cancer death. Despite some Avasimibe CI-1011 progress in the treatment of cancers, existing therapies are limited in their ability to cure malignancies and to prevent me tastases and relapses. Surgery, radiofrequency abla tion therapy and chemotherapy are all directed at reducing the bulk of the tumor mass. However, on completion of therapy there is ultimately regrowth of tumor and relapse of diseases in the majority of cases. Although the idea of tumor stem cells has been proposed for a number of decades, demonstration of their existence has only occurred within the last ten years. Recently, HCC progression has been thought to be driven by cancer stem cells through their capacity for self renewal, production of heterogene ous progeny, resistance to chemotherapy and to lim itlessly divide.
Advances were first achieved in he matological malignancies, with the first CSC demon strated in acute myeloid leukemia. However, using similar strategies and technologies, and taking ad vantage of available surface markers, CSCs have been more recently demonstrated Doramapimod in a growing range of epithelial and other solid organ malignancies, sug gesting that the majority of malignancies are de pendent on such a compartment. Furthermore, many potentially and biologically significant surface mark ers and pathways that can modulate these stem progenitor cells in cancer tissue have been suc cessfully identified based on their dual role both in embryogenic stem cell development and tumor acti vation or suppression.
In this review, we demonstrate a brief and up to date review of molecular signaling in liver CSC and present insights into new therapeutic strategies for liver CSCs. Liver stem cells in human liver regeneration The liver is both an exocrine and an endocrine gland, which performs complex functions and has the phenomenal ability to regenerate. This process ena bles the recovery of the lost mass without endanger ing the viability of the entire organism. Many studies suggest that the existence of two basic types of liver regeneration. After acute liver injury, he patic stem cells take part in normal tissue repair and homeostasis quickly. In contrast, liver regenera tion after loss of hepatic tissue does not depend on these kinds of cells, but on the proliferation of the existing mature hepatocytes, the parenchymal cells of the organ.
In addition, other cells such as endothelial cells, Kuppfer cells, and Ito cells may also contribute to regeneration of the lost hepatic tissue. The normal liver has been estimated to be re placed by normal tissue approximately once a year or more. Therefore replacement rate of the normal adult liver was calculated to be 0.005 0.0025 at any time. However, this slow normal renewal rate differs from the rapid proliferate response to loss of hepatic mass. In rodents, when two thirds of the liver is resected the remaining rem nant can regrow to the original liver size in approxi mately 10 days. In response to this sti