Abstract 3356: A controversial study on well reported liver cancer stem cell marker

Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC Recent studies suggest that the presence of cancer stem cells (CSC) could be linked with patients’ survival. The ability of cancers to grow indefinitely has fueled the idea that cancer and stem cells may have common underlying mechanisms. It has been suggested that tumors are initiated from cancer stem cells (CSCs) with proliferation potential drives the growth of cancer. CSCs are resistant to chemotherapy and radiation. However, the suggested cancer stem cell markers in human hepatocellular carcinoma cells are variable and confused. In this study, we profiled some of the most reported CSC markers, including CD133, epithelial cell adhesion molecule (EpCAM), aldehyde dehydrogenase (ALDH), CD90, CD24, c-kit, global-H and stemness genes in eight human hepatocellular carcinoma cell lines. Through specific marker expressed cell sorting by FACs aria or magnetic beads, the CSC associated drug resistance and tumorigenicity were further evaluated. However, there is no obvious difference among parental group, marker-positive group and marker-negative group in these CSC characteristics evaluated. It seems no good correlation between reported markers in liver cancer stem cells. Therefore, presence of markers alone should be taken with caution as single prognostic parameters. Through harsh culture condition, spheroid cell grew and had been isolated, which perform CSC-like properties. Moreover, forced activation of an ESC-like gene expression program can reprogram HCC cells into CSC-like cells and achieve pathologic self-renewal. The ability to create induced cancer stem cells (iCSC) may provide opportunities to better define the biology of cancer stem cells in order to trace or eliminate them in human patients. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3356.