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BIOMARKER:

ARID2 mutation

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Other names: ARID2, AT-Rich Interaction Domain 2, BAF200, AT-Rich Interactive Domain-Containing Protein 2, AT Rich Interactive Domain 2 (ARID, RFX-Like), Zinc Finger Protein With Activation Potential, ARID Domain-Containing Protein 2, BRG1-Associated Factor 200, Zipzap/P200, DKFZp686G052, FLJ30619, CSS6
Entrez ID:
Related biomarkers:
2ms
ARID2 mutations may relay a distinct subset of cutaneous melanoma patients with different outcomes. (PubMed, Sci Rep)
Melanoma patients with ARID mutations exhibited higher prevalence of markers associated with ICI response, including TMB-H, and immune-related signatures. Our data also suggests improved survival outcome in patients with ARID2 mutations, irrespective of anti-PD1 therapy.
Journal • Tumor mutational burden • PD(L)-1 Biomarker • MSi-H Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • ARID1A (AT-rich interaction domain 1A) • NF1 (Neurofibromin 1) • IFNG (Interferon, gamma) • ARID2 (AT-Rich Interaction Domain 2)
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PD-L1 expression • TMB-H • MSI-H/dMMR • BRAF mutation • ARID1A mutation • NF1 mutation • RAS mutation • ARID2 mutation
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VENTANA PD-L1 (SP142) Assay
6ms
Evaluation of association of mutation in ARID family of genes with outcomes in cutaneous melanoma (SITC 2023)
Conclusions Melanoma patients with ARID mutations exhibited higher prevalence of markers associated with ICI response, including TMB-H, PD-L1 and immune-related signatures. Our data also suggests improved survival outcome in patients with ARID2 mutations, although no additional OS benefit was observed with anti-PD-L1 therapy.
Tumor mutational burden • PD(L)-1 Biomarker • MSi-H Biomarker • IO biomarker
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KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • ARID1A (AT-rich interaction domain 1A) • NF1 (Neurofibromin 1) • IFNG (Interferon, gamma) • ARID2 (AT-Rich Interaction Domain 2)
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PD-L1 expression • TMB-H • MSI-H/dMMR • BRAF mutation • ARID1A mutation • NF1 mutation • RAS mutation • ARID2 mutation
|
VENTANA PD-L1 (SP142) Assay
9ms
Mutational landscape of SWI/SNF complex genes reveal correlation to predictive biomarkers for immunotherapy sensitivity in lung adenocarcinoma patients. (PubMed, ESMO Open)
The research presented in this study shows that mutations in the ARID gene family, including ARID1A, ARID1B, and ARID2, are primarily responsible for the sensitive response to immunotherapy treatment in patients with lung adenocarcinoma.
Journal • Tumor mutational burden • IO biomarker
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TMB (Tumor Mutational Burden) • ARID1A (AT-rich interaction domain 1A) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • SMARCB1 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily B, Member 1) • ARID1B (AT-Rich Interaction Domain 1B) • ARID2 (AT-Rich Interaction Domain 2)
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ARID1A mutation • SMARCA4 mutation • SMARCB1 mutation • ARID2 mutation
1year
HR/HER2 de novo metastatic breast cancer: a true peculiar entity? (PubMed, Drugs Context)
Altogether genomic, biological and clinical findings highlight HR/HER2 dnMBC as a peculiar entity as compared with rMBC and deserve a dedicated treatment algorithm. This article is part of the Tackling clinical complexity in breast cancer Special Issue: https://www.drugsincontext.com/special_issues/tackling-clinical-complexity-in-breast-cancer/.
Clinical • Review • Journal • Tumor mutational burden • Metastases
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HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • TMB (Tumor Mutational Burden) • ARID2 (AT-Rich Interaction Domain 2)
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HR positive • HER-2 negative • ER mutation • ESR1 mutation • EGFR positive • ARID2 mutation
1year
Comprehensive profiling of EGFR mutation subtypes reveals genomic-clinical associations in non-small-cell lung cancer patients on first-generation EGFR inhibitors. (PubMed, Neoplasia)
Furthermore, mutational profiles, such as top frequently mutated genes and mutational signatures of patients with various EGFR subtype mutations were significantly different. Our study analyzed the mutational landscape of NSCLC patients harboring cEGFR and uEGFR mutations, revealing specific genomic characteristics associated with uEGFR mutations that might explain the poor prognosis of first-generation EGFR-TKIs.
Journal • Tumor mutational burden
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EGFR (Epidermal growth factor receptor) • TMB (Tumor Mutational Burden) • ARID2 (AT-Rich Interaction Domain 2)
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EGFR mutation • TMB-H • EGFR L858R • EGFR exon 19 deletion • ARID2 mutation
1year
Mutational pattern of SWI/SNF pathway genes in lung adenocarcinoma patients reveal uneven correlation with immunotherapy sensitivity (AACR 2023)
In summary, the mutational landscape of 5 major SWI/SNF pathway genes were classified. The research presented also shows that mutations in the ARID gene family, including ARID1A, ARID1B, and ARID2, are primarily responsible for the sensitive response to immunotherapy treatment in patients with SWI/SNF mutant lung adenocarcinoma.
Clinical • Tumor mutational burden • IO biomarker
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TMB (Tumor Mutational Burden) • ARID1A (AT-rich interaction domain 1A) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • SMARCB1 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily B, Member 1) • ARID1B (AT-Rich Interaction Domain 1B) • ARID2 (AT-Rich Interaction Domain 2)
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ARID1A mutation • SMARCA4 mutation • SMARCB1 mutation • ARID2 mutation
1year
Eribulin inhibits cell growth in cutaneous squamous cell carcinoma cell lines and a novel patient-derived xenograft harboring TP53 and ARID2 mutations (ISID 2023)
cSCC-PDX models responded well to both eribulin and cisplatin treatments. In addition, we developed a unique cSCC-PDX model that maintains the characteristics of a patient's tumor. This PDX model could help researchers who are exploring novel therapeutic strategies for cSCC.
Preclinical
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TP53 (Tumor protein P53) • ARID2 (AT-Rich Interaction Domain 2)
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TP53 mutation • ARID2 mutation
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cisplatin • Halaven (eribulin mesylate)
almost2years
Hepatocellular carcinoma after a sustained virological response by direct-acting antivirals harbors TP53 inactivation. (PubMed, Cancer Med)
Our dataset potentially serves as a fundamental resource for the genomic characteristics of HCV-SVR-DAA tumors. Our comprehensive genetic profiling by WES revealed significant differences in the mutation rate of several driver genes between HCV-positive tumors and HCV-SVR tumors. Furthermore, it was revealed that the frequency of samples with mutations in TP53 was significantly higher in HCV-SVR-DAA tumors than in HCV-SVR-IFN tumors.
Journal
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TP53 (Tumor protein P53) • ARID2 (AT-Rich Interaction Domain 2) • PREX2 (Phosphatidylinositol-3,4,5-Trisphosphate Dependent Rac Exchange Factor 2)
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TP53 mutation • ARID2 mutation • PREX2 mutation
2years
BRD4 inhibition induces synthetic lethality in ARID2-deficient hepatocellular carcinoma by increasing DNA damage. (PubMed, Oncogene)
Interestingly, JQ1, a selective inhibitor of bromodomain protein BRD4, uniquely suppressed the growth of ARID2- deficient HCC cells...However, as both ARID2 and BRD4 are disrupted, the expression of these DNA repair-related genes in response to DNA damage are hindered, resulting in DSB accumulation and cell apoptosis. Taken together, this study discloses that BRD4 inhibition may induce synthetic lethality in ARID2-deficient HCC cells, which might provide a potential therapeutic strategy for HCC patients with ARID2 mutations.
Journal • BRCA Biomarker • Synthetic lethality
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BRCA1 (Breast cancer 1, early onset) • RAD51 (RAD51 Homolog A) • ARID2 (AT-Rich Interaction Domain 2) • BRD4 (Bromodomain Containing 4) • TP53BP1 (Tumor Protein P53 Binding Protein 1)
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ARID2 mutation
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JQ-1
over2years
ARID1A, ARID1B, and ARID2 Mutations Serve as Potential Biomarkers for Immune Checkpoint Blockade in Patients With Non-Small Cell Lung Cancer. (PubMed, Front Immunol)
Finally, a nomogram was established to guide the clinical use of ICIs. The results show that patients with NSCLC who have ARID1A, ARID1B, and ARID2 mutations of the SWI/SNF complex were more likely to benefit from ICI therapy.
Clinical • Journal • Checkpoint inhibition • IO biomarker
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ARID1A (AT-rich interaction domain 1A) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • ARID1B (AT-Rich Interaction Domain 1B) • ARID2 (AT-Rich Interaction Domain 2)
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ARID1A mutation • ARID2 mutation
over2years
Comprehensive characterization of distinct genetic alterations in metastatic breast cancer across various metastatic sites. (PubMed, NPJ Breast Cancer)
Seven potential MBC driver mutations showed similar preferential enrichment in specific metastatic sites. This large-scale study identified new MBC genetic alterations according to various metastatic sites and highlights their potential role in breast cancer organotropism.
Journal
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ER (Estrogen receptor) • TP53 (Tumor protein P53) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • ATRX (ATRX Chromatin Remodeler) • TSC2 (TSC complex subunit 2) • AURKA (Aurora kinase A) • RICTOR (RPTOR Independent Companion Of MTOR Complex 2) • ARID2 (AT-Rich Interaction Domain 2)
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TP53 mutation • ER mutation • ARID2 mutation
almost3years
Journal
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NPM1 (Nucleophosmin 1) • KMT2D (Lysine Methyltransferase 2D) • ARID2 (AT-Rich Interaction Domain 2)
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NPM1 mutation • KMT2D mutation • ARID2 mutation
3years
ARID2 deficiency promotes tumor progression and is associated with higher sensitivity to chemotherapy in lung cancer. (PubMed, Oncogene)
Moreover, we demonstrated that ARID2 deficiency impairs DNA repair, enhancing the sensitivity of the cells to DNA-damaging agents. Our findings support that ARID2 is a bona fide tumor suppressor gene in lung cancer that may be exploited therapeutically.
Journal
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ARID2 (AT-Rich Interaction Domain 2)
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ARID2 mutation