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GNAS (Neuroendocrine secretory protein 55) is a gene that drives cell growth when it is altered. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Colorectal cancer, Pancreatic ductal adenocarcinoma, Breast cancer and 5 more.
UniProt has no function text for O95467; HGNC names it "GNAS complex locus".
CIViC holds 17 clinical evidence items and 0 assertions across 5 variants, naming Trametinib, Palbociclib, Vemurafenib and Gefitinib and others. Open Targets scores its association with cancer at 0.77 (direct and indirect evidence; datatypes genetic literature 0.30, affected pathway 0.61, literature 0.98, genetic association 0.03, somatic mutation 0.97, animal model 0.25). IntOGen calls it a driver in 12 cohorts (11 activating, 1 loss-of-function), covering Invasive Breast Carcinoma, Colorectal Adenocarcinoma, Oesophageal Adenocarcinoma, Hepatocellular Carcinoma, Lung Adenocarcinoma, Medulloblastoma and others.
In plain words · GNAS (Neuroendocrine secretory protein 55) is a gene that drives cell growth when it is altered. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Colorectal cancer, Pancreatic ductal adenocarcinoma, Breast cancer and 5 more.
GNAS (Neuroendocrine secretory protein 55) is a gene that drives cell growth when it is altered. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Colorectal cancer, Pancreatic ductal adenocarcinoma, Breast cancer and 5 more.
UniProt has no function text for O95467; HGNC names it "GNAS complex locus". Location: Cytoplasmic vesicle, secretory vesicle; Secreted (UniProt).
No product in this corpus aims at GNAS 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 tumour suppressor (IntOGen finds it knocked out more often than chance), 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 GNAS: RNA low tissue specificity; no normal tissue stained high; highest cancer staining colorectal cancer (5 of 12 high). Distribution: 8 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Colorectal cancer, Pancreatic ductal adenocarcinoma, Breast cancer (all types), Bladder & urothelial cancer, Oesophageal cancer, Skin cancer (all types), Hepatocellular carcinoma and more); Open Targets associates it with 1 specific cancer type at or above 0.5 (pituitary adenoma 3, multiple types). (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt O95467; CIViC gene GNAS; IntOGen GNAS; Human Protein Atlas GNAS tissue; Open Targets ENSG00000087460 associations
First described 1998. Earliest sequence paper UniProt cites for the protein: Hayward B.E. et al, Proc. Natl. Acad. Sci. U.S.A, 1998, "Bidirectional imprinting of a single gene: human GNAS1 encodes distinct maternally, paternally and biallelically derived proteins". Source.
Sources: HGNC HGNC:4392 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt O95467 (protein name, function text, keywords and locations (REST API)); CIViC gene GNAS (17 evidence items, 0 assertions, 5 variants; diseases: Colorectal Cancer, Pseudomyxoma Peritonei, Appendix Cancer, Melanoma, Lung Non-small Cell Carcinoma and 9 more (GraphQL API, CC0)); Open Targets ENSG00000087460 (association with cancer (MONDO_0004992) 0.77; per-cancer scores at or above 0.5: colorectal cancer 0.67, gastric cancer 0.51, ovarian cancer 0.51, melanoma 0.57, skin cancer 0.57 (GraphQL API, CC0)); IntOGen GNAS (driver in 12 cohorts (Act 11, LoF 1); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
UniProt has no function text for O95467; HGNC names it "GNAS complex locus". Location: Cytoplasmic vesicle, secretory vesicle; Secreted (UniProt). Locus 20q13.32 (HGNC).
RNA: low tissue specificity, detected in all normal tissues.
No normal tissue stained high.
Medium only: breast cancer, carcinoid, cervical cancer, glioma.
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 |
|---|---|---|---|---|
| Pancreatic ductal adenocarcinoma | 2-4% | R201 hotspot mutation (IPMN-derived tumours) | cBioPortal: 76 of 2,336, 3.3% (R201H 39, R201C 21, R201S 3), in pdac_msk_2024; 7 of 179, 3.9% (R201C 4, R201H 2), in paad_tcga_pan_can_atlas_2018; 10 of 383, 2.6%, in paad_qcmg_uq_2016; 9 of 395, 2.3%, in pancreas_msk_2024; 5 of 109 in paad_utsw_2015; GNAS was a recurrent gene in the TCGA analysis and KRAS wild-type tumours carried GNAS among their drivers (Cancer Genome Atlas 2017). GNAS mutations in 66% of 132 IPMNs, KRAS or GNAS in 96%, carried into the invasive cancer in 7 of 8 IPMN-associated carcinomas and absent from other cysts and from non-IPMN cancers (Wu 2011); 27 of 456 QCMG tumours were IPMN with invasion (cBioPortal histology). | cBioPortal (TCGA) |
Approximate, population-level figures; the measure column says what was counted. Ranges show the midpoint as a bar.
A cancer next to a cyst is not necessarily from the cyst, so removing the cyst does not always remove the risk, and surveillance must cover the whole gland.
It is the caution attached to the sidedness rule: a tumour at the hepatic flexure and one at the caecum are both called right-sided and are not the same disease.
Risk stratification of a cyst cannot assume the nearby cancer came from it, and the whole gland stays at risk after cyst resection.
It is the reference multi-platform dataset and the reason a KRAS wild-type report is treated as a search for another driver rather than as an absence.
The evidence that molecular cyst-fluid testing can spare operations, now part of specialist practice although not a universal standard.
The reporting standard behind every modern precursor study and the reason a pathology report now says low or high grade rather than PanIN-2.
It fixes the order of events, with the initiating mutation present in the smallest visible lesion, and it warns that finding mutant KRAS in a duct does not mean cancer.
A GNAS mutation in cyst fluid says the cyst is an IPMN, and in a cancer it says the cancer came from one, which is the molecular basis of cyst triage.
Query for this target: (TITLE:"GNAS" OR ABSTRACT:"GNAS" OR TITLE:"GNAS complex locus" OR ABSTRACT:"GNAS complex locus" OR TITLE:"Neuroendocrine secretory protein 55" OR ABSTRACT:"Neuroendocrine secretory protein 55" OR TITLE:"NESP55" OR ABSTRACT:"NESP55" OR TITLE:"GNASXL" OR ABSTRACT:"GNASXL" OR TITLE:"SCG6" OR ABSTRACT:"SCG6") 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 GNAS, not a curated reading list.
Shares IPMNs with co-occurring invasive cancers: neighbours but not always relatives, A combination of molecular markers and clinical features improve the classification of pancreatic cysts, Integrated genomic characterization of pancreatic ductal adenocarcinoma, Oesophageal cancer.
Shares Pathways of progression from intraductal papillary mucinous neoplasm to pancreatic ductal adenocarcinoma based on molecular features, Presence of somatic mutations in most early-stage pancreatic intraepithelial neoplasia, A combination of molecular markers and clinical features improve the classification of pancreatic cysts, Hepatocellular carcinoma.
Shares Pathways of progression from intraductal papillary mucinous neoplasm to pancreatic ductal adenocarcinoma based on molecular features, IPMNs with co-occurring invasive cancers: neighbours but not always relatives, Classifying colorectal cancer by tumor location rather than sidedness highlights a continuum in mutation profiles and consensus molecular subtypes, A combination of molecular markers and clinical features improve the classification of pancreatic cysts.
Shares Integrated genomic characterization of pancreatic ductal adenocarcinoma, Bladder & urothelial cancer, Hepatocellular carcinoma, CIViC.
Shares Integrated genomic characterization of pancreatic ductal adenocarcinoma, Oesophageal cancer, IntOGen, Gastric & gastro-oesophageal junction cancer.
Shares Classifying colorectal cancer by tumor location rather than sidedness highlights a continuum in mutation profiles and consensus molecular subtypes, A combination of molecular markers and clinical features improve the classification of pancreatic cysts, Integrated genomic characterization of pancreatic ductal adenocarcinoma, Hepatocellular carcinoma.
Shares Presence of somatic mutations in most early-stage pancreatic intraepithelial neoplasia, Recurrent GNAS mutations define an unexpected pathway for pancreatic cyst development, Pancreatic ductal adenocarcinoma.
Shares Presence of somatic mutations in most early-stage pancreatic intraepithelial neoplasia, A combination of molecular markers and clinical features improve the classification of pancreatic cysts, Integrated genomic characterization of pancreatic ductal adenocarcinoma, Oesophageal cancer.