Industry news, page-1683

@Davisite reply function not working

Another thing to consider is that there are significantly more writers increasing methylation within cells than erasers that demethylate. I realise the key methylators are METTL3 and METTL14, with information coming out about the unique role of METTL16. The other writers play more of a supportive role fascilitating the work of METTL3, METTL14, and METTL16.



There is an enormous amount of available data supporting the relationship between depleted m6A levels and tumorigenesis. I put this table together this morning that highlights 287 gastric cancer patients with excellent follow-up information highlighting high FTO expression (low m6A) have 49.7% greater chance or mortality than low/medium FTO expression when all other factors are taken into account. FTO expression correlated with response and resistance to immune checkpoint blockade treatment as well as advanced cancer stages. FTO played such an important role in therapy response it is being considered a novel potential predictor and target for gastric cancers.



Also, for the first time ever, HER2 monoclonal antibody (Trastuzumab - Herceptin) resistance has been linked to decreased m6A levels (FTO overexpression / METTL3-METTL14 suppression). Increasing m6A levels increased sensitivity of resistant breast cancer cells to trastuzumab. This paper focused on METTL14 supression, but others will follow FTO overexpression in time. There is also the nice in vivo synergy between FTO KD and trastuzumab.