ArticleCancer reports (Hoboken, N.J.)2022
The effects of ARID1A mutations on colorectal cancer and associations with PD-L1 expression by stromal cells.
Article in Cancer reports (Hoboken, N.J.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Cellular characteristics of the immune microenvironment of colorectal cancer and progress in immunotherapy research.Annals of medicine · 2025Review
- Evaluating the efficacy of PARP inhibitor in ARID1A-deficient colorectal cancer: ACancer biomarkers : section A of Disease markers · 2025Article
- The role of SWI/SNF complexes in digestive system neoplasms.Medical oncology (Northwood, London, England) · 2024Review
- Response to PD-1 inhibitor in SMARCB1‑deficient undifferentiated rectal carcinoma with low TMB, proficient MMR and BRAF V600E mutation: a case report and literature review.Diagnostic pathology · 2024Review
- Review
- Low level of ARID1A contributes to adaptive immune resistance and sensitizes triple-negative breast cancer to immune checkpoint inhibitors.Cancer communications (London, England) · 2023Article
- Association between Tumor Mutational Burden, Stromal CD8Cancers · 2023Article
- Roles of ARID1A variations in colorectal cancer: a collaborative review.Molecular medicine (Cambridge, Mass.) · 2022Review
- The effects of ARID1A mutations on colorectal cancer and associations with PD-L1 expression by stromal cells.Cancer reports (Hoboken, N.J.) · 2022Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundARID1A is a component of the SWI/SNF complex, which controls the accessibility of proteins to DNA. ARID1A mutations are frequently observed in colorectal cancers (CRCs) and have been reported to be associated with high mutational burden and tumor PD-L1 expression in vitro.
aimTo clarify the role of ARID1A mutation in CRC. METHOD AND
resultsWe used next generation sequencing (NGS) and immunohistochemistry on clinically obtained samples. A total of 201 CRC tissues from Niigata University and Niigata Center Hospital were processed by NGS using the CANCERPLEX panel. Immunohistochemistry for ARID1A, PD-L1, MLH1, and MSH2 was performed on 66 propensity-matched (33 microsatellite instability-high [MSI-H] and 33 microsatellite-stable [MSS]) cases among 499 cases from Kyushu University. TCGA data were downloaded from cBioPortal. NGS showed significantly more mutations in ARID1A mutated CRCs (p = 0.01), and the trend was stronger for right-sided CRCs than left-sided. TCGA data confirmed these findings (p < 0.01). BRAF V600E and ATM mutations were also found at higher frequencies. Immunohistochemistry showed that 30% of MSI-H CRCs had ARID1A loss, while this was true in only 6% of MSS CRCs. In both MSI-H and MSS, PD-L1 expression by stromal cells was enhanced in the ARID1A-mutant groups (90% vs 39% in MSI-H, 100% vs 26% in MSS).
conclusionWe found a higher mutational burden in ARID1A-mutant CRCs, and IHC study showed that ARID1A loss was correlated with high PD-L1 expression in stromal cells regardless of MSI status. These data support the idea that mutant ARID1A is a potential biomarker for CRCs.
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