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APC (Adenomatous polyposis coli protein) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and an approved or late-stage drug is recorded against it. Tied to Colorectal cancer, Gastric & gastro-oesophageal junction cancer, Hepatocellular carcinoma and 5 more.
Tumour suppressor. Promotes rapid degradation of CTNNB1 and participates in Wnt signalling as a negative regulator. APC activity is correlated with its phosphorylation state.
CIViC holds 5 clinical evidence items and 0 assertions across 2 variants, naming JW55, G007-LK, Nirogacestat and Regorafenib. Open Targets scores its association with cancer at 0.91 (direct and indirect evidence; datatypes genetic literature 0.79, affected pathway 0.86, literature 1.00, genetic association 0.90, somatic mutation 0.97, animal model 0.88). IntOGen calls it a driver in 43 cohorts (2 activating, 41 loss-of-function), covering Acute Myeloid Leukaemia, Anal Squamous Cell Carcinoma, Cholangiocarcinoma, Colon Adenocarcinoma, Colorectal Adenocarcinoma, Cutaneous Squamous Cell Carcinoma and others. In OnCo, 1 product record names it (Nirogacestat).
In plain words · APC (Adenomatous polyposis coli protein) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and an approved or late-stage drug is recorded against it. Tied to Colorectal cancer, Gastric & gastro-oesophageal junction cancer, Hepatocellular carcinoma and 5 more.
APC (Adenomatous polyposis coli protein) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and an approved or late-stage drug is recorded against it. Tied to Colorectal cancer, Gastric & gastro-oesophageal junction cancer, Hepatocellular carcinoma and 5 more.
Tumour suppressor. Promotes rapid degradation of CTNNB1 and participates in Wnt signalling as a negative regulator.
No product in this corpus aims at APC yet. Because the protein is lost rather than overactive, drugs either restore its function or exploit the weakness its loss leaves (synthetic lethality).
Tumour-specific alteration: 1 of 1 medicines aimed at it name a mutant, fusion, exon or hotspot in their mechanism (Nirogacestat), an alteration absent from normal cells. HPA APC: RNA tissue enhanced (brain 39 nTPM); high antibody staining in 14 normal tissues; highest cancer staining prostate cancer (6 of 11 high). Distribution: 8 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Colorectal cancer, Gastric & gastro-oesophageal junction cancer, Hepatocellular carcinoma, Prostate cancer, Oesophageal cancer, Biliary tract cancer (all types), Anal cancer (squamous cell carcinoma) and more); Open Targets associates it with 22 specific cancer types at or above 0.5 (familial adenomatous polyposis 1, classic familial adenomatous polyposis, colorectal cancer, gastric adenocarcinoma and proximal polyposis of the stomach, colon carcinoma, colorectal adenocarcinoma and more). (Rule 4 of scripts/fetch-target-specificity.ts.)
Sources: FDA label (DailyMed); Human Protein Atlas APC tissue; Open Targets ENSG00000134982 associations
First described 1991. Earliest sequence paper UniProt cites for the protein: Joslyn et al, Cell, 1991, "Identification of deletion mutations and three new genes at the familial polyposis locus". Source.
Sources: HGNC HGNC:583 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P25054 (protein name, function text, keywords and locations (REST API)); CIViC gene APC (5 evidence items, 0 assertions, 2 variants; diseases: Colorectal Cancer, Colon Carcinoma, Desmoid Tumour (GraphQL API, CC0)); Open Targets ENSG00000134982 (association with cancer (MONDO_0004992) 0.91; per-cancer scores at or above 0.5: non-small cell lung carcinoma 0.56, colorectal cancer 0.86, gastric cancer 0.81, oesophageal cancer 0.55, hepatocellular carcinoma 0.74, prostate cancer 0.65 (GraphQL API, CC0)); IntOGen APC (driver in 43 cohorts (Act 2, LoF 41); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Tumour suppressor. Promotes rapid degradation of CTNNB1 and participates in Wnt signalling as a negative regulator. APC activity is correlated with its phosphorylation state. Activates the GEF activity of SPATA13 and ARHGEF4. Plays a role in hepatocyte growth factor (HGF)-induced cell migration. Required for MMP9 up-regulation via the JNK signalling pathway in colorectal tumour cells. Location: Cell junction, adherens junction; Cytoplasm, cytoskeleton; Cell projection, lamellipodium; Cell projection, ruffle membrane (UniProt). Locus 5q22.2 (HGNC).
RNA: tissue enhanced (brain 39 nTPM), detected in all normal tissues.
Medium: Adrenal gland, Bone marrow, Cervix, Colon, Endometrium, Epididymis, Esophagus, Fallopian tube.
Medium only: carcinoid, endometrial cancer, head and neck cancer, lung 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 |
|---|---|---|---|---|
| Colorectal cancer | 58-77% | Inactivating mutation (WNT pathway gatekeeper) | cBioPortal: 5,400 of 7,237, 74.6%, in crc_msk_2026; 867 of 1,134, 76.5%, in crc_msk_2017; 1,145 of 1,516, 75.5%, in crc_eo_2020; 387 of 534, 72.5%, in coadread_tcga_pan_can_atlas_2018; 168 of 224, 75.0%, in coadread_tcga_pub; 361 of 619, 58.3%, in coadread_dfci_2016; 451 of 1,015, 44.4%, in crc_sysucc_2022. Deep deletion adds 40 of 7,237 (crc_msk_2026) and 18 of 592 (TCGA), and structural variants disrupt APC in a further 54 of 7,237 samples. The TCGA analysis found WNT signalling altered in 93% of tumours (Cancer Genome Atlas Network 2012); adding intronic APC splice alterations and large in-frame CTNNB1 deletions took oncogenic WNT alterations to 96% of 1,134 prospectively sequenced cancers (Yaeger 2018). | cBioPortal (TCGA) |
| Prostate cancer | 2-10% | Activating CTNNB1 exon 3 mutation, or APC inactivation | cBioPortal mutation: CTNNB1 89 of 2,260, 3.9%, in prostate_msk_2024; 23 of 424, 5.4%, in prad_mcspc_mskcc_2020; 19 of 444, 4.3%, in prad_su2c_2019; 11 of 494, 2.2%, in prad_tcga_pan_can_atlas_2018. APC mutation 176 of 2,260, 7.8%, in prostate_msk_2024; 36 of 424, 8.5%, in prad_mcspc_mskcc_2020; 31 of 444, 7.0%, in prad_su2c_2019, with deep deletion adding 1 to 10%. The CTNNB1 records cluster on the degron: in prostate_msk_2024, S37F 9, T41A 9, D32Y 7, T41I 7, S45P 6 of 94 records. | cBioPortal (TCGA) |
Approximate, population-level figures; the measure column says what was counted. Ranges show the midpoint as a bar.
If a childhood exposure to colibactin-producing Escherichia coli writes APC mutations into the colon decades before a tumour appears, then the rise in early-onset bowel cancer may be preventable by something done in childhood rather than by screening alone.
A three-continent cohort from high-incidence countries, and the origin of the idea that a shared frameshift (ELF3) could be a vaccine target in a cancer with few targets. CTNNB1 and STK11 from this list recur in the MSK data.
It fills the gap between the primary-tumour atlases and the castration-resistant series by describing the disease at the moment most treatment decisions are actually made, and it identifies SPOP as a favourable marker rather than a neutral one.
It sets the baseline the adenoma-carcinoma sequence starts from and warns against reading a driver mutation found in tissue, or in stool or blood, as evidence of cancer.
It turned sidedness from an epidemiological curiosity into a mechanistic statement, and it is the reason a wild-type mitogenic report on a left-sided tumour is read as ligand dependence rather than as an absence.
It gives a genetic account of both immunotherapy failures: why some mismatch repair deficient tumours resist, and why the microsatellite-stable majority has no T cells in it to begin with.
It is the clearest mechanistic answer to why microsatellite-stable colorectal cancer resists immunotherapy, and the rationale for every TGF-beta plus checkpoint combination now in trials in this disease.
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.
Query for this target: (TITLE:"APC" OR ABSTRACT:"APC" OR TITLE:"APC regulator of Wnt signaling pathway" OR ABSTRACT:"APC regulator of Wnt signaling pathway" OR TITLE:"Adenomatous polyposis coli protein" OR ABSTRACT:"Adenomatous polyposis coli protein" OR TITLE:"DP2" OR ABSTRACT:"DP2" OR TITLE:"DP3" OR ABSTRACT:"DP3" OR TITLE:"DP2.5" OR ABSTRACT:"DP2.5") 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 APC, not a curated reading list.
Shares Integrated genomic analysis reveals mutated ELF3 as a potential gallbladder cancer vaccine candidate, Genetic mechanisms of immune evasion in colorectal cancer, Nirogacestat, Clinical sequencing defines the genomic landscape of metastatic colorectal cancer.
Shares Recurrent R-spondin fusions in colon cancer, Comprehensive molecular characterization of human colon and rectal cancer, Wnt / β-catenin, Hepatocellular carcinoma.
Shares TGF-beta drives immune evasion in genetically reconstituted colon cancer metastasis, A genetic model for colorectal tumorigenesis, Clinical sequencing defines the genomic landscape of metastatic colorectal cancer, Genetic alterations during colorectal-tumor development.
Shares Biliary tract cancer (all types), Neuroendocrine tumours, Oesophageal cancer, CIViC.
Shares Biliary tract cancer (all types), Oesophageal cancer, Hepatocellular carcinoma, CIViC.
Shares Recurrent R-spondin fusions in colon cancer, Wnt / β-catenin, IntOGen, Open Targets Platform.
Shares Colorectal cancer (KEGG map), Oesophageal cancer, Hepatocellular carcinoma, CIViC.
Shares Biliary tract cancer (all types), Oesophageal cancer, Hepatocellular carcinoma, CIViC.