Research Goal
Recent research has provided comprehensive insight into the genetic and epigenetic alterations in livercancer and has identified many relevant pathways affected. Based on this knowledge it is the aim of this consortium to delineate complex superordinate mechanisms that shape liver carcinogenesis. Research area A (Protumorigenic mechanisms in chronic viral infection, NASH, and hepatic inflammation) will analyze the relevant oncogenic mechanisms of the two leading liver cancer etiologies in the Western World, chronic hepatitis C (A01, A02) and non-alcoholic fatty liver disease (A02-04) as well as their common effector chronic inflammation (A05, A06). Research area B (Tumor cell autonomous mechanisms, tumor cell plasticity, and tumor-environment cross-talk) analyses the role of the respective key mechanisms that shape the tumor cell response to its environment, such as inflammation-tumor suppressor genes interaction (B01), metabolic reprogramming (B02), intracellular regulatory mechanisms (B03, B04, B07), and liver cell plasticity (B05, B06). Research area C (New therapeutic approaches) aims at novel interventional approaches towards integrative mechanisms addressing the broadly acting oncogenic factor MYC (C01, C02), epigenetic targeting (C02), neoangiogenesis (C03), cytokinemechanisms (C04), and (viro-)immunological effector mechanisms (C05-07). As liver cancer represents an ideal model system of solid cancer, the goals of the SFB/TR 209 are of relevance beyond liver cancer for other tumor diseases.
