Carolin Mogler

This study uses single-nucleus RNA sequencing and spatial transcriptomics to compare primary and metastatic leiomyosarcoma, identifying antigen-presenting fibroblasts associated with metastasis.

This study uses pan-cancer phosphoproteomics to identify therapeutic targets and improve precision oncology by analyzing 1,998 tumor samples and developing new scores for kinase activity and immune response.

This study uses an in ovo model to show that the CAM platform supports tumor-stroma coevolution in pancreatic cancer, preserving patient-specific features and enabling functional analysis of stromal interactions.

This study shows that high-speed mass spectrometers reduce performance differences between DDA and DIA proteomics, but current LC-MS methods still lack comprehensive proteome coverage.

This study shows that HIRA-mediated H3.3 deposition maintains hepatocyte identity during aging, and its loss leads to metabolic dysfunction and fibrosis, which can be partially reversed by tissue regeneration.

Exome and transcriptome sequencing of salivary basal cell adenomas reveals a recurrent FBXW11 p.F517S mutation, exclusive with CTNNB1 p.I35T, together accounting for 94% of cases.

This study identifies a mitochondria-regulated p53 circuit that links genomic instability and inflammation in senescent cells, showing p53 suppresses inflammation without affecting cell cycle arrest.

The paper profiles proteomes from 1,220 FFPE tumors across six cancers, identifies a new normalization method, and reports a comprehensive pan-cancer proteome resource.

This study shows that NFAT5 in endothelial cells limits hypoxia-induced maladaptive remodeling of pulmonary arterioles by restricting HIF1-mediated Pdgfb expression.

This study shows that Dnmt3a regulates placental vascularization and fetal growth by controlling DNA methylation in endothelial cells, identifying it as a key factor in placental function.

This study shows that Caspase-8 promotes angiogenesis in endothelial cells through a cell death-independent mechanism involving p38 MAPK activation and VE-cadherin destabilization.