Table 1 The characteristics of the 23 eligible studies
From: Roles of ARID1A variations in colorectal cancer: a collaborative review
Author and country | Publication year | Type of CRC | ARID1A variation (%) | ARID1A expression | Roles of ARID1A | Clinicopathologic features or biological effects of ARID1A | Antibodies of ARID1A | References |
|---|---|---|---|---|---|---|---|---|
Jones, USA | 2012 | CRC | 12/119, 10% | Downregulated | Suppressor | ARID1A inactivation promoted CRC development | NA | Jones et al. (2012) |
Chou, Australia | 2014 | CRC | 110/1876, 5.9%; | Loss of expression | Suppressor | No significant relationship between loss expression of ARID1A and the OS of CRC; Loss expression of ARID1A was associated with multiple clinical features, BRAFV600E variation and loss of mismatch repair protein expression (all P < 0.01) | Sigma 1: 100 | Chou et al. (2014) |
Cajuso, Finland | 2014 | CRC | 18/46, 39% | Downregulated | Suppressor | Exome sequencing showed that ARID1A play an important role in microsatellite-unstable CRC via DNA binding activity and transcription coactivator activity | Santa Clara | Cajuso et al. (2014) |
Xie, China | 2014 | CRC | 26/86, 30.2% | Loss of expression | Suppressor | Loss of ARID1A significantly associated with poor differentiation of CRC (P = 0.0009) | Rabbit antibodies Sigma 1:500 | Xie et al. (2014) |
Ye, USA | 2014 | CRC | 22/257, 9% | Loss of expression | Suppressor | ARID1A loss was significantly associated with various clinicopathological features of CRC (all P < 0.05), and with a trend toward a worse OS (P > 0.05) | polyclonal antibody Sigma- 1:100 | Ye et al. (2014) |
Wei, China | 2014 | CRC | 54/209, 25.8% | Loss of expression | Suppressor | ARID1A loss was correlated to late TNM stage, distant metastasis, and poor pathological classification (all P < 0.05) | Santa Cruz Biotechnology | Wei et al. (2014) |
Lee, Korea | 2015 | CRC | 12/196, 6.1% | Loss of expression | Suppressor | Loss of ARID1A expression was significantly correlated with negative lymphatic invasion (P = 0.003) in CRC, and with expanding tumor border (CRC, P = 0.010) | Rabbit polyclonal, Sigma 1:100 | Lee et al. (2015) |
Lee, USA | 2016 | CRC | 49/552, 8.9% | Loss of expression | Suppressor | ARID1A loss was associated with mismatch-repair protein deficiency. poor differentiation, lymphovascular invasion, and higher pT stage (all P < 0.05) | Rabbit polyclonal, Sigma, 1:300 | Lee et al. (2016) |
Agaimy, Germany | 2016 | Colon, small bowel, and stomach cancer | 2/13, 15.4% | Loss of expression | Suppressor | NA | Rabbit polyclonal Abcam, 1:100 | Agaimy et al. (2016) |
Fountzilas, USA | 2018 | CRC | 16/36, 44% | Loss of expression | Suppressor | ARID1A variations independently predicted for unfavorable DFS (HR = 1.99, 95%CI 1.11–3.54, P = 0.020) | NA | Fountzilas et al. (2018) |
Wan, China | 2018 | CRC | 3/16, 18.8% | Loss of expression | Suppressor | NA | MygeneSeq technology | Wan et al. (2018) |
Sen, USA | 2019 | CRC | 24/164, 14.6% | Loss of expression | Suppressor | The expression of ARID1A plays a key role in KRAS-mutated CRC cells | Cell Signaling, 1:500 | Sen et al. (2019) |
Kishida, Japan | 2019 | CRC | 10/218, 4.6% | Loss of expression | Suppressor | Loss expression of ARID1A was significantly correlated to younger age, lymphatic invasion, and lymph node metastasis | Rabbit monoclonal, 1:500 | Kishida et al. (2019) |
Xu, China | 2020 | sCRC | 1/28, 3.6% | Frameshift variation | Suppressor | ARID1A variations and the deficiency of its protein expression were significantly involved in advanced tumor depth, poor differentiation, lymphatic metastasis, BRAF V600E variation, MMR deficiency and MSI phenotype in tumors of CRC patients | NA | Xu et al. (2020) |
Tokunaga-1,USA | 2020 | CRC | 468/5726, 8% | Downregulated | Suppressor | ARID1A variations could regulate DNA repair pathways | NA | Tokunaga et al. (2020) |
Tokunaga-2,USA | 2020 | CRC | 50/619, 8% | Downregulated | Suppressor | ARID1A variation was significantly associated with a favourable immune profile indicative of a higher likelihood of response to immune checkpoint inhibitors | NA | Tokunaga et al. (2020) |
Tokunaga-3,USA | 2020 | CRC | 104/1099, 10% | Downregulated | Suppressor | ARID1A variation was associated with right-sided primary tumor location and earlier tumor stage | NA | Tokunaga et al. (2020) |
Tokunaga-4,USA | 2020 | CRC | 58/534, 11% | Downregulated | Suppressor | ARID1A variations lead to strong immune activation in CRC | NA | (Tokunaga et al. 2020) |
Erfani, Iran | 2020 | CRC | 12/18, 66.7% | Loss or low expression | Suppressor | No significant relationship was found between the loss of ARID1A and the OS or the clinicopathological features in CRC | Rabbit antibody Sigma 1:200 | Erfani et al. (2020) |
Villatoro, USA | 2020 | Colorectal adenocarcinoma | 16/338, 4.7%; | Deficiency | Suppressor | No difference in disease-specific or disease-free survival was found for ARID1A deficiency (all P > 0.05) | Abcam | Villatoro et al. (2020) |
Stein, USA | 2020 | pCRC PM | pCRC: 179/617, 29%, PM: 42/348, 12% | Variation | Suppressor | NA | Primary antibody clones | Stein et al. (2020) |
Wang-1, China | 2020 | CRC | 76/156, 48.7% | Downregulated | Suppressor | NA | NA | Wang et al. (2020) |
Wang-2, China | 2020 | CRC | 17/225, 7.6% | Downregulated | Suppressor | NA | NA | Wang et al. (2020) |
Jiang, China | 2020 | CRC | 89/1234, 7.2% | Variation | Suppressor | CRC patients with ARID1A variation showed a significantly longer DFS/PFS (HR = 0.74, P = 0.0026) | NA | Jiang et al. (2020) |
Huang, China | 2021 | CRC | 65/630, 10.3% | Variation | Suppressor | NA | NA | (Huang et al. 2021) |
Perna, Spain | 2021 | HG-CRCs | 12/29, 41.4% | Loss of expression | Suppressor | The differences in survival were not statistically significant (HR = 0.58, 95% CI = 0.23–1.49, P = 0.257) | Polyclonal Sigma, 1:500 | Perna et al. (2021) |
Kamori, Japan | 2021 | CRC | 20/201, 10% | Variation | Suppressor | Tumor histological grade was significantly correlated with ARID1A variation status in those patients with right-sided CRC | Rabbit polyclonal, | Kamori et al. (2021) |