Abstract
Abstract Cancer stem cells (CSCs) have been discovered in cancers of many tissues but they have not been explored for gastric cancer. A candidate approach was taken to isolate putative gastric cancer stem cells from primary gastric cancer specimens because surface markers have been used to describe CSCs from different cancers. Cells dissociated from biopsy samples extracted from primary tumour and non-tumour sites of the same patient were analyzed by flow cytometry. Cell surface markers surveyed include CD45 for hematopoietic cells, CD31 for endothelial cells, CD44, CD133, CD34, CD117, CD166, CD90 and EpCAM as potential cancer stem cell markers. EpCAM levels were found to be higher in cells isolated from the tumor than non-tumor sites. Using median fluorescence intensity, it was found that cells at the tumor site express 1.2-1.7 fold higher level of EpCAM. This was observed in histopathologically distinct types of gastric tumors, namely intestinal subtypes that are well, moderately and poorly differentiated. Data from diffused type gastric tumors were not as consistent mainly because of sampling difficulties. 100,000 EpCAM-positive cells form xenograft tumors in NOD/SCID mice whereas 500,000 EpCAM-negative cells from a fraction that was not hematopoietic (CD45-negative), endothelial (CD31-negative) nor fibroblastic (CD140b-negative) were unable to do so. To further enrich for gastric cancer stem cells, the EpCAM-positive cells were sorted based on EpCAM+CD44+ or EpCAM+CD133+ cells. To expand the tumor material, we generated xenograft tumors directly from fresh tumor pieces. Histological analyses verified that the xenograft tumors recapitulate those in the patient samples. Cells dissociated from the xenograft tumor were then subjected to CSC identification assays. To date, three lines of xenograft tumors were generated from tumor tissues of well, moderately and poorly differentiated histological subtype of gastric cancers. As few as 1000 EpCAM+CD44+ cells were able to initiate tumors in NOD/SCID mice whereas 20,000 EpCAM+CD44- cells were required to do so. We are currently doing limiting dilution assays to estimate the number of cancer initiating cells in each fraction we isolate from the xenografts. We were unable to see differential tumorigenic potentials in EpCAM+CD133+ and EpCAM+CD133- fractions. In conclusion, we have identified a subpopulation of gastric cancer cells that potentially mark gastric cancer stem cells as characterized by their cancer-initiating potential. 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 3371.
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