Hampe lab

more information on CRTD website

Research focus

The research interest in our group is to unravel the molecular pathways that are implicated in the development of gastrointestinal and hepatological disorders. We employ modern functional, genetic, genomic and epigenomic approaches (GWAS, snRNA-Seq, snATAC--Seq, spatial transcriptomics, DNA-methylation and tissue-specific mouse KO-models) to understand the molecular mechanisms of liver physiology and regeneration in health and disease.

Genome-wide association studies

Studies of genetic risk factors of complex disorders, and specifically, genome-wide association studies (GWAS) have been widely employed in the study of complex disorders. Through close cooperation with German and international hospitals and research centers we have actively recruited large cohorts with complex disorders and use these for the identification of novel susceptibility genes for gallstone disease, alcoholic liver cirrhosis, colonic diverticular disease (diverticulosis, diverticulitis), colorectal cancer, hemochromatosis, inflammatory bowel disease and sarcoidosis.

Epigenetics of liver physiology and regeneration in health and disease

Epigenetics describes heritable changes in gene expression without changing the DNA sequence. We focus on changes in DNA methylation in combination with single nuclei RNA-Seq, snATAC-Seq, spatially resolved transcriptomics and Methyl-Seq to identify disease driving molecular pathways in liver diseases, such as non-alcoholic fatty liver disease (NAFLD), hepatocellular carcinoma and colorectal liver metastases. We have investigated DNA methylation to understand the progression and pathogenesis of NAFLD, and we have used DNA methylation as a molecular clock to track the epigenetic signature of obesity in human liver. We reported the first combined positional analysis of transcriptomes and methylomes across three micro-dissected zones (pericentral, intermediate and periportal) of human liver. In this study, we identified pronounced anti-correlated transcriptional and methylation gradients including a core of 271 genes controlling zonated metabolic and morphogen networks and observed a prominent porto-central gradient of DNA methylation at 46 transcription factor binding sites.

Role of genetic factors in development of FLD

Liver disease can be a result of several risk factors such as obesity, T2D, genetic factors, intestinal dysbiosis, excessive alcohol consumption etc. In our group we focus on genes, which have been identified by GWAS to be involved in many liver diseases, such as NAFLD, ALD, cirrhosis and hepatocellular carcinoma. We employ genetically modified models to understand physiology, biochemistry and involved molecular pathways in disease development to develop diagnostic and therapeutical targets.

Team