Recent advances provide additional support for the liver TISC concept and, importantly, may aid therapeutic decision making by allowing risk assessment. Targeted anti-TISC therapies hold significant promise, but a better understanding of the origin and phenotype of www.selleckchem.com/products/MG132.html these cells appears necessary. Significant progress has been made in liver stem cell and liver cancer
stem cell research in the last 2 years. Although normal and cancerous liver stem cells or LPCs naturally share many characteristics and markers, on most accounts, the two fields have been moving forward independently. The dual focus of the conference provided an opportunity to gather insight or update one’s knowledge of the other field. In addition, the conference
identified commonalities that may serve as a basis for future advances. For Lumacaftor example, new markers of normal LPCs may be useful for further fractionation of heterogeneous TISC populations. Conversely, signaling pathways and transcription factors regulating TISC characteristics may also play a role in noncancerous liver regeneration. In addition, new cell-culture or in vivo cell-delivery systems will likely benefit research on both normal and cancerous liver stem cells or LPCs. The hope is that increased exchange and collaboration between the two fields will accelerate the development of therapies for patients with liver disease and liver cancer. The American Association for the Study of Liver Disease Henry M. and Lillian Stratton Basic Research Single Topic Conference “Stem Cells in Liver Diseases and Cancer: Discovery and Promise” was held in Atlanta, GA, March 19-20, 2011. The meeting provided an overview and update on ongoing research efforts seeking to obtain a detailed
understanding of stem cell biology in liver disease and cancer for the development of new therapies. This review is dedicated to Nelson Fausto, a leader in the field. “
“Ischemia-reperfusion injury (IRI) is a major limiting event for successful Cyclooxygenase (COX) liver transplantation, and CD4+ T cells and invariant natural killer T (iNKT) cells have been implicated in promoting IRI. We hypothesized that hepatic overexpression of CD39, an ectonucleotidase with antiinflammatory functions, will protect liver grafts after prolonged cold ischemia. CD39-transgenic (CD39tg) and wildtype (WT) mouse livers were transplanted into WT recipients after 18 hours cold storage and pathological analysis was performed 6 hours after transplantation. Serum levels of alanine aminotransferase and interleukin (IL)-6 were significantly reduced in recipients of CD39tg livers compared to recipients of WT livers. Furthermore, less severe histopathological injury was demonstrated in the CD39tg grafts. Immune analysis revealed that CD4+ T cells and iNKT cells were significantly decreased in number in the livers of untreated CD39tg mice.