Projects

Forschungsnetzwerk zur Früherkennung und Prävention- LiSyM-Krebs

Ein Netzwerk von Klinikern, Wissenschaftlern und Datenmanagern hat sich zur Aufgabe gemacht, Methoden zu entwickeln, um Patienten mit einem hohen Risiko für ein Leberkarzinom frühzeitig, in Vorstadien der Tumorentwicklung, identifizieren zu können. Gemeinsam bilden sie das „Systemmedizinische Forschungsnetzwerk zur Früherkennung und Prävention von Leberkrebs“, LiSym-Krebs, das vom Bundesministerium für Bildung und Forschung ...

SMART-NAFLD : A Systems Medicine Approach to Early Detection and Prevention of Hepatocellular Carcinoma in Non-Alcoholic Fatty Liver Disease

The massive increase in obesity is leading to an alarming rise in non-alcoholic liver disease (NAFLD). This development will lead to a dramatic increase in liver diseases such as hepatocellular carcinoma (HCC). A particular challenge is that NAFLD-associated HCCs, for reasons still unknown, not only occur in association with advanced liver fibrosis/cirrhosis, ...

DEEP-HCC - Detailed Analysis of the Spatial Organization of the Development of Hepatocellular Carcinoma

C-TIP-HCC- Mechanism-based Multiscale Model to Dissect the Tipping Point from Liver Cirrhosis to Hepatocellular Carcinoma

The ultimate goal of the C-TIP-HCC is a „mechanistic multiscale model to describe dynamic changes in regenerative nodes across a tipping point (TIP) towards development in patients with cirrhosis to facilitate early monitoring and intervention“ and facilitate intervention“. To achieve this, we will conduct in-depth studies on cirrhotic regenerative nodes.

In chronic diseases, at some point the liver can suddenly stop functioning. This is called acute-on-chronic liver failure, or ACLF. This is the leading cause of death in liver patients and is often provoked by the use of transcription or freely available drugs or alcohol abuse. For this condition we need an effective treatment quickly. LiSyM-Pillar III researches the factors that contribute significantly to ACLF. What exactly happens then? Are there any early signs that would enable ACLF to be ...

This comprises the whole LiSyM network

One of the tasks of the healthy liver is to store fat. Yet, at some stage, too much fat makes the liver sick. One critical time point occurs when a healthy fatty liver becomes inflamed and progresses to steatohepatitis, or NASH. LiSyM-Pillar I will identify what events lead to this transition. Does it occur in all parts of the liver? Which molecules indicate that it is taking place? Can the degeneration be stopped or undone - and if so, how?

In one in five people with NAFLD, the functioning liver cells, the hepatocytes, are replaced by connective tissue. Eventually this fibrosis becomes irreversible. In this state the liver is like a ‘scar that never heals’. Through it, the liver loses many of its vital functions. LiSyM-Pillar II wants to know more about which factors promote fibrosis and the conditions under which fibrosis becomes irreversible How can fibrosis be diagnosed as early as possible? Researchers in the pillar are also ...

Dr. Nachiket Vartak (TU University, Dortmund) investigates the role of a particular protein - the GTPase Rab18 - in initiating NAFLD. He tries to influence Rab18 pharmacologically so that NAFLD is not initiated. Vartak also analyzes how bile acids leave the liver. He hopes to find ways to improve the flow of bile in a liver with dysfunctional bile flow.

Dr. Madlen Matz-Soja (University of Leipzig) investigates the importance of a control mechanism - the hedgehog signaling pathway - for fatty liver disease. She has shown that the signaling pathway directs how liver cells in NAFLD accumulate fat. Hedgehog also affects sex hormones in the liver. Therefore, Matz-Soya hopes to clarify why women and men suffer from cirrhosis and liver cancer with varying degrees of frequency.

Dr. Ahmed Ghallab (TU University, Dortmund) deals with chronic liver damage caused by toxins. In addition, he investigates processes associated with cholestasis - when bile accumulates in the bile ducts. Ghallab has been able to explain basic mechanisms of acute cholestasis, using a method for intravital two-photon microscopy, which he developed.