Metabolic low-grade inflammation in obesity results in metabolic and oncogenic disorders. Our aim is to decipher the missing link between obesity-induced inflammation and cancer progression to ultimately develop strategies for therapeutic approaches.
Obesity is a current health burden in Western countries that creates a predisposition to numerous disorders such as T2DM and cancer. Our group aims to dissect the role of the obesity-associated low-grade inflammation in cancer, especially in hepatocellular and colorectal carcinoma. To this end, we are using self-generated sophisticated mouse models enabling restriction of transgene expression to a specific cell type or even to different organs. We have combined Cre/loxP with Dre/rox technologies to achieve these goals.
We aim to dissect the link between obesity-induced inflammation and cancer by using sophisticated transgenic mice models.
In addition to promoting cancer, interleukin (IL) 6 and other inflammatory mediators also have beneficial metabolic characteristics for the human body. The research team aims to understand why IL 6 helps the body during acute inflammation, but has a negative effect under chronic inflammatory conditions.
In 2013, PD Dr. Wunderlich and his group enjoyed a scientific breakthrough when they decoded the importance of interleukin 6 in liver cancer development. In lean mice, IL-6 signaling is necessary to promote liver cancerogenesis via Mcl-1 stabilization, whereas in obese mice Mcl-1 stabilization occurs independent of IL-6Rα signaling. Here, another yet to be identified factor that compensates in obesity for IL-6Rα deficiency activates similar signaling pathways that promote HCC development. Thus, identifying this factor might help to combat this often fatal disorder.