ArticleTechnology in cancer research & treatment2018
Loss of ARID1A Expression Correlates With Tumor Differentiation and Tumor Progression Stage in Pancreatic Ductal Adenocarcinoma.
Article in Technology in cancer research & treatment, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Molecular interplay of ARID1A in gastrointestinal cancers.Medical oncology (Northwood, London, England) · 2025Review
- Drivers of Pancreatic Cancer: Beyond the Big 4.Cancers · 2025Review
- The cross-talk between the macro and micro-environment in precursor lesions of pancreatic cancer leads to new and promising circulating biomarkers.Journal of experimental & clinical cancer research : CR · 2024Review
- The Role of Genetic Mutations in Mitochondrial-Driven Cancer Growth in Selected Tumors: Breast and Gynecological Malignancies.Life (Basel, Switzerland) · 2023Review
- Review
- [Multiple primary malignancies combined with SWI/SNF complex-deficient gastric cancer: a case report and literature review].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Review
- Relationship between cellular morphology and abnormality of SWI/SNF complex subunits in pancreatic undifferentiated carcinoma.Journal of cancer research and clinical oncology · 2022Article
- Article
- Targeting the alterations of ARID1A in pancreatic cancer: tumorigenesis, prediction of treatment, and prognostic value.American journal of translational research · 2022Review
- Article
- Co-existing TP53 and ARID1A mutations promote aggressive endometrial tumorigenesis.PLoS genetics · 2021Article
- LncRNA GAS5 inhibits the proliferation and invasion of ovarian clear cell carcinoma via the miR-31-5p/ARID1A axis.The Kaohsiung journal of medical sciences · 2021Article
- ARID1A serves as a receivable biomarker for the resistance to EGFR-TKIs in non-small cell lung cancer.Molecular medicine (Cambridge, Mass.) · 2021Review
- Single-PanIN-seq unveils thateLife · 2021Article
- Exploiting vulnerabilities of SWI/SNF chromatin remodelling complexes for cancer therapy.Oncogene · 2021Review
- Molecular Alterations in Pancreatic Cancer: Transfer to the Clinic.International journal of molecular sciences · 2021Review
- The Role ofFrontiers in oncology · 2021Review
- Non-coding RNAs in Pancreatic Ductal Adenocarcinoma.Frontiers in oncology · 2020Review
- Article
- A pipeline for rapidly generating genetically engineered mouse models of pancreatic cancer using in vivo CRISPR-Cas9-mediated somatic recombination.Laboratory investigation; a journal of technical methods and pathology · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the AT-rich interactive domain 1A gene, which encodes a subunit of the Switch/Sucrose nonfermentable chromatin remodeling complex, can result in loss of protein expression and are associated with different cancers. Here, we used immunohistochemistry to investigate the significance of AT-rich interactive domain 1A loss in 73 pancreatic ductal adenocarcinoma cases with paired paracancerous normal pancreatic tissues. The relationship between levels of the AT-rich interactive domain 1A protein product, BAF250a, and clinicopathological parameters in the 73 pancreatic cancer specimens was also analyzed. We found that the expression of AT-rich interactive domain 1A in normal pancreatic tissue was higher than that in tumor tissue. Loss of AT-rich interactive domain 1A expression in pancreatic tumors was associated with tumor differentiation ( P = .002) and tumor stage ( P = .048). Meanwhile, BAF250a protein levels were not related to lymph node metastasis, distant metastasis, sex, or age and were not associated with survival. Transfection of the pancreatic cancer cell lines AsPC-1 and PANC-1 with small-interfering RNA specific for AT-rich interactive domain 1A resulted in elevated messenger RNA and protein expression levels of B-cell lymphoma-2 (Bcl-2), CyclinD1, and Kirsten rat sarcoma viral oncogene (KRAS). The AT-rich interactive domain 1A expression level in the cells was increased following microRNA-31 (miR-31) inhibitor transfection. Our data provide additional evidence that AT-rich interactive domain 1A might function as a tumor suppressor gene in pancreatic carcinogenesis.
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