As for all stem cells, oncogenically transformed cancer stem cells (CSCs) are defined by their ability for self-renewal and multipotency. The CSC hypothesis states that, although CSCs represent a rare population of cells within a tumor, their high tumorigenic capacity drives tumorigenesis. Due to their intrinsic stem cell-like properties, CSC proliferation generates more CSCs, and all the differentiated cell types that compose the bulk of the tumor. Non-CSCs in the tumor have been shown to proliferate at a faster rate than CSCs, but have little tumor-initiating potential. Because CSCs exhibit increased resistance to toxic and chemical insults, this specific subpopulation of cells is believed to underlie resistance to chemotherapy and disease relapse. In fact, the CSC model posits that all CSCs must be eradicated to eliminate a tumor and prevent its recurrence.
Unlike the differentiated cancer cells in a tumor, CSCs have been shown to form new tumors when xenotransplanted into immunodeficient animal models. Although inconsistencies in these studies have questioned the validity of the CSC hypothesis, it is possible that different types of cancer involve distinct modes of tumorigenesis, or a combination of mechanisms. A critical experimental limitation is the ability of researchers to identify and isolate CSCs from other tumor cells. To address this need, we present a table of molecules identified in the current literature as markers of CSCs detected in specific malignancies.