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A number of studies provide evidence for the existence of ovarian cancer stem cells, defined by functional attributes, foremost the ability to reconstruct the heterogeneity of the original tumor in immunocompromised mice through asymmetric cell division. As satisfying as the concept of an ovarian cancer stem cell is to explain the origins of ovarian cancer, can this concept be applied universally to explain the diversity in the histologic types of epithelial ovarian cancer? Can the unique features of an ovarian cancer stem cell population be exploited to therapeutically disarm these cells? Herein we explore these questions, beginning with a brief description of cancer stem cells in general and then turning more specifically to what is known about ovarian cancer stem cells. We then explore the potential for therapeutic targeting of these cells, and what the future holds for implementation of such approaches toward improving survival of women with ovarian cancer. [ABSTRACT FROM AUTHOR]

Cancer, and more specifically metastatic cancer, continues to be a leading cause of death worldwide. One of the most common organs in which metastatic cancer is diagnosed, and where it is often fatal, is the liver. This is not surprising given the large volume of nutrient-rich blood filtered through the fenestrated sinusoids of the liver. And while progress has been made in our understanding and treatment of metastatic disease, the majority of treatments are still ultimately unsuccessful in the metastatic setting. In the case of liver metastasis, even after apparently successful initial treatment, 5 year survival remains relatively low. Yet, although metastatic disease is associated with poor prognosis, the process of metastasis itself is known to be highly inefficient. The reasons for this inefficiency and the failure of cancer cells to form large vascularised metastases are, at least initially, twofold – cell death and dormancy. Dormant solitary metastatic cells and micrometastases have been proposed to be responsible, at least in part, for treatment failure and recurrence months to decades following initial treatment. Here we review experimental and clinical evidence regarding metastatic dormancy and discuss the implications of dormant cell populations for treatment of metastatic disease. [ABSTRACT FROM AUTHOR]