# FYN

Source: https://onco.cc/targets/fyn/  
OnCo record `fyn` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

FYN (Tyrosine-protein kinase Fyn) is a protein kinase, an enzyme that switches other proteins on by adding phosphate groups. The public catalogues list it as a drug target, and an approved or late-stage drug is recorded against it. Tied to Non-Hodgkin lymphoma, Leukaemia, Myeloproliferative neoplasms and 2 more.

## Summary

Non-receptor tyrosine-protein kinase that plays a role in many biological processes including regulation of cell growth and survival, cell adhesion, integrin-mediated signalling, cytoskeletal remodeling, cell motility, immune response and axon guidance. Inactive FYN is phosphorylated on its C-terminal tail within the catalytic domain. Following activation by PKA, the protein subsequently associates with PTK2/FAK1, allowing PTK2/FAK1 phosphorylation, activation and targeting to focal adhesions.

Open Targets scores its association with cancer at 0.74 (direct and indirect evidence; datatypes clinical 0.96, affected pathway 0.92, literature 0.97, genetic association 0.00, animal model 0.42).

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: FYN proto-oncogene, Src family tyrosine kinase; Tyrosine-protein kinase Fyn; MGC45350
- Tags: cancer-genes-wave
- Symbol: FYN
- Class: kinase
- Biology: Non-receptor tyrosine-protein kinase that plays a role in many biological processes including regulation of cell growth and survival, cell adhesion, integrin-mediated signalling, cytoskeletal remodeling, cell motility, immune response and axon guidance. Inactive FYN is phosphorylated on its C-terminal tail within the catalytic domain. Following activation by PKA, the protein subsequently associates with PTK2/FAK1, allowing PTK2/FAK1 phosphorylation, activation and targeting to focal adhesions. Involved in the regulation of cell adhesion and motility through phosphorylation of CTNNB1 (beta-catenin) and CTNND1 (delta-catenin). Regulates cytoskeletal remodeling by phosphorylating several proteins including the actin regulator WAS and the microtubule-associated proteins MAP2 and MAPT. Promotes cell survival by phosphorylating AGAP2/PIKE-A and preventing its apoptotic cleavage. Location: Cytoplasm; Nucleus; Cell membrane; Perikaryon (UniProt). Locus 6q21 (HGNC).
- Where found: Non-Hodgkin lymphoma: Open Targets association 0.69 with non-Hodgkin lymphoma (MONDO_0018908); Leukaemia: Open Targets association 0.62 with leukaemia (MONDO_0005059); Myeloproliferative neoplasms: Open Targets association 0.61 with myeloproliferative neoplasm (MONDO_0020076); Chronic myeloid leukaemia: Open Targets association 0.60 with chronic myelogenous leukaemia, BCR-ABL1 positive (MONDO_0011996); Acute lymphoblastic leukaemia: Open Targets association 0.56 with acute lymphoblastic leukaemia (MONDO_0004967)

## Notes

- 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: Open Targets known-drug datatype score 0.97. Evidence tier "approved-drug" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.
- Lymphoma, RHOA G17V and the epigenetic mutations of T-follicular-helper lymphoma: A single substitution, G17V, in the small GTPase RHOA produces a protein that does not bind GTP and that blocks the wild-type protein as well. It is specific to the tumour cell, whereas the TET2 mutations that accompany it are found in non-tumour haematopoietic cells too, which places the TET2 lesion earlier, in the stem cell, and makes this lymphoma a disease that grows out of clonal haematopoiesis. Frequency: RHOA G17V in 68% of angioimmunoblastic T-cell lymphoma samples, with every G17V case also carrying a TET2 mutation (Sakata-Yanagimoto 2014); independently, in 22 of 35 angioimmunoblastic cases, 67%, and 8 of 44 peripheral T-cell lymphoma not otherwise specified, 18%, alongside recurrent TET2, DNMT3A and IDH2 mutations and less frequent FYN, ATM, B2M and CD58 lesions (Palomero 2014). What it changes about treatment: Not through an approved test. The hypomethylating agents are used in this disease on the strength of the TET2 and DNMT3A biology rather than on a mutation result, and azacitidine-containing regimens have shown activity in T-follicular-helper histology specifically.

## Sources

- HGNC HGNC:4037: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:4037
- UniProt P06241: https://www.uniprot.org/uniprotkb/P06241/entry
- NCBI Gene 2534: https://www.ncbi.nlm.nih.gov/gene/2534
- Ensembl ENSG00000010810: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000010810
- Sakata-Yanagimoto et al., Nat Genet 2014: somatic RHOA G17V in angioimmunoblastic T-cell lymphoma: https://doi.org/10.1038/ng.2872
- Palomero et al., Nat Genet 2014: recurrent mutations in epigenetic regulators, RHOA and FYN in peripheral T-cell lymphoma: https://doi.org/10.1038/ng.2873

## Connected records

- collections: [Open Targets Platform](https://onco.cc/collections/open-targets/)
- cancers: [Acute lymphoblastic leukaemia](https://onco.cc/cancers/all-leukemia/), [Chronic myeloid leukaemia (CML)](https://onco.cc/cancers/cml/), [Leukaemia (all types)](https://onco.cc/cancers/leukaemia/), [Myeloproliferative neoplasms (PV, ET, myelofibrosis)](https://onco.cc/cancers/myeloproliferative-neoplasms/), [Nodal T-follicular helper cell lymphoma, angioimmunoblastic type (angioimmunoblastic T-cell lymphoma)](https://onco.cc/cancers/angioimmunoblastic-t-cell-lymphoma/), [Non-Hodgkin lymphoma (all types)](https://onco.cc/cancers/non-hodgkin-lymphoma/), [Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma)](https://onco.cc/cancers/peripheral-t-cell-lymphoma/)
- pathways: [Clonal haematopoiesis (CHIP)](https://onco.cc/pathways/clonal-haematopoiesis/), [Epigenetic reprogramming](https://onco.cc/pathways/epigenetic-reprogramming/)
- biomarkers: [RHOA G17V](https://onco.cc/biomarkers/rhoa-g17v/)

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