# ELL

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

## TL;DR

ELL (RNA polymerase II elongation factor ELL) is a protein that switches other genes on and off. The public catalogues list it as an oncogene driver, a tumour suppressor and a fusion partner, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Ovarian cancer, Breast cancer, Skin cancer and 1 more.

## Summary

Elongation factor component of the super elongation complex (SEC), a complex required to increase the catalytic rate of RNA polymerase II transcription by suppressing transient pausing by the polymerase at multiple sites along the DNA. Elongation factor component of the little elongation complex (LEC), a complex required to regulate small nuclear RNA (snRNA) gene transcription by RNA polymerase II and III. Specifically required for stimulating the elongation step of RNA polymerase II- and III-dependent snRNA gene transcription.

Open Targets scores its association with cancer at 0.65 (direct and indirect evidence; datatypes literature 0.53, genetic association 0.27, somatic mutation 0.98). IntOGen calls it a driver in 2 cohorts (1 activating, 1 loss-of-function), covering Melanoma, Ovarian Epithelial Tumour.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: elongation factor for RNA polymerase II; RNA polymerase II elongation factor ELL; Men; ELL1; PPP1R68; C19orf17
- Tags: cancer-genes-wave
- Symbol: ELL
- Class: transcription
- Biology: Elongation factor component of the super elongation complex (SEC), a complex required to increase the catalytic rate of RNA polymerase II transcription by suppressing transient pausing by the polymerase at multiple sites along the DNA. Elongation factor component of the little elongation complex (LEC), a complex required to regulate small nuclear RNA (snRNA) gene transcription by RNA polymerase II and III. Specifically required for stimulating the elongation step of RNA polymerase II- and III-dependent snRNA gene transcription. ELL also plays an early role before its assembly into in the SEC complex by stabilising RNA polymerase II recruitment/initiation and entry into the pause site. Required to stabilise the pre-initiation complex and early elongation. Location: Nucleus; Nucleus speckle; Nucleus, Cajal body (UniProt). Locus 19p13.11 (HGNC).
- Where found: Ovarian cancer: IntOGen driver in 1 cohort (OVT); Breast cancer: Open Targets association 0.55 with breast cancer (MONDO_0007254); Skin cancer: Open Targets association 0.51 with skin cancer (MONDO_0002898); Melanoma: IntOGen driver in 1 cohort (MEL)

## 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; IntOGen calls it a loss-of-function (LoF) driver in 1 cohort; UniProt disease notes describe a translocation or gene fusion involving the gene. Evidence tier "cohort-driver" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.

## Sources

- HGNC HGNC:23114: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:23114
- UniProt P55199: https://www.uniprot.org/uniprotkb/P55199/entry
- NCBI Gene 8178: https://www.ncbi.nlm.nih.gov/gene/8178
- Ensembl ENSG00000105656: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000105656

## Connected records

- collections: [IntOGen](https://onco.cc/collections/intogen/), [Open Targets Platform](https://onco.cc/collections/open-targets/)
- cancers: [Breast cancer (all types)](https://onco.cc/cancers/breast-cancer/), [Melanoma](https://onco.cc/cancers/melanoma/), [Ovarian cancer](https://onco.cc/cancers/ovarian/), [Skin cancer (all types)](https://onco.cc/cancers/skin-cancer/)

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