ARID1B

Overview

ARID1B encodes a subunit of the SWI/SNF chromatin-remodeling complex, serving as a paralog of ARID1A. Like ARID1A, ARID1B regulates chromatin accessibility and transcription. In cancer genomics, ARID1B has been characterized alongside ARID1A in small cell lung cancer (SCLC), where both genes show low somatic mutation rates compared to contexts such as ovarian clear cell carcinoma and gastric cancer.

Alterations observed in the corpus

  • ARID1B exhibits a low somatic mutation rate (3.0%) in SCLC, characterized alongside ARID1A as a SWI/SNF complex member in a study of chromatin remodeling and BET inhibitor sensitivity PMID:22037554
  • ARID1B mutations identified in breast cancer WES of 100 tumors, implicating SWI/SNF chromatin remodeling complex in breast cancer PMID:22722201
  • ARID1B is identified as a significantly mutated gene in melanoma WES of 121 tumors (Broad cohort), highlighting SWI/SNF complex subunit alterations in cutaneous melanoma PMID:22817889
  • Mutated in neuroblastoma (Broad WES/WGS, 240 tumors); ARID1B identified among recurrently mutated chromatin-remodeling genes PMID:23334666
  • Somatic mutation in chromatin-remodeling gene cluster; collectively mutated in 12/24 ACC cases in exome-sequencing discovery cohort PMID:23778141
  • Flagged as SWI/SNF chromatin-remodeling complex partner of ARID1A in sinonasal AdCC literature context; no coding mutations reported in the sequenced cohort PMID:24418857
  • Non-catalytic BAF subunit (BAF250B) invoked in the context of SWI/SNF biology in SCCOHT; not mutated in this cohort but discussed as relevant to ovarian tumorigenesis PMID:24658004
  • Loss-of-function mutation in 1% (range 1–3%) of HCCs (WES, n=1,289); chromatin-modifier trunk driver classified as non-actionable PMID:24798001
  • Frameshift/nonsense mutations in 3/22 (14%) carcinosarcoma cases; co-occurs with ARID1A mutations in 3 cases, suggesting combined SWI/SNF complex disruption PMID:25233892
  • Candidate dark-matter driver and chromatin-remodeling gene; among 93 mutations across 57 epigenetic regulator genes in 80/402 (20.0%) papillary thyroid carcinomas in the TCGA PTC cohort PMID:25417114
  • Synthetic lethal partner with ARID1A in PDA; ARID1A-deficient PDA cell lines are vulnerable to ARID1B depletion; also part of SWI/SNF chromatin-remodeling lesions in >42% of PDA cases PMID:25855536
  • Mouse-model gCIS shared between local and metastatic medulloblastoma recurrences but absent from diagnostic samples; identified as a recurrence-specific driver in the Shh subgroup PMID:26760213
  • ARID1B, as part of the SWI/SNF complex, mutated in 36% ATC vs 6% PDTC (P = 1×10⁻⁴) in a 341-gene targeted sequencing cohort (n=117 advanced thyroid tumors); SWI/SNF disruption was the first such report in advanced thyroid cancer PMID:26878173

Cancer types (linked)

  • SCLC: Low mutation rate (3.0%) reported in SCLC cohort; characterized alongside ARID1A as part of the BAF/SWI/SNF complex PMID:22037554

Co-occurrence and mutual exclusivity

  • ARID1B co-characterized with ARID1A as SWI/SNF paralog in SCLC; ARID1A loss is the functionally dominant alteration driving BET inhibitor sensitivity PMID:22037554

Therapeutic relevance

  • BET bromodomain inhibitors (e.g., JQ1) show enhanced activity in ARID1A-deficient SCLC; whether ARID1B loss confers a similar dependency is not yet established PMID:22037554

Open questions

  • Functional consequences of ARID1B mutation in SCLC are not explicitly characterized; only mutation frequency reported alongside ARID1A.
  • Whether ARID1B loss recapitulates the synthetic lethal relationship with BET inhibitors seen for ARID1A loss remains to be determined.

Sources

  • PMID:22037554 — ARID1A Governs Genomic Stability and Proliferation in SCLC via c-MYC/PARP1 Suppression Driving Vulnerability to BET Inhibitors

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