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AFDN (Afadin) 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 Breast cancer, Skin cancer, Colorectal cancer and 2 more.
Belongs to an adhesion system, probably together with the E-cadherin-catenin system, which plays a role in the organisation of homotypic, interneuronal and heterotypic cell-cell adherens junctions (AJs). Nectin- and actin-filament-binding protein that connects nectin to the actin cytoskeleton. May play a key role in the organisation of epithelial structures of the embryonic ectoderm.
Open Targets scores its association with cancer at 0.66 (direct and indirect evidence; datatypes literature 0.94, animal model 0.59, genetic association 0.00, somatic mutation 0.85). IntOGen calls it a driver in 3 cohorts (1 activating, 2 loss-of-function), covering Invasive Breast Carcinoma, Colorectal Adenocarcinoma.
In plain words · AFDN (Afadin) 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 Breast cancer, Skin cancer, Colorectal cancer and 2 more.
AFDN (Afadin) 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 Breast cancer, Skin cancer, Colorectal cancer and 2 more.
Belongs to an adhesion system, probably together with the E-cadherin-catenin system, which plays a role in the organisation of homotypic, interneuronal and heterotypic cell-cell adherens junctions (AJs).
No product in this corpus aims at AFDN 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 1993. Earliest sequence paper UniProt cites for the protein: Prasad et al, Cancer Res, 1993, "Cloning of the ALL-1 fusion partner, the AF-6 gene, involved in acute myeloid leukemias with the t(6;11) chromosome translocation". Source.
Sources: HGNC HGNC:7137 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P55196 (protein name, function text, keywords and locations (REST API)); Open Targets ENSG00000130396 (association with cancer (MONDO_0004992) 0.66; per-cancer scores at or above 0.5: colorectal cancer 0.53, melanoma 0.55, skin cancer 0.58, breast cancer 0.57, lung cancer 0.51 (GraphQL API, CC0)); IntOGen AFDN (driver in 3 cohorts (Act 1, LoF 2); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Belongs to an adhesion system, probably together with the E-cadherin-catenin system, which plays a role in the organisation of homotypic, interneuronal and heterotypic cell-cell adherens junctions (AJs). Nectin- and actin-filament-binding protein that connects nectin to the actin cytoskeleton. May play a key role in the organisation of epithelial structures of the embryonic ectoderm. Essential for the organisation of adherens junctions. Location: Cell junction, adherens junction (UniProt). Locus 6q27 (HGNC).
Query for this target: (TITLE:"AFDN" OR ABSTRACT:"AFDN" OR TITLE:"afadin, adherens junction formation factor" OR ABSTRACT:"afadin, adherens junction formation factor" OR TITLE:"Afadin" OR ABSTRACT:"Afadin" OR TITLE:"AF-6" OR ABSTRACT:"AF-6" OR TITLE:"AF6" OR ABSTRACT:"AF6" OR TITLE:"MLLT4" OR ABSTRACT:"MLLT4") 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 AFDN, not a curated reading list.