Delighted to announce that @antonvenhuizen.bsky.social has received a Marie Skłodowska-Curie Actions Postdoctoral Fellowship Award, working with @melissa-gammons1.bsky.social to further understanding of the rare genetic disease Robinow Syndrome www.cimr.cam.ac.uk/news/cimr-re...

10 Must-Read Posts in GI Oncology This Week oncodaily.com/oncolibrary/... #OncoDaily #Oncology #Cancer #Health #Medicine #MedEd #MedOnc #MedNews #GIOnc

10 Must-Read Posts in GI Oncology This Week - OncoDaily

10 Must-Read Posts in GI Oncology This Week / cancer, cancer care, cancer treatment, clinical trials, colorectal cancer, esophageal cancer, gastric cancer, GI

oncodaily.com

Excited to share that work from my PhD in the @mauricelab.bsky.social has been published in @cp-iscience.bsky.social. ❔️Why do mutations in two Wnt pathway genes lead to different clinical features in hepatocellular carcinoma? 📄Read the paper for our insights: doi.org/10.1016/j.is...

I had an amazing week full of great talks and discussions at the Gordon Research Seminar and Conference on Wnt signalling in Maine, US. I also had the honour of leading the GRS panel discussion and was selected to present work from the Gammons lab during the GRC. Many thanks to the organisers!

Yesterday, @antonvenhuizen.bsky.social successfully defended his thesis "Molecular mechanisms of the β-catenin destruction complex in health and disease", which describes the versatile field of WNT regulator AXIN1. We are super proud and wish Dr. Venhuizen all the best in Cambridge!

Our first selected oral presentation comes from Elisabeth Chapman from the @melissa-gammons1.bsky.social group at the CIMR @thecimr.bsky.social telling us about her research into casein kinase 1 regulation of Wnt signalosome assembly. #WNTUK2025

Hello! Although we are still in the other place, this will become our main social media feed. We're part of the University of Cambridge Clinical School Cell biology, molecular mechanisms of human disease

Excited about our pre-print on AXIN1 mutations in HCC! We found that AXIN1 mutations drive low but physiologically relevant levels of Wnt/β-catenin signaling, while being permissive to YAP/TAZ activation. This helps explain why mutations in AXIN1 and β-catenin are linked to distinct HCC subtypes.

bioRxiv Cancer Bio@biorxiv-cancer.bsky.social · 2y ago

Hepatocellular carcinoma-associated AXIN1 mutations drive low levels of Wnt/β-catenin pathway activity that allow for niche-independent growth and YAP/TAZ signaling https://www.biorxiv.org/content/10.1101/2024.11.28.625941v1