Targeting ARID1A mutations in cancer
Abstract
Genes encoding SWI/SNF chromatin remodeling complex subunits are collectively mutated in approximately 20% of human cancers. ARID1A is a SWI/SNF subunit gene whose protein product binds DNA. ARID1A gene alterations result in loss of function. It is the most commonly mutated member of the SWI/SNF complex, being aberrant in ∼6% of cancers overall, including ovarian clear cell cancers (∼45% of patients) and uterine endometrioid cancers (∼37%). ARID1A has a crucial role in regulating gene expression that drives oncogenesis or tumor suppression. In particular, ARID1A participates in control of the PI3K/AKT/mTOR pathway, immune responsiveness to cancer, EZH2 methyltransferase activity, steroid receptor modulation, DNA damage checkpoints, and regulation of p53 targets and KRAS signaling. A variety of compounds may be of benefit in ARID1A-altered cancers: immune checkpoint blockade, and inhibitors of mTOR, EZH2, histone deacetylases, ATR and/or PARP. ARID1A alterations may also mediate resistance to platinum chemotherapy and estrogen receptor degraders/modulators.
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ARID1A regulates DNA damage checkpoints and sensitizes cells to DNA damage response (DDR) targeting agents.
“ARID1A regulates DNA damage checkpoints and sensitizes cells to DNA damage response (DDR) targeting agents67–69.”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [69]
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- Authors
- Mullen, J., Kato, S., Sicklick, J. K., & Kurzrock, R.
- Affiliations
- University of California San Diego (US)
- UC San Diego Health System (US)
- WIN Consortium (FR)
- Corresponding author
- Kato, Shumei
- Venue
- Cancer Treatment Reviews
- Publisher
- Elsevier BV
- Published
- 2021-11
- Volume
- 100
- Pages
- 102287
- ISSN
- 0305-7372 (ISSN-L)
- OpenAlex
- W3197896101
- Cited by
- 186
- References
- 88
- Citations by year
- 2026: 27 · 2025: 47 · 2024: 56 · 2023: 28 · 2022: 28
- FWCI
- 3.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Cancer Treatment Reviews (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Health Sciences › Medicine › Reproductive Medicine › Ovarian cancer diagnosis and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- ARID1A mutation, SWI/SNF complex, ovarian clear cell carcinoma, endometrioid endometrial cancer, PI3K/AKT/mTOR pathway, EZH2, immune checkpoint blockade, mTOR inhibitors, histone deacetylase inhibitors, ATR inhibitors, PARP inhibitors, platinum resistance, estrogen receptor modulators, KRAS signaling, DNA damage checkpoint, cancer therapy resistance
- MeSH terms
- Poly(ADP-ribose) Polymerase Inhibitors, Immune Checkpoint Inhibitors, Animals, DNA-Binding Proteins, Enzyme Inhibitors, Humans, Mutation, Neoplasms, Transcription Factors, Molecular Targeted Therapy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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