Large-scale multiomic analysis identifies non-coding somatic driver mutations and nominates ZFP36L2 as a driver gene for pancreatic ductal adenocarcinoma Background The identification and characterisation of somatic cancer driver mutations in the non-coding genome remains challenging. Objective To broadly characterise non-coding driver mutations for p...

So excited that our manuscript is now online! Led by the super talented @junzhong.bsky.social & Aidan O'Brien in my lab with lots of help from Minal Patel @kconnelly92.bsky.social Jason Hoskins @efsunarda.bsky.social @struangrant.bsky.social and others. Very grateful to our team and collaborators!!

Always one of the best moments in research and very pound to be in the @amundadottir.bsky.social team!

Allelic effects on KLHL17 expression underlie a pancreatic cancer genome-wide association signal at chr1p36.33 - Nature Communications Allele-preferential transcription factor binding can influence pancreatic ductal adenocarcinoma risk loci function. Here, the authors show allele-specific JunB and JunD binding at chr1p36.33 and propo...

www.nature.com/articles/s41...

Very excited to share our research identifying a mechanism underlying PDAC risk at chr1p36.33 via KLHL17 gene regulation. Project led by a super talented Research Fellow @kconnelly92.bsky.social who is on the job market. Now online at Nature Communications

Very excited to share our research identifying a mechanism underlying PDAC risk at chr1p36.33 via KLHL17 gene regulation. Project led by a super talented Research Fellow @kconnelly92.bsky.social who is on the job market. Now online at Nature Communications