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ERG (Transcriptional regulator ERG) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, a biomarker and a fusion partner, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Sarcomas, Prostate cancer, Non-Hodgkin lymphoma and 4 more.
Transcriptional regulator. May participate in transcriptional regulation through the recruitment of SETDB1 histone methyltransferase and subsequent modification of local chromatin structure.
CIViC holds 1 clinical evidence item and 0 assertions across 1 variant. Open Targets scores its association with cancer at 0.72 (direct and indirect evidence; datatypes genetic literature 0.61, literature 1.00, genetic association 0.03, somatic mutation 0.83, animal model 0.57). IntOGen calls it a driver in 1 cohort (1 activating, 0 loss-of-function), covering Angiosarcoma.
In plain words · ERG (Transcriptional regulator ERG) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, a biomarker and a fusion partner, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Sarcomas, Prostate cancer, Non-Hodgkin lymphoma and 4 more.
ERG (Transcriptional regulator ERG) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, a biomarker and a fusion partner, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Sarcomas, Prostate cancer, Non-Hodgkin lymphoma and 4 more.
Transcriptional regulator. May participate in transcriptional regulation through the recruitment of SETDB1 histone methyltransferase and subsequent modification of local chromatin structure.
No product in this corpus aims at ERG yet. Drugs fit a pocket that exists only in one shape of the mutant protein and hold it there, off.
Tumour-specific alteration: the catalogues call it an oncogene driver (IntOGen cohort analysis finds it activated more often than chance) and a fusion partner (UniProt records a translocation); 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 ERG: RNA tissue enhanced (blood vessel 38 nTPM); high antibody staining in 2 normal tissues. Distribution: 5 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Sarcomas (soft tissue, bone, GIST), Prostate cancer, Lymphoma, Leukaemia, Neuroendocrine tumours); Open Targets associates it with 0 specific cancer types at or above 0.5. (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt P11308; CIViC gene ERG; IntOGen ERG; Human Protein Atlas ERG tissue; Open Targets ENSG00000157554 associations
First described 1987. Earliest sequence paper UniProt cites for the protein: Rao V.N. et al, Science, 1987, "erg, a human ets-related gene on chromosome 21: alternative splicing, polyadenylation, and translation". Source.
Sources: HGNC HGNC:3446 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P11308 (protein name, function text, keywords and locations (REST API)); CIViC gene ERG (1 evidence items, 0 assertions, 1 variants; diseases: B-lymphoblastic Leukaemia/lymphoma (GraphQL API, CC0)); Open Targets ENSG00000157554 (association with cancer (MONDO_0004992) 0.72; per-cancer scores at or above 0.5: prostate cancer 0.58, sarcoma 0.67, neuroendocrine neoplasm 0.52, acute lymphoblastic leukaemia 0.54, non-Hodgkin lymphoma 0.56, leukaemia 0.56 (GraphQL API, CC0)); IntOGen ERG (driver in 1 cohort (Act 1, LoF 0); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
What a pathology or genomic report can say about this target, each with the thresholds approvals use.
Transcriptional regulator. May participate in transcriptional regulation through the recruitment of SETDB1 histone methyltransferase and subsequent modification of local chromatin structure. Location: Nucleus; Cytoplasm (UniProt). Locus 21q22.2 (HGNC).
RNA: tissue enhanced (blood vessel 38 nTPM), detected in many normal tissues.
Medium: Adrenal gland, Appendix, Bone marrow, Breast, Bronchus, Kidney, Liver, Lymph node.
RNA group enriched: Kidney Renal Clear Cell Carcinoma 17 pTPM, Prostate Adenocarcinoma 41 pTPM.
No cancer stained high; medium in liver cancer, pancreatic cancer, stomach cancer.
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 | 25-46% | Gene fusion putting ERG under an androgen-responsive promoter | cBioPortal structural variants, samples with an ERG rearrangement: 152 of 333, 45.6%, in prad_tcga_pub, which reproduces the 46% the TCGA paper reports; 203 of 494, 41.1%, in prad_tcga_pan_can_atlas_2018; 305 of 1,013, 30.1%, in prad_p1000; 104 of 424, 24.5%, in prad_mcspc_mskcc_2020; 127 of 504, 25.2%, in prad_mskcc_2017; 544 of 2,260, 24.1%, in prostate_msk_2024; 528 of 2,069, 25.5%, in prad_msk_stopsack_2021; 134 of 444, 30.2%, in prad_su2c_2019; 62 of 150, 41.3%, in prad_su2c_2015. TMPRSS2 is the partner in almost all of them: 194 of the 203 TCGA PanCancer events, 305 of 305 in prad_p1000 and 128 of 134 in prad_su2c_2019, with SLC45A3 and NDRG1 supplying the rest. | cBioPortal (TCGA) |
Approximate, population-level figures; the measure column says what was counted. Ranges show the midpoint as a bar.
What a prostate cancer sequencing report looks like in practice, and the numerical basis for two clinical rules: do not expect checkpoint immunotherapy to work unless the tumour is mismatch repair deficient, and do not treat a CDK12 alteration as if it were a BRCA alteration.
It is the quantitative answer to why prostate cancer has so few targeted therapies. The common events are not druggable, the druggable ones are individually rare, and no trial can be powered on a driver present in 2% of men without an international basket.
It is the reason a prostate cancer fusion frequency quoted without an ancestry is unsafe. In this cohort the founder event that defines almost half of Western tumours is uncommon, and the fusion-negative, CHD1-deleted route dominates instead.
The genomic definition of advanced prostate cancer, and the evidence that made molecular testing standard in it. The 19.3 percent DNA repair figure is the direct ancestor of PROfound, TRITON3, PROpel and TALAPRO-2, and the 8 percent germline figure is why a tumour result in this disease has implications for a man's relatives.
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.
A different picture of how a cancer genome is built, and one that explains why prostate cancer has few point mutations and a great deal of structural damage. It is also why whole-genome rather than exome sequencing is the right assay for this disease.
It established the fusion-negative side of the prostate cancer taxonomy and made SPOP the disease's signature point mutation, in a ubiquitin ligase adaptor rather than in a kinase, which is part of why prostate cancer has so few druggable drivers.
The explanation for why prostate cancer has so few targeted drugs outside the hormone axis and the DNA-repair genes: it is a quiet genome with structural rather than point-mutational damage, and the recurrent changes sit in the machinery that reads DNA rather than in kinases.
Query for this target: (TITLE:"ERG" OR ABSTRACT:"ERG" OR TITLE:"ETS transcription factor ERG" OR ABSTRACT:"ETS transcription factor ERG" OR TITLE:"Transcriptional regulator ERG" OR ABSTRACT:"Transcriptional regulator ERG" OR TITLE:"erg-3" OR ABSTRACT:"erg-3" OR TITLE:"p55" OR ABSTRACT:"p55") 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 ERG, not a curated reading list.
Shares The TMPRSS2-ERG rearrangement, ERG expression and prostate cancer outcomes: a cohort study and meta-analysis, Punctuated evolution of prostate cancer genomes, Whole-genome and transcriptome sequencing of prostate cancer identifies new genetic alterations driving disease progression, Chromoplexy.
Shares Exome sequencing identifies recurrent SPOP, FOXA1 and MED12 mutations in prostate cancer, The long tail of oncogenic drivers in prostate cancer, The mutational landscape of lethal castration-resistant prostate cancer, TCGA: the molecular taxonomy of primary prostate cancer.
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 The TMPRSS2-ERG rearrangement, ERG expression and prostate cancer outcomes: a cohort study and meta-analysis, Exome sequencing identifies recurrent SPOP, FOXA1 and MED12 mutations in prostate cancer, Whole-genome and transcriptome sequencing of prostate cancer identifies new genetic alterations driving disease progression, The long tail of oncogenic drivers in prostate cancer.
Shares Exome sequencing identifies recurrent SPOP, FOXA1 and MED12 mutations in prostate cancer, The long tail of oncogenic drivers in prostate cancer, TCGA: the molecular taxonomy of primary prostate cancer, CIViC.
Shares The long tail of oncogenic drivers in prostate cancer, The mutational landscape of lethal castration-resistant prostate cancer, Leukaemia (all types), CIViC.
Shares The long tail of oncogenic drivers in prostate cancer, The mutational landscape of lethal castration-resistant prostate cancer, Neuroendocrine tumours, CIViC.
Shares Leukaemia (all types), Sarcomas (soft tissue, bone, GIST), Acute lymphoblastic leukaemia, CIViC.