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CNTRL (Centriolin) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as an oncogene driver, a tumour suppressor and a fusion partner, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Leukaemia, Nasopharyngeal carcinoma, Cutaneous squamous cell carcinoma and 1 more.
Involved in cell cycle progression and cytokinesis. During the late steps of cytokinesis, anchors exocyst and SNARE complexes at the midbody, thereby allowing secretory vesicle-mediated abscission.
Open Targets scores its association with cancer at 0.67 (direct and indirect evidence; datatypes literature 0.71, affected pathway 0.94, genetic association 0.00, somatic mutation 0.45). IntOGen calls it a driver in 3 cohorts (1 activating, 2 loss-of-function), covering Cutaneous Squamous Cell Carcinoma, Nasopharyngeal Carcinoma, Thymoma.
In plain words · CNTRL (Centriolin) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as an oncogene driver, a tumour suppressor and a fusion partner, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Leukaemia, Nasopharyngeal carcinoma, Cutaneous squamous cell carcinoma and 1 more.
CNTRL (Centriolin) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as an oncogene driver, a tumour suppressor and a fusion partner, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Leukaemia, Nasopharyngeal carcinoma, Cutaneous squamous cell carcinoma and 1 more.
Involved in cell cycle progression and cytokinesis. During the late steps of cytokinesis, anchors exocyst and SNARE complexes at the midbody, thereby allowing secretory vesicle-mediated abscission.
No product in this corpus aims at CNTRL yet. Because the protein is lost rather than overactive, drugs either restore its function or exploit the weakness its loss leaves (synthetic lethality).
First described 2000. Earliest sequence paper UniProt cites for the protein: Guasch et al, Blood, 2000, "FGFR1 is fused to the centrosome-associated protein CEP110 in the 8p12 stem cell myeloproliferative disorder with t(8;9)(p12;q33)". Source.
Sources: HGNC HGNC:1858 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt Q7Z7A1 (protein name, function text, keywords and locations (REST API)); Open Targets ENSG00000119397 (association with cancer (MONDO_0004992) 0.67; per-cancer scores at or above 0.5: leukaemia 0.57 (GraphQL API, CC0)); IntOGen CNTRL (driver in 3 cohorts (Act 1, LoF 2); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Involved in cell cycle progression and cytokinesis. During the late steps of cytokinesis, anchors exocyst and SNARE complexes at the midbody, thereby allowing secretory vesicle-mediated abscission. Location: Cytoplasm, cytoskeleton, microtubule organizing center, centrosome; Midbody, Midbody ring (UniProt). Locus 9q33.2 (HGNC).
Query for this target: (TITLE:"CNTRL" OR ABSTRACT:"CNTRL" OR TITLE:"centriolin" OR ABSTRACT:"centriolin" OR TITLE:"Centriolin" OR ABSTRACT:"Centriolin" OR TITLE:"CEP1" OR ABSTRACT:"CEP1" OR TITLE:"CEP110" OR ABSTRACT:"CEP110") 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 CNTRL, not a curated reading list.
Shares Nasopharyngeal carcinoma, IntOGen, Open Targets Platform.
Shares Thymoma (WHO types A, AB, B1, B2 and B3), IntOGen, Open Targets Platform.
Shares Leukaemia (all types), IntOGen, Open Targets Platform.
Shares Leukaemia (all types), IntOGen, Open Targets Platform.
Shares Nasopharyngeal carcinoma, IntOGen.
Shares Nasopharyngeal carcinoma, IntOGen.
Shares Nasopharyngeal carcinoma, IntOGen.