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    BIOMARKER:

    ARID1A mutation

    i
    Other names: ARID1A, AT-Rich Interaction Domain 1A, SWI/SNF-Related, Matrix-Associated, Actin-Dependent Regulator Of Chromatin Subfamily F Member 1, AT-Rich Interactive Domain-Containing Protein 1A, AT Rich Interactive Domain 1A (SWI-Like), ARID Domain-Containing Protein 1A, SWI/SNF Complex Protein P270, BRG1-Associated Factor 250a, SWI-Like Protein, Osa Homolog 1, SMARCF1, C1orf4, BAF250, HOSA1, OSA1, AT Rich Interactive Domain 1A (SWI- Like), Chromatin Remodeling Factor P250, BRG1-Associated Factor 250, OS
    Entrez ID:
    8289
    Related biomarkers:
    Mutation
    CNA
    Others
    1d
    Prognostic Implications of SMARCA4, ARID1A, and Other BAF Mutations in Non-Small Cell Lung Cancer. (PubMed, Cancer Med)
    A growing body of evidence indicates that BAF complex mutations have important prognostic implications. These may be leveraged for risk stratification and therapeutic selection in patients with non-small cell lung cancer.
    Review • Journal • IO biomarker
    |
    EGFR (Epidermal growth factor receptor) • ARID1A (AT-rich interaction domain 1A) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4)
    |
    EGFR mutation • ARID1A mutation
    1d
    The immunotherapy era in ovarian clear cell carcinoma: current evidence and future perspective. (PubMed, Front Immunol)
    This review highlights OCCC molecular underpinnings and therapeutic challenges, emphasizing the need for innovative, multi-targeted strategies. Advances in understanding genetic-immunological interplay in OCCC may enable more effective and durable treatments and improved patient outcomes.
    Review • Journal • PD(L)-1 Biomarker • IO biomarker
    |
    PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • ARID1A (AT-rich interaction domain 1A) • IL6 (Interleukin 6) • LAG3 (Lymphocyte Activating 3) • HIF1A (Hypoxia inducible factor 1, alpha subunit) • IL10 (Interleukin 10)
    |
    PIK3CA mutation • ARID1A mutation
    1d
    Targeting synthetic lethality: an effective therapeutic approach in ovarian and endometrial cancers. (PubMed, Ther Adv Med Oncol)
    WEE1 inhibitors have shown encouraging results in combination with chemotherapy, increasing the objective response rate in patients with platinum-resistant TP53-mutated ovarian cancer. ATR inhibitors are currently being evaluated in ARID1A-mutated tumours, with preliminary results confirming their therapeutic potential.
    Review • Journal • BRCA Biomarker • PARP Biomarker
    |
    TP53 (Tumor protein P53) • PTEN (Phosphatase and tensin homolog) • HRD (Homologous Recombination Deficiency) • ARID1A (AT-rich interaction domain 1A) • BRCA (Breast cancer early onset)
    |
    TP53 mutation • HRD • PTEN mutation • ARID1A mutation • BRCA mutation
    3d
    Genomic Characteristics of Bladder Cancer: An AACR Project GENIE Study. (PubMed, Int J Mol Sci)
    Distinct patterns of co-occurrence, including TP53 with RB1, and mutual exclusivity, including TP53 with FGFR3 or KDM6A, revealed distinct molecular subtypes. This study highlights the extensive heterogeneity of bladder cancer, and our findings emphasize the clinical importance of molecular stratification and support the need for further mechanistic and prospective studies to inform the development of targeted therapies.
    Retrospective data • Journal
    |
    TP53 (Tumor protein P53) • FGFR3 (Fibroblast growth factor receptor 3) • RB1 (RB Transcriptional Corepressor 1) • ARID1A (AT-rich interaction domain 1A) • TERT (Telomerase Reverse Transcriptase) • KMT2D (Lysine Methyltransferase 2D) • KDM6A (Lysine Demethylase 6A)
    |
    TP53 mutation • ARID1A mutation • FGFR3 mutation
    3d
    Retrospective review of metastatic hormone receptor-positive inflammatory breast cancer patients reveals poor responses to cyclin dependent kinase 4/6 inhibition. (PubMed, Breast Cancer Res)
    Patients with metastatic HR+HER2- IBC demonstrated a shorter time on treatment suggesting shorter duration of response on CDKI + HT, which is markedly inferior to reported data for non-IBC patients from phase III trials.
    Retrospective data • Journal
    |
    HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR1 (Fibroblast growth factor receptor 1) • ARID1A (AT-rich interaction domain 1A) • CCND1 (Cyclin D1)
    |
    HER-2 positive • TP53 mutation • HR positive • HER-2 negative • PIK3CA mutation • ARID1A mutation • ESR1 mutation • HR positive + HER-2 negative • HER-2 negative + HR positive + ESR1 mutation
    |
    Ibrance (palbociclib) • Verzenio (abemaciclib) • Kisqali (ribociclib)
    5d
    MAP4 phosphorylation induced by ARID1A loss sensitizes colorectal cancer cells to EMP. (PubMed, Cell Death Dis)
    Here, we performed a synthetic lethal drug screening in an approved drug library with ARID1A isogenic CRC cell lines and identified estramustine phosphate sodium (EMP), an FDA approved antimicrotubule chemotherapy drug, as a synthetic lethal partner of ARID1A...Furthermore, we identified that MAP4 is phosphorylated by PI3K, which is activated by ARID1A loss. These findings highlight MAP4 as a key regulator of microtubule dynamics in ARID1A-deficient cells and unveil a novel synthetic lethality relationship between ARID1A and EMP.
    Journal
    |
    ARID1A (AT-rich interaction domain 1A) • MAP4 (Microtubule Associated Protein 4) • PI3K (Phosphoinositide 3-kinases)
    |
    ARID1A mutation
    |
    Emcyt (estramustine)
    5d
    Therapeutic opportunities in EBV-positive gastric cancer subtypes. (PubMed, Ther Adv Med Oncol)
    Lastly, EBVaGC is more likely to express the PI3K and ARID1A mutations, which can potentially be treated using PI3K/mTOR dual inhibitors and Akt/PARP inhibitors. These six subtypes could aid the selection of more successful treatments for EBVaGC, thereby improving the current overall survival and prognosis of patients.
    Review • Journal • Tumor mutational burden • MSi-H Biomarker • PARP Biomarker • IO biomarker
    |
    TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • ARID1A (AT-rich interaction domain 1A)
    |
    TMB-H • MSI-H/dMMR • TP53 wild-type • ARID1A mutation
    9d
    Endometrial carcinomas with solid basaloid morphology and geographic necrosis: clinicopathological and molecular features of 18 cases. (PubMed, Virchows Arch)
    Endometrial carcinomas with SB-GN represent a distinct and aggressive tumor group characterized by solid growth pattern, prominent necrosis, frequent basaloid morphology, high rates of CTNNB1 mutations, and aberrant β-catenin staining. Our results demonstrate that endometrial carcinomas with SB-GN and PiMHECs share similar clinicopathologic and molecular profiles, supporting a unified biological spectrum.
    Journal
    |
    TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PGR (Progesterone receptor) • PTEN (Phosphatase and tensin homolog) • ARID1A (AT-rich interaction domain 1A) • POLE (DNA Polymerase Epsilon) • CTNNB1 (Catenin (cadherin-associated protein), beta 1)
    |
    TP53 mutation • PIK3CA mutation • PTEN mutation • ARID1A mutation • POLE mutation
    10d
    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
    |
    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)
    |
    KRAS mutation • EGFR wild-type • ARID1A mutation • STK11 mutation • KEAP1 mutation
    13d
    Targeting WEE1 in ARID1A/TP53 Concurrent Mutant Colorectal Cancer by Exploiting RLoop Accumulation and DNA Repair Deficiencies. (PubMed, Adv Sci (Weinh))
    Moreover, though CRISPR knockout screening, it is found that concurrent AKT blockade significantly augmented the antitumor effects of the WEE1 inhibitor. In conclusion, WEE1 inhibition offers a promising therapeutic strategy for ARID1A/TP53 concurrent mutant CRC.
    Journal
    |
    TP53 (Tumor protein P53) • ARID1A (AT-rich interaction domain 1A) • DRD (DNA Repair Deficiency) • ATF3 (Activating Transcription Factor 3)
    |
    TP53 mutation • ARID1A mutation • DDR
    17d
    Descriptive Genomic Analysis of Ampullary Carcinoma Utilizing the AACR Project GENIE Dataset. (PubMed, Curr Issues Mol Biol)
    Reduced survival rates were seen in populations with the TP53 or KRAS mutation. This study provides a detailed descriptive genomic landscape of ampullary carcinoma, highlighting frequent mutations between patient groups and the mutational burden of the DNA damage response pathway in ampullary cancer, laying important groundwork for the development of therapeutic targets and more individualized treatment regimens.
    Journal • Tumor mutational burden
    |
    HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • ARID1A (AT-rich interaction domain 1A) • KMT2D (Lysine Methyltransferase 2D) • SMAD4 (SMAD family member 4) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • APC (APC Regulator Of WNT Signaling Pathway)
    |
    TP53 mutation • KRAS mutation • PIK3CA mutation • HER-2 mutation • ARID1A mutation
    25d
    Establishment of novel cholangiocarcinoma cell lines with ARID1A deficiency and preclinical validation of synthetic lethality therapies. (PubMed, Sci Rep)
    Based on this molecular finding, we performed drug screening and demonstrated that these ARID1A-deficient CCA cell lines are hypersensitive to inhibition by both PI3K/AKT and PARP inhibitors. The SiSP-K01 and SiSP-K05 cell lines are therefore critical new preclinical models suitable for functional studies of ARID1A deficiency and the development of targeted therapies for CCA.
    Preclinical • Journal • PARP Biomarker
    |
    ARID1A (AT-rich interaction domain 1A)
    |
    ARID1A mutation