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. 2008 Oct 12;1(1):4.
doi: 10.1186/1757-2215-1-4.

Ovarian cancer: emerging concept on cancer stem cells

Moorthy P Ponnusamy  1 , Surinder K Batra
Affiliations

Ovarian cancer: emerging concept on cancer stem cells

Moorthy P Ponnusamy et al. J Ovarian Res. .

Abstract

Emerging evidence suggests that the capacity of a tumor to grow and propagate is dependent on a small subset of cells within a tumor, termed cancer stem cells. In fact, cancer cells, like stem cells, can proliferate indefinitely through a dysregulated cellular self-renewal capacity. Cancer stem cells may originate due to the distribution into self-renewal and differentiation pathways occurring in multi-potential stem cells, tissue-specific stem cells, progenitor cells and cancer cells. Recent studies have shown that ovarian cancer also contains stem cells or tumor-initiating cells. Moreover, ovarian serous adenocarcinomas were disaggregated and subjected to growth conditions to select for self-renewing, non-adherent spheroids previously shown to be derived from tissue stem cells. A recent study showed that epithelial ovarian cancer was derived from a sub population of CD44+, CD117+ and CD133+ cells. The existence of cancer stem cells would explain why only a small minority of cancer cells is capable of extensive proliferation of the tumor. In this review, we have discussed the studies on ovarian cancer stem cells along with the molecular pathways that could be involved in these cancer stem cells.

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Figures

Figure 1
Figure 1
Origin of cancer stem cells. Self-renewal and differentiation potentials are the features of stem cells. Progenitor cells, the product of stem cells that lose the activity of self-renewal, could differentiate into mature cells, which have the feature of differentiation. The hypothesis is that cancer stem cells are caused by transforming mutations occurring in multi-potential stem cells, tissue-specific stem cells, progenitor cells, mature cells, and cancer cells.
Figure 2
Figure 2
Schematic diagram of signaling pathways that are involved in normal and cancer stem cell biology. Wnt, Shh and Notch1 pathways have been shown to contribute to the self-renewal of stem cells and/or progenitors in a variety of organs, including the ovarian system. When deregulated, these pathways can contribute to oncogenesis. Mutations of these pathways have been associated with a number of carcinomas.
Figure 3
Figure 3
Schematic diagram representing the histological types and its specific mutations in ovarian carcinoma.
See this image and copyright information in PMC

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