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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
    10d
    Transarterial Chemoembolization Modulates the Exosomal miR-32-5p/cGAS-STING Axis Mediated Macrophage Ferroptosis, Triggers Immune Remodeling, and Enhances Anti-PD-1/L1 Efficacy in HCC. (PubMed, Research (Wash D C))
    Such a combined treatment led to excellent tumor control and enhanced survival without loss of acceptable toxicity profiles. The essential role of ferroptosis was confirmed by the use of Fer-1 to inhibit the chemical reactions, which revealed a new approach by which TACE-resistant exosomal miR-32-5p could inhibit the progression of HCC and complement the anti-PD-L1 therapeutic effects through ferroptosis using TAM, providing insights as well as potential therapeutic objectives in the treatment of HCC.
    Journal
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    CD8 (cluster of differentiation 8) • IL6 (Interleukin 6) • TNFA (Tumor Necrosis Factor-Alpha) • ARID1B (AT-Rich Interaction Domain 1B) • STING (stimulator of interferon response cGAMP interactor 1) • CCL2 (Chemokine (C-C motif) ligand 2) • CD68 (CD68 Molecule) • CGAS (Cyclic GMP-AMP Synthase) • CD86 (CD86 Molecule)
    13d
    Acute Leukemia with BCL11B Rearrangements: Genetic Landscape, BCL11B Expression, and Therapeutic Response. (PubMed, Hum Pathol)
    Clinically, newly diagnosed patients, most treated with venetoclax based regimens, achieved high remission rates. Our data delineate the structural diversity of BCL11B rearrangements identified by OGM and show that BCL11B activation cannot be reliably inferred from partner gene identity alone. BCL11B immunohistochemistry as a practical surrogate for assessing BCL11B activation is recommended in routine practice.
    Journal
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    CCDC6 (Coiled-Coil Domain Containing 6) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • ARID1B (AT-Rich Interaction Domain 1B) • CDK6 (Cyclin-dependent kinase 6) • TNFAIP3 (TNF Alpha Induced Protein 3) • LMO2 (LIM Domain Only 2) • BCL11B (BAF Chromatin Remodeling Complex Subunit BCL11B) • GAPDH (Glyceraldehyde-3-Phosphate Dehydrogenase) • TLX1 (T Cell Leukemia Homeobox 1)
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    Venclexta (venetoclax)
    20d
    Analysis of SWI Complex Subunits in 69 Cases of TTF-1 Negative Non-Small Cell Lung Carcinoma. (PubMed, Diagn Cytopathol)
    The uniqueness of this study lies in the large number of cases, with their specimens obtained via cytopathological methods and immunostained with all five common SWI markers. This study contributes to the familiarity and awareness of pathologists and oncologists by highlighting the importance of cytomorphology and immunohistochemical profile of SWI/SNF-deficient NSCLC-NOS, facilitating earlier diagnosis, and may ultimately lead to more specific and novel therapeutic targets.
    Journal
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    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) • NKX2-1 (NK2 Homeobox 1) • NAPSA (Napsin A Aspartic Peptidase)
    25d
    SWITCH: Cemiplimab Plus Gemcitabine in Patients With Metastatic Pancreatic Adenocarcinoma (clinicaltrials.gov)
    P2, N=43, Recruiting, University of California, San Diego | Not yet recruiting --> Recruiting
    Enrollment open
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    ARID1A (AT-rich interaction domain 1A) • PBRM1 (Polybromo 1) • SMARCB1 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily B, Member 1) • ARID1B (AT-Rich Interaction Domain 1B)
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    gemcitabine • Libtayo (cemiplimab-rwlc)
    2ms
    SWI/SNF complex alterations predict immunotherapy response in bladder cancer. (PubMed, Front Immunol)
    SWI/SNF alterations define an immunotherapy-responsive stratification of UBC. The accompanying genotype-specific prognostic models provide a ready-to-test framework for guiding precision immunotherapy.
    Journal • Tumor mutational burden • IO biomarker
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    TMB (Tumor Mutational Burden) • ARID1A (AT-rich interaction domain 1A) • PBRM1 (Polybromo 1) • 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)
    2ms
    Synovial sarcoma reprograms transcription by GBAF activation of polycomb targets and loss of CBAF enhancers. (PubMed, Nat Commun)
    Disruption of Arid1a or Arid1b (both CBAF-specific) retains synovial sarcoma character, while Smarcb1 (PBAF- and CBAF-specific) or Pbrm1 (PBAF-specific) disruption does not, although all accelerate SS18::SSX-driven tumorigenesis in mice. Thus, the synovial sarcomagenesis mechanism involves SS18::SSX reprogramming transcription positively through GBAF redistribution to activate polycomb-targeted developmental genes, and negatively by loss of normal CBAF localization and function.
    Journal
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    ARID1A (AT-rich interaction domain 1A) • PBRM1 (Polybromo 1) • SMARCB1 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily B, Member 1) • ARID1B (AT-Rich Interaction Domain 1B) • SS18 (SS18 Subunit Of BAF Chromatin Remodeling Complex)
    2ms
    Human stem cell models for group 3 medulloblastoma uncover JARID1B as a regulator of the chromatin landscape. (PubMed, bioRxiv)
    Knockdown of JARID1B in human G3MB cell lines reduced growth, supporting potential as a therapeutic target. We conclude that a MYC-TGFβ-JARID1B axis represses target genes to drive G3MB and present new humanized models for G3MB to understand epigenetic dysregulation in G3MB.
    Journal
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    ARID1B (AT-Rich Interaction Domain 1B) • KDM5B (Lysine Demethylase 5B)
    2ms
    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)
    2ms
    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)
    2ms
    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
    3ms
    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
    3ms
    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)