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MYC (Myc proto-oncogene protein) 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 Non-Hodgkin lymphoma, Skin cancer, Multiple myeloma and 5 more. This dossier gathers the 0 products (0 approved), 0 trials, 0 pathways and 0 resistance routes in the corpus that involve it, with external identifiers so it can be joined to UniProt, ChEMBL, Open Targets and the rest of biology.
Transcription factor that binds DNA in a non-specific manner, yet also specifically recognises the core sequence 5'-CAC[GA]TG-3'. Activates the transcription of growth-related genes. Binds to the VEGFA promoter, promoting VEGFA production and subsequent sprouting angiogenesis. Regulator of somatic reprogramming, controls self-renewal of embryonic stem cells. Functions with TAF6L to activate target gene expression through RNA polymerase II pause release. Positively regulates transcription of HNRNPA1, HNRNPA2 and PTBP1 which in turn regulate splicing of pyruvate kinase PKM by binding repressively to sequences flanking PKM exon 9, inhibiting exon 9 inclusion and resulting in exon 10 inclusion and production of the PKM M2 isoform. Location: Nucleus, nucleoplasm; Nucleus, nucleolus; Nucleus; Cytoplasm (UniProt). Locus 8q24.21 (HGNC).
| Cancer | Prevalence | Measure | Note | Source |
|---|---|---|---|---|
| Pancreatic ductal adenocarcinoma | 4-13% | Amplification | cBioPortal high-level amplification: 23 of 183, 12.6%, in paad_tcga_pan_can_atlas_2018; 13 of 109, 11.9%, in paad_utsw_2015; 98 of 2,336, 4.2%, in pdac_msk_2024; 11 of 395, 2.8%, in pancreas_msk_2024. MYC amplification was uniquely associated with poor outcome and the adenosquamous subtype among 109 microdissected cancers (Witkiewicz 2015); squamous-feature cancers showed intercellular heterogeneity for MYC amplification (Hayashi 2020); KDM6A loss activates a MYC super-enhancer (Andricovich 2018). | cBioPortal (TCGA) |
| Colorectal cancer | 4-5% | High-level amplification (8q24) | cBioPortal high-level amplification: 354 of 7,237, 4.9%, in crc_msk_2026; 46 of 1,134, 4.1%, in crc_msk_2017; 71 of 1,516, 4.7%, in crc_eo_2020; 30 of 592, 5.1%, in coadread_tcga_pan_can_atlas_2018; 11 of 257 in coadread_tcga_pub. The TCGA integrative analysis concluded that MYC-directed transcriptional activation and repression is central to the disease even where the gene is not amplified, because APC loss switches it on (Cancer Genome Atlas Network 2012). | cBioPortal (TCGA) |
Approximate, population-level figures; the measure column says what was counted. Ranges show the midpoint as a bar.
No product in the corpus is aimed at this target yet.
No trial in the corpus names this target or one of its products.
No recorded escape route names this target.
No pathway diagram carries this target as a node.
No companion diagnostic in the registry measures this target.
No model entry for this target yet; check the cancer entries on the models page.
No open questions recorded for this target yet. Suggest one.
Query for this target: (TITLE:"MYC" OR ABSTRACT:"MYC" OR TITLE:"MYC proto-oncogene, bHLH transcription factor" OR ABSTRACT:"MYC proto-oncogene, bHLH transcription factor" OR TITLE:"Myc proto-oncogene protein" OR ABSTRACT:"Myc proto-oncogene protein" OR TITLE:"c-Myc" OR ABSTRACT:"c-Myc" OR TITLE:"bHLHe39" OR ABSTRACT:"bHLHe39") 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 MYC, not a curated reading list.
The dossier as machine-readable JSON, at /api/v1/dossiers/myc-gene.json: identifiers from HGNC, Ensembl, UniProt and ChEMBL, products with status, trials, pathways, hotspots, open questions and assays. The full entity record is in the open API at /api/v1/entities/myc-gene.json. Licence CC BY-NC 4.0.