# SMARCA2

Source: https://onco.cc/targets/smarca2/  
OnCo record `smarca2` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

SMARCA2 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Salivary gland cancers.

## Summary

ATPase involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Component of SWI/SNF chromatin remodeling complexes that carry out key enzymatic activities, changing chromatin structure by altering DNA-histone contacts within a nucleosome in an ATP-dependent manner. Binds DNA non-specifically.

CIViC holds 2 clinical evidence items and 0 assertions across 2 variants. IntOGen calls it a driver in 1 cohort (1 activating, 0 loss-of-function), covering Salivary Carcinoma.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: SWI/SNF related BAF chromatin remodeling complex subunit ATPase 2; SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2; BAF190; hSNF2a; hBRM; Sth1p; SNF2LA; SNF2; SWI2; SNF2L2
- Tags: cancer-genes-wave
- Symbol: SMARCA2
- Class: oncogene
- Biology: ATPase involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Component of SWI/SNF chromatin remodeling complexes that carry out key enzymatic activities, changing chromatin structure by altering DNA-histone contacts within a nucleosome in an ATP-dependent manner. Binds DNA non-specifically. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a postmitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to postmitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. Location: Nucleus (UniProt). Locus 9p24.3 (HGNC).
- Where found: Salivary gland cancers: IntOGen driver in 1 cohort (SACA)

## Notes

- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: IntOGen calls it an activating (Act) driver in 1 cohort; CIViC holds 2 clinical evidence items on its variants. Evidence tier "clinical-evidence" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.

## Sources

- HGNC HGNC:11098: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:11098
- UniProt P51531: https://www.uniprot.org/uniprotkb/P51531/entry
- NCBI Gene 6595: https://www.ncbi.nlm.nih.gov/gene/6595
- Ensembl ENSG00000080503: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000080503

## Connected records

- collections: [CIViC](https://onco.cc/collections/civic/), [IntOGen](https://onco.cc/collections/intogen/)
- cancers: [Salivary gland cancers](https://onco.cc/cancers/salivary-gland/)
- pathways: [SWI/SNF chromatin remodelling](https://onco.cc/pathways/swi-snf-chromatin/)

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JSON: https://onco.cc/api/v1/entities/smarca2.json