Jens Timmer

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.

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, ...

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 ...

This comprises the whole LiSyM network

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 ...

Upon stimulation of cells with transforming growth factorb(TGF-b),Smad proteins form trimeric complexes and activate a broad spectrum of target genes. It remains unresolved which of the possible Smad complexes are formed in cellular contexts and how these contribute to gene expression. Combining quantitative mass spectrometry with a computational selection strategy, we investigate Smad complexes in the mouse hepatoma cell line Hepa1-6.

In this study we identify most relevant Smad complexes in liver-derived cells, the contribution of the Smad complexes on target gene expression, and the role of Smad abundance and Smad2 phosphorylation in hepatocellular carcinoma

ODE model describes dynamics of IFNalpha-induced signaling in Huh7.5 cells for a time scale up to 32 hours after stimulation with IFNalpha. The model consists of an IFN receptor model, formation/degradation and cytoplasmic/nuclear shuttling of STAT1-homodimers, STAT1-STAT2-heterodimers and STAT1-STAT2-IRF9 (ISGF3) complexes. On top, formation of feedback proteins STAT1, STAT2, IRF9, USP18, SOCS1, SOCS3 and IRF2 and corresponding influences on IFNalpha signaling dynamics was incorporated. The model ...

Taken from https://github.com/Benchmarking-Initiative/Benchmark-Models See the github repository for license Import and execute the model in d2d

Taken from https://github.com/Benchmarking-Initiative/Benchmark-Models License according to the github repository's license Import and execute with d2d

Jamboree presentation