Stem cells represent a cellular compartment that is partially characterized by regenerative capacity and multipotential differentiation capabilities. In these characteristics, they resemble cancer cells and it is thought that these self-renewing stem cells are at risk for neoplastic transformation by oncogenic mutations. Recently, the same repair, apoptotic and senescence effector mechanisms involved in limiting normal stem cell life span have also been found to be involved in aging and in cancer susceptibility. Studies in Drosophila and Caenorhabditis elegans have implicated free radical production, the rate of cellular metabolism, and DNA repair in the aging of these species which have been corroborated by investigations of mammalian cells and animal models. Further association between stem cell and cancer biology have been buttressed by the identification of putative cancer stem cells in human carcinoma. An in depth discussion of the intersect between stem cell biology, cancer, and senescence would therefore be timely. A goal of the proposed symposium is to explore the cancer stem cells in the context of the rapidly advancing understanding of stem cell biology and aging. Activation of telomerase and more rarely a recombinogenic mechanism (Alternative Lengthening of Telomeres; ALT) can maintain telomeres allowing cancer cells to escape senescence. The targeting of cancer stem cells and other telomerase positive cancer cell populations to either die by apoptosis or undergo induced “premature” senescence will a major theme during the last two days of the conference.