RT @FunImmune: We are excited to announce that today, @HRMrqz successfully defended her PhD thesis! . A new Doctor has emerged from our lab….

RT @SusselLab: We are excited to share our latest publication in @GenesDev!

RT @EurPancClub: Did YOU fill out the survey on the shortage of PERT 🤔??. From the #EPC Public Affairs Committee!!. Help us analyze the cur….

Many thanks to collaborators @JonathanBaldan, #PhilSeymour, @CVRift ,#JaneHasselby, @albin_san and all members of @ARNesLab for comments. Work supported by funding from @cancer_dk.@UCPH_BRIC.

Next steps: We’ll explore mechanisms behind the impaired regeneration, potentially leading to a new understanding of cancer risk factors and opportunities to prevent cancerous changes in the pancreas.

Despite minimal differences in normal pancreas function, aged mice had reduced capacity to recover from pancreatitis, showing tissue atrophy and fibroinflammatory stroma. A key finding in how aging affects recovery.

The study found a pre-existing proinflammatory state in the pancreas of aged mice, similar to conditions that predispose individuals to cancer. This could be key to understanding how aging impacts cancer risk.

Age is the biggest risk factor for pancreatic cancer (PDAC), but the underlying causes are still unclear. Kristina’s work focuses on how aging affects pancreas regeneration and cancer susceptibility.

I am excited to see this story by my talented Master's Student, Kristina Høj. Her research dives into age-related decline in pancreas regeneration and how it’s linked to a proinflammatory response to injury. @AGA_GHAdvances,@UCPH_BRIC,

RT @KenOliveLab: The Olive Lab is looking for a postdoc to lead our translational program on RAS inhibition in pancreatic cancer. Should ha….

Excited to see your future successes! #Research #PancreaticCancer #Organoids.

In collaboration with colleagues at Herlev Hospital and Rigshospitalet, Katarzyna will work towards precision therapy in pancreatic ductal adenocarcinoma and strategies to overcome therapy resistance using organoids.

Kudos to Katarzyna Radke for winning a fellowship from the UEG! @ARNeslab, @UCPH_BRIC, @UCPH_Research, @my_ueg

Many thanks to collaborators #CarloMaurer, #JaneHasselby, #LucBowens, #CharlesJDavid, #IlseRooman, #OrenParnas, #VéroniqueLefebvre, @ErlerLab @DelgiornoKathy.Work supported by funding from @cancer_dk @novonordiskfond , @UCPH_BRIC.

Reach out for discussion and sharing notes! More studies aiming at boosting the inherent healing capacity of the pancreas to come.

Second evidence, Sox4 leads to fibroblast activation, collagen deposition, and macrophage polarization, suggesting that Sox4 has a protective effect by limiting a conducive environment for disease progression.

The absence of metaplastic cell types leads to non-autonomous effects on the tissue microenvironment. First evidence: the pancreas appears stiff (noticeable by sight and touch!).

Acinar cells can adopt alternative phenotypes during tissue injury, suggesting a division of labour in tissue regeneration. Our in vivo analysis demonstrate that Sox4 is a master regulator, driving tuft cell specification and gastric metaplasia in acinar plasticity.

Sox4 is activated in acinar cells upon pancreatic injury in mouse and human, akin to a stress sensor. We found that Sox4 restricts rather than promote tissue injury in experimental pancreatitis.

New Paper! Jonathan Baldan, Juan Camacho and Marta Ballester from the lab find a genetic program driven by Sox4 promoting the resolution of tissue injury in pancreas regeneration and cancer. @JonathanBaldan @AGA_Gastro @UCPH_BRIC #tuft_cells #plasticity