{Reference Type}: Journal Article
{Title}: KMT2C and KMT2D aberrations in breast cancer.
{Author}: Tinsley E;Bredin P;Toomey S;Hennessy BT;Furney SJ;
{Journal}: Trends Cancer
{Volume}: 10
{Issue}: 6
{Year}: 2024 Jun 6
{Factor}: 19.161
{DOI}: 10.1016/j.trecan.2024.02.003
{Abstract}: KMT2C and KMT2D are histone lysine methyltransferases responsible for the monomethylation of histone 3 lysine 4 (H3K4) residues at gene enhancer sites. KMT2C/D are the most frequently mutated histone methyltransferases (HMTs) in breast cancer, occurring at frequencies of 10-20% collectively. Frequent damaging and truncating somatic mutations indicate a tumour-suppressive role of KMT2C/D in breast oncogenesis. Recent studies using cell lines and mouse models to replicate KMT2C/D loss show that these genes contribute to oestrogen receptor (ER)-driven transcription in ER+ breast cancers through the priming of gene enhancer regions. This review provides an overview of the functions of KMT2C/D and outlines the recent clinical and experimental evidence of the roles of KMT2C and KMT2D in breast cancer development.