RRAS2
RRAS2 (Ras-related protein R-Ras2) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Endometrial cancer, Ovarian cancer and Breast cancer.
Overview
GTP-binding protein with GTPase activity, involved in the regulation of MAPK signalling pathway and thereby controlling multiple cellular processes. Regulates craniofacial development.
CIViC holds 1 clinical evidence item and 0 assertions across 1 variant. Open Targets scores its association with cancer at 0.76 (direct and indirect evidence; datatypes genetic literature 0.61, literature 0.93, genetic association 0.00, somatic mutation 0.88, animal model 0.30). IntOGen calls it a driver in 2 cohorts (2 activating, 0 loss-of-function), covering Endometrial Carcinoma.
- Target · the protein and the cell it sits on
- Drug · antibody, small molecule, cell or radioligand
- Effect · signal, damage or kill
In plain words · RRAS2 (Ras-related protein R-Ras2) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Endometrial cancer, Ovarian cancer and Breast cancer.
- 1 · What it is
RRAS2 (Ras-related protein R-Ras2) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Endometrial cancer, Ovarian cancer and Breast cancer.
- 2 · What goes wrong in cancer
GTP-binding protein with GTPase activity, involved in the regulation of MAPK signalling pathway and thereby controlling multiple cellular processes. Regulates craniofacial development.
- 3 · How drugs use it
No product in this corpus aims at RRAS2 yet. Drugs fit a pocket that exists only in one shape of the mutant protein and hold it there, off.
External identifiers
Sources: HGNC HGNC:17271 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P62070 (protein name, function text, keywords and locations (REST API)); CIViC gene RRAS2 (1 evidence items, 0 assertions, 1 variants; diseases: (GraphQL API, CC0)); Open Targets ENSG00000133818 (association with cancer (MONDO_0004992) 0.76; per-cancer scores at or above 0.5: ovarian cancer 0.58, endometrial cancer 0.51, breast cancer 0.52 (GraphQL API, CC0)); IntOGen RRAS2 (driver in 2 cohorts (Act 2, LoF 0); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Biology
GTP-binding protein with GTPase activity, involved in the regulation of MAPK signalling pathway and thereby controlling multiple cellular processes. Regulates craniofacial development. Location: Cell membrane; Golgi apparatus membrane (UniProt). Locus 11p15.2 (HGNC).
- Endometrial cancer: Open Targets association 0.51 with endometrial cancer (MONDO_0011962); IntOGen driver in 2 cohorts (UCEC)
- Ovarian cancer: Open Targets association 0.58 with ovarian cancer (MONDO_0008170)
- Breast cancer: Open Targets association 0.52 with breast cancer (MONDO_0007254)
Notes
top- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: IntOGen calls it an activating (Act) driver in 2 cohorts; CIViC holds 1 clinical evidence items on its variants. Evidence tier "clinical-evidence" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.
Latest papers
topQuery for this target: (TITLE:"RRAS2" OR ABSTRACT:"RRAS2" OR TITLE:"RAS related 2" OR ABSTRACT:"RAS related 2" OR TITLE:"Ras-related protein R-Ras2" OR ABSTRACT:"Ras-related protein R-Ras2" OR TITLE:"TC21" OR ABSTRACT:"TC21") 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 RRAS2, not a curated reading list.