FYN

Overview

First described 1986. Earliest sequence paper UniProt cites for the protein: Kawakami et al, Mol. Cell. Biol, 1986, "Isolation and oncogenic potential of a novel human src-like gene". Source.

Sources: HGNC HGNC:4037 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P06241 (protein name, function text, keywords and locations (REST API)); Open Targets ENSG00000010810 (association with cancer (MONDO_0004992) 0.74; per-cancer scores at or above 0.5: acute lymphoblastic leukaemia 0.56, non-Hodgkin lymphoma 0.69, chronic myelogenous leukaemia, BCR-ABL1 positive 0.60, myeloproliferative neoplasm 0.61, leukaemia 0.62 (GraphQL API, CC0))

• 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.