PBRM1 and ARID2 (cBioPortal). Chromatin-regulating gene mutations were present in about 20% of patients and associated with improved survival (Sausen 2015); ARID1A was among the significantly mutated genes of the first exome cohorts (Biankin 2012, Cancer Genome Atlas 2017).
- Colorectal cancer: inactivating mutation in 9 to 13%, named a new driver by the TCGA analysis (Cancer Genome Atlas Network 2012), and overwhelmingly a hypermutated-class event (65.2% of MSI-high against 6.3% of microsatellite-stable samples in crc_msk_2026), alongside KMT2D and KMT2C.

## Sources

- HGNC HGNC:11110: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:11110
- UniProt O14497: https://www.uniprot.org/uniprotkb/O14497/entry
- NCBI Gene 8289: https://www.ncbi.nlm.nih.gov/gene/8289
- Ensembl ENSG00000117713: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000117713

## Connected records

- collections: [CIViC](https://onco.cc/collections/civic/), [IntOGen](https://onco.cc/collections/intogen/), [Open Targets Platform](https://onco.cc/collections/open-targets/)
- cancers: [Bladder & urothelial cancer](https://onco.cc/cancers/urothelial/), [Breast cancer (all types)](https://onco.cc/cancers/breast-cancer/), [Colorectal cancer](https://onco.cc/cancers/colorectal/), [Endometrial cancer](https://onco.cc/cancers/endometrial/), [Gallbladder cancer](https://onco.cc/cancers/gallbladder/), [Gastric & gastro-oesophageal junction cancer](https://onco.cc/cancers/gastric/), [Hepatocellular carcinoma](https://onco.cc/cancers/hcc/), [Lung cancer (all types)](https://onco.cc/cancers/lung-cancer/), [Non-Hodgkin lymphoma (all types)](https://onco.cc/cancers/non-hodgkin-lymphoma/), [Pancreatic ductal adenocarcinoma](https://onco.cc/cancers/pancreatic/)
- pathways: [SWI/SNF chromatin remodelling](https://onco.cc/pathways/swi-snf-chromatin/)
- key papers: [Biliary cancer: utility of next-generation sequencing for clinical management](https://onco.cc/key-papers/paper-javle-biliary-ngs-cancer-2016/), [Clinical implications of genomic alterations in the tumour and circulation of pancreatic cancer patients](https://onco.cc/key-papers/paper-sausen-ctdna-pancreatic-resection-nat-commun-2015/), [Comprehensive molecular characterization of human colon and rectal cancer](https://onco.cc/key-papers/paper-tcga-colorectal-comprehensive-characterization-nature-2012/), [Genomic analyses identify molecular subtypes of pancreatic cancer](https://onco.cc/key-papers/paper-bailey-molecular-subtypes-pancreatic-nature-2016/), [Genomic characterization of biliary tract cancers identifies driver genes and predisposing mutations](https://onco.cc/key-papers/paper-wardell-biliary-drivers-germline-j-hepatol-2018/), [Genomic profiling of Indian gallbladder carcinoma: mutational insights in a high-incidence population](https://onco.cc/key-papers/paper-suryavanshi-indian-gallbladder-genomics-jco-go-2025/), [Integrated genomic characterization of pancreatic ductal adenocarcinoma](https://onco.cc/key-papers/paper-tcga-pancreatic-integrated-characterisation-cancer-cell-2017/), [Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes](https://onco.cc/key-papers/paper-biankin-pancreatic-exomes-axon-guidance-nature-2012/), [Population-Specific Immunogenomic Alterations in Gallbladder Cancer and Prognostic Significance](https://onco.cc/key-papers/paper-zhu-population-specific-immunogenomics-gallbladder-cancer-mod-pathol-2025/), [Regional differences in gallbladder cancer pathogenesis: insights from a multi-institutional comparison of tumor mutations](https://onco.cc/key-papers/paper-narayan-gallbladder-regional-mutations-cancer-2019/)

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