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ETV1 (ETS translocation variant 1) is a protein that switches other genes on and off. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor, a biomarker and a fusion partner, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Lung cancer, Pancreatic ductal adenocarcinoma, Breast cancer and 4 more.
Transcriptional activator that binds to DNA sequences containing the consensus pentanucleotide 5'-CGGA[AT]-3'. Required for olfactory dopaminergic neuron differentiation; may directly activate expression of tyrosine hydroxylase (TH).
CIViC holds 2 clinical evidence items and 0 assertions across 1 variant, naming Trametinib. Open Targets scores its association with cancer at 0.74 (direct and indirect evidence; datatypes genetic literature 0.61, literature 0.97, genetic association 0.42, somatic mutation 0.83, animal model 0.39). IntOGen calls it a driver in 2 cohorts (1 activating, 1 loss-of-function), covering Invasive Breast Carcinoma, Colon Adenocarcinoma.
In plain words · ETV1 (ETS translocation variant 1) is a protein that switches other genes on and off. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor, a biomarker and a fusion partner, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Lung cancer, Pancreatic ductal adenocarcinoma, Breast cancer and 4 more.
ETV1 (ETS translocation variant 1) is a protein that switches other genes on and off. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor, a biomarker and a fusion partner, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Lung cancer, Pancreatic ductal adenocarcinoma, Breast cancer and 4 more.
Transcriptional activator that binds to DNA sequences containing the consensus pentanucleotide 5'-CGGA[AT]-3'. Required for olfactory dopaminergic neuron differentiation; may directly activate expression of tyrosine hydroxylase (TH).
No product in this corpus aims at ETV1 yet. Transcription factors have no pocket to plug, so drugs either degrade them or block the partner protein they need to dock on DNA.
Tumour-specific alteration: the catalogues call it an oncogene driver (IntOGen cohort analysis finds it activated more often than chance) and a tumour suppressor (IntOGen finds it knocked out more often than chance) and a fusion partner (UniProt records a translocation), so the direction differs between cohorts but the alteration is somatic either way; what a medicine would aim at or exploit is the altered form or its loss, absent from normal cells; no corpus medicine is aimed at it yet. HPA ETV1: RNA tissue enhanced (brain 124 nTPM, salivary gland 85 nTPM); no normal tissue stained high. Distribution: 7 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Lung cancer (all types), Pancreatic ductal adenocarcinoma, Breast cancer (all types), Colorectal cancer, Prostate cancer, Gastric & gastro-oesophageal junction cancer, Sarcomas (soft tissue, bone, GIST)); Open Targets associates it with 0 specific cancer types at or above 0.5. (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt P50549; CIViC gene ETV1; IntOGen ETV1; Human Protein Atlas ETV1 tissue; Open Targets ENSG00000006468 associations
First described 1995. Earliest sequence paper UniProt cites for the protein: Jeon I.-S. et al, Oncogene, 1995, "A variant Ewing's sarcoma translocation (7;22) fuses the EWS gene to the ETS gene ETV1". Source.
Sources: HGNC HGNC:3490 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P50549 (protein name, function text, keywords and locations (REST API)); CIViC gene ETV1 (2 evidence items, 0 assertions, 1 variants; diseases: Lung Cancer, Pancreatic Cancer (GraphQL API, CC0)); Open Targets ENSG00000006468 (association with cancer (MONDO_0004992) 0.74; per-cancer scores at or above 0.5: gastric cancer 0.52, prostate cancer 0.57, sarcoma 0.50, lung cancer 0.53 (GraphQL API, CC0)); IntOGen ETV1 (driver in 2 cohorts (Act 1, LoF 1); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Transcriptional activator that binds to DNA sequences containing the consensus pentanucleotide 5'-CGGA[AT]-3'. Required for olfactory dopaminergic neuron differentiation; may directly activate expression of tyrosine hydroxylase (TH). Location: Nucleus (UniProt). Locus 7p21.2 (HGNC).
RNA: tissue enhanced (brain 124 nTPM, salivary gland 85 nTPM), detected in many normal tissues.
No normal tissue stained high.
RNA cancer enhanced: Glioblastoma Multiforme 86 pTPM.
No cancer sample stained medium or high.
Human Protein Atlas version 25.1, antibody staining at reliability approved, enhanced or supported; used under CC BY-SA 3.0. Staining counts are patients per level in the atlas cohort, not population prevalence.
| Cancer | Prevalence | Measure | Note | Source |
|---|---|---|---|---|
| Prostate cancer | 1-14% | Fusion of a non-ERG ETS transcription factor, usually to TMPRSS2 or SLC45A3 | cBioPortal, samples: in prad_tcga_pub, ETV1 29 of 333 (8.7%), ETV4 16 (4.8%) and FLI1 4 (1.2%), matching the TCGA paper's 8%, 4% and 1%; in prad_tcga_pan_can_atlas_2018, ETV1 11, ETV4 12 and ETV5 2 of 494; in prad_p1000, ETV1 45, ETV4 23 and FLI1 5 of 1,013; in prad_su2c_2019, ETV1 22, ETV4 12, ETV5 3 and FLI1 1 of 444. Counting any ETS fusion together: 224 of 494, 45.3%, in prad_tcga_pan_can_atlas_2018; 378 of 1,013, 37.3%, in prad_p1000; 172 of 444, 38.7%, in prad_su2c_2019; 564 of 2,260, 25.0%, in prostate_msk_2024. | cBioPortal (TCGA) |
Approximate, population-level figures; the measure column says what was counted. Ranges show the midpoint as a bar.
The reference classification of prostate cancer as it presents, and the source of the two numbers that drive most molecular treatment decisions in the disease: a quarter with a PI3K or MAPK lesion, which is the rationale for capivasertib in PTEN-deficient disease, and a fifth with DNA repair inactivation, which is the rationale for PARP inhibitors.
The most common single molecular event in prostate cancer, present in roughly half of tumours in most series, and the reason prostate cancer is classified by fusion status. It is also a standing reminder that finding the driver and drugging it are different problems: no ETS-directed therapy has reached the clinic.
Query for this target: (TITLE:"ETV1" OR ABSTRACT:"ETV1" OR TITLE:"ETS variant transcription factor 1" OR ABSTRACT:"ETS variant transcription factor 1" OR TITLE:"ETS translocation variant 1" OR ABSTRACT:"ETS translocation variant 1" OR TITLE:"ER81" OR ABSTRACT:"ER81") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about ETV1, not a curated reading list.
Shares TMPRSS2-ERG fusion (and the other ETS rearrangements), Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer, TCGA: the molecular taxonomy of primary prostate cancer, IntOGen.
Shares TMPRSS2-ERG fusion (and the other ETS rearrangements), Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer, TCGA: the molecular taxonomy of primary prostate cancer, Sarcomas (soft tissue, bone, GIST).
Shares TCGA: the molecular taxonomy of primary prostate cancer, CIViC, IntOGen, Breast cancer (all types).
Shares TCGA: the molecular taxonomy of primary prostate cancer, CIViC, IntOGen, Open Targets Platform.
Shares TMPRSS2-ERG fusion (and the other ETS rearrangements), TCGA: the molecular taxonomy of primary prostate cancer, Prostate cancer.
Shares Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer, Prostate cancer.
Shares TCGA: the molecular taxonomy of primary prostate cancer, Pancreatic ductal adenocarcinoma, Prostate cancer, Colorectal cancer.
Shares TMPRSS2-ERG fusion (and the other ETS rearrangements), Prostate cancer.