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    GENE:

    ARID1B (AT-Rich Interaction Domain 1B)

    i
    Other names: ARID1B, AT-Rich Interaction Domain 1B, AT-Rich Interactive Domain-Containing Protein 1B, AT Rich Interactive Domain 1B (SWI1-Like), ARID Domain-Containing Protein 1B, BRG1-Associated Factor 250b, BAF250B, P250R, DAN15, OSA2, BRG1-Binding Protein HELD/OSA1, BRG1-Binding Protein ELD/OSA1, ELD (Eyelid)/OSA Protein, Osa Homolog 2, ELD/OSA1, KIAA1235, BRIGHT, 6A3-5, MRD12, HOsa2, CSS1
    4d
    Dedifferentiated Cervical Mesonephric Adenocarcinoma: Report of 2 Cases of a Previously Undescribed Phenomenon. (PubMed, Int J Gynecol Pathol)
    Both tumors exhibited aggressive behavior with rapid local recurrence or metastasis of the undifferentiated carcinoma component. PVs in SWI/SNF genes may be associated with the process of dedifferentiation.
    Journal
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    KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • 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) • GATA3 (GATA binding protein 3) • PAX8 (Paired box 8)
    15d
    Genomic Profile and Clinicopathological Analyses of Wild-Type Gastrointestinal Stromal Tumors. (PubMed, Mol Cancer Res)
    Considering the rarity and heterogeneity of WT-GISTs, a regulatory detection procedure should be established for WT-GISTs, including NGS for qWT-GISTs, to identify the molecular mechanisms and potential therapeutic targets. Implications: WT-GISTs are heterogenous tumors which should be managed using different treatments and follow-up strategies.
    Journal
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    HIF1A (Hypoxia inducible factor 1, alpha subunit) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase) • ARID1B (AT-Rich Interaction Domain 1B) • PLCG2 (Phospholipase C Gamma 2)
    15d
    Genomic pathogenic alterations in the SWI/SNF complex compromise the outcomes of immunotherapy in Chinese patients with KRAS-mutant NSCLC by downregulating STING expression. (PubMed, BMC Med)
    In KRAS-mut NSCLCs with or without STK11/KEAP1 mutations, the GPAs in the DNA-binding genes ARID1A/ARID2 affected the outcomes of immunotherapy, possibly through the downregulation of STING expression.
    Journal • IO biomarker
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    KRAS (KRAS proto-oncogene GTPase) • STK11 (Serine/threonine kinase 11) • ARID1A (AT-rich interaction domain 1A) • KEAP1 (Kelch Like ECH Associated Protein 1) • PBRM1 (Polybromo 1) • 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) • STING (stimulator of interferon response cGAMP interactor 1) • ARID2 (AT-Rich Interaction Domain 2)
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    KRAS mutation • EGFR wild-type • ARID1A mutation • STK11 mutation • KEAP1 mutation
    25d
    Shifted assembly and function of mSWI/SNF family subcomplexes underlie targetable dependencies in dedifferentiated endometrial carcinomas. (PubMed, bioRxiv)
    Further, treatment with clinical-grade SMARCA4/2 ATPase inhibitors markedly attenuates DDEC cell proliferation and tumor growth in vivo and synergizes with carboplatin-based chemotherapy to extend survival. These findings reveal the oncogenic contributions of shifted mSWI/SNF family complex stoichiometry and resulting gene regulatory dysregulation and suggest therapeutic utility of mSWI/SNF small molecule inhibitors in DDEC/UEC and other cBAF-disrupted cancer types.
    Journal
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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)
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    carboplatin
    1m
    Clinical Risk Stratification and Modifiable Risk Factors for Hepatitis B Virus-Related Follicular Lymphoma. (PubMed, Immunotargets Ther)
    Integrated clinicopathological features into prediction system may provide precise risk stratification for HBV-positive FL. Modifiable DNA methylation acts as the potential targets for the combined treatment strategy to delay POD24 occurrence.
    Journal
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    MYC (V-myc avian myelocytomatosis viral oncogene homolog) • KMT2A (Lysine Methyltransferase 2A) • ARID1B (AT-Rich Interaction Domain 1B) • EP300 (E1A binding protein p300) • TNFRSF1A (TNF Receptor Superfamily Member 1A) • CXCR5 (C-X-C Motif Chemokine Receptor 5)
    2ms
    Shifted assembly and function of mSWI/SNF family subcomplexes underlie targetable dependencies in dedifferentiated endometrial carcinomas. (PubMed, Nat Genet)
    Furthermore, treatment with clinical-grade SMARCA4 and/or SMARCA2 ATPase inhibitors markedly attenuates DDEC cell proliferation and tumor growth in vivo and synergizes with carboplatin-based chemotherapy to extend survival. These findings reveal the oncogenic contributions of shifted mSWI/SNF family complex stoichiometry and resulting gene-regulatory dysregulation and suggest therapeutic utility of mSWI/SNF small molecule inhibitors in DDEC/UECs and other cBAF-disrupted cancer types.
    Journal
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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) • SMARCA2 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily A, Member 2)
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    carboplatin
    2ms
    Distinct genomic subgroups and mutational patterns in undifferentiated/dedifferentiated endometrial carcinoma. (PubMed, BMC Cancer)
    Our analysis revealed distinct architectures and actionable alterations in UDEC. The identification of molecular subgroups provides a promising framework for prognostic stratification. Collectively, our findings not only advance our understanding of UDEC biology but also illuminate potential translational applications.
    Journal
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    PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • 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) • KMT2B (Lysine Methyltransferase 2B)
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    PTEN mutation
    3ms
    ARID1A regulates histone octamer transfer activity of human canonical BAF complex. (PubMed, Nucleic Acids Res)
    Remarkably, we find that the ARID1A subunit of cBAF is largely dispensable for nucleosome binding, nucleosome sliding, and adenosine triphosphatase activity, but ARID1A is required for cBAF to transfer histone octamers between DNA templates. Our study reveals a biochemical function of ARID1A/ARID1B in BAF-mediated chromatin remodeling, suggesting a model in which dysregulation of histone octamer transfer activity of BAF complexes may be relevant to cancer formation.
    Journal
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    ARID1A (AT-rich interaction domain 1A) • ARID1B (AT-Rich Interaction Domain 1B)
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    ARID1A mutation
    3ms
    ARID1A and ARID1B safeguard B cell identity, prevent myeloid transformation and expose therapeutic vulnerabilities in lymphoma. (PubMed, bioRxiv)
    Transcriptomic analysis revealed major alterations in cell adhesion/migration pathways, cytokine-receptor interactions and DNA repair mechanisms. Collectively, these findings reveal stage-specific and compensatory roles for ARID1A and ARID1B in B cell development, uncover a mechanism by which SWI/SNF loss in early progenitors can drive transformation towards myeloid leukemia, and suggests context-dependent therapeutic vulnerabilities.
    Journal
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    ARID1A (AT-rich interaction domain 1A) • CD19 (CD19 Molecule) • ARID1B (AT-Rich Interaction Domain 1B) • FLI1 (Fli-1 Proto-Oncogene ETS Transcription Factor) • CBFA2T3 (CBFA2/RUNX1 Partner Transcriptional Co-Repressor 3)
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    ARID1A mutation
    3ms
    Genomic profiling guided therapy for synchronous SCC and CLL of the parotid gland: a rare case report. (PubMed, J Surg Case Rep)
    He received six cycles of cemiplimab followed by cetuximab-based targeted therapy, based on rising circulating DNA levels. This case emphasizes the value of genetic profiling and tools like TMB, FISH, and immunohistochemistry for risk stratification and personalized treatment in managing advanced or complex parotid malignancies, including synchronous SCC and CLL, to optimize patient outcomes.
    Journal • Tumor mutational burden • PD(L)-1 Biomarker
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    TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • MSH2 (MutS Homolog 2) • PMS2 (PMS1 protein homolog 2) • ARID1B (AT-Rich Interaction Domain 1B)
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    TP53 mutation • TMB-H
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    Erbitux (cetuximab) • Libtayo (cemiplimab-rwlc)
    4ms
    A novel SWI/SNF complex promotes triple-negative breast cancer progression. (PubMed, Cell Mol Biol Lett)
    This research enhances the understanding of the intricate roles played by SWI/SNF complex components in TNBC and bridges the gap between the structural specificity of SWI/SNF assembly and the progression of cancer. These findings could potentially unveil novel therapeutic targets for TNBC, thereby advancing the development of more efficacious treatment approaches for this highly aggressive malignancy.
    Journal
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    SMARCB1 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily B, Member 1) • ARID1B (AT-Rich Interaction Domain 1B)
    4ms
    Clinicopathological and genomic analysis of SWI/SNF chromatin remodeling abnormalities with a focus on SMARCA4 in cancer of unknown primary. (PubMed, J Cancer Res Clin Oncol)
    This study demonstrated SWI/SNF chromatin remodeling abnormalities in CUP and the association between SMARCA4 deficiency and U-CUP. It suggests a potential strategy for selecting an ICI regimen for CUP, particularly U-CUP, with SMARCA4 deficiency.
    Journal • IO biomarker
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    ARID1A (AT-rich interaction domain 1A) • PBRM1 (Polybromo 1) • 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) • SMARCA2 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily A, Member 2)