Ovarian tumor initiating cell populations persist following paclitaxel and carboplatin chemotherapy treatment in vivo

Kulkarni-Datar, Kashmira; Oršulić, Sandra; Foster, Rosemary; Rueda, Bo R.

doi:10.1016/j.canlet.2013.06.014

Cited by 26 publications

(31 citation statements)

References 57 publications

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“…Chemotherapy resistance is another feature commonly associated with TICs (11,28–30). We first verified that TIC culture conditions enriched for cells with carboplatin resistance by measuring viability across a range of concentrations in ACI23 and OV90 cells (Figure 5A).…”

Section: Resultsmentioning

confidence: 99%

NFκB Promotes Ovarian Tumorigenesis via Classical Pathways That Support Proliferative Cancer Cells and Alternative Pathways That Support ALDH+ Cancer Stem–like Cells

et al. 2017

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Understanding the mechanisms supporting tumor-initiating cells (TIC) is vital to combat advanced stage recurrent cancers. Here we show that in advanced ovarian cancers NF-kB signaling via the RelB transcription factor supports TIC populations by directly regulating the cancer stem-like associated enzyme aldehyde dehydrogenase (ALDH). Loss of RelB significantly inhibited spheroid formation, ALDH expression and activity, chemoresistance, and tumorigenesis in subcutaneous and intrabursal mouse xenograft models of human ovarian cancer. RelB also affected expression of the ALDH gene ALDH1A2. Interestingly, classical NF-kB signaling through the RelA transcription factor was equally important for tumorigenesis in the intrabursal model, but had no effect on ALDH. In this case, classical signaling via RelA was essential for proliferating cells, whereas the alternative signaling pathway was not. Our results show how NF-kB sustains diverse cancer phenotypes via distinct classical and alternative signaling pathways, with implications for improved understanding of disease recurrence and therapeutic response.

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Section: Resultsmentioning

confidence: 99%

NFκB Promotes Ovarian Tumorigenesis via Classical Pathways That Support Proliferative Cancer Cells and Alternative Pathways That Support ALDH+ Cancer Stem–like Cells

et al. 2017

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“…Likewise, the size of CD133 expressing subpopulations within individual EOC samples shows high variability with ranges of !15% (Baba et al 2009, Kryczek et al 2012 to as much as 92% (Stewart et al 2011). While one study described enhanced tumourigenicity in clonal spheroid lines which lacked CD133 expression (Kusumbe et al 2009), most other studies have shown, albeit inconsistently, an association of CD133-expressing cells and tumourigenic potential (Curley et al 2009, Silva et al 2011, Stewart et al 2011, Kryczek et al 2012, Kulkarni-Datar et al 2013.…”

Section: Cd133mentioning

confidence: 99%

“…Similarly, CD133 combined with the murine stem cell marker LY6A defined a tumourigenic subpopulation of a murine EOC cell line (Kulkarni-Datar et al 2013). The role of CD133 alone in defining enriched populations of CSC has also been examined in primary human tumour/ascites cells (Stewart et al 2011) and primary human tumour cells passaged in NOD/ SCID xenografts (Curley et al 2009).…”

Section: Cd133mentioning

confidence: 99%

Epithelial ovarian cancer stem cells: underlying complexity of a simple paradigm

Garson¹,

Vanderhyden²

2015

Reproduction

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The lack of significant progress in the treatment of epithelial ovarian cancer (EOC) underscores the need to gain a better understanding of the processes that lead to chemoresistance and recurrence. The cancer stem cell (CSC) hypothesis offers an attractive explanation of how a subpopulation of cells within a patient's tumour might remain refractory to treatment and subsequently form the basis of recurrent chemoresistant disease. This review examines the literature defining somatic stem cells of the ovary and fallopian tube, two tissues that give rise to EOC. In addition, considerable research has been reviewed, that has identified subpopulations of EOC cells, based on marker expression (CD133, CD44, CD117, CD24, epithelial cell adhesion molecule, LY6A, ALDH1 and side population (SP)), which are enriched for tumour initiating cells (TICs). While many studies identified either CD133 or CD44 as markers useful for enriching for TICs, there is little consensus. This suggests that EOC cells may have a phenotypic plasticity that may preclude the identification of universal markers defining a CSC. The assay that forms the basis of quantifying TICs is the xenograft assay. Considerable controversy surrounds the xenograft assay and it is essential that some of the potential limitations be examined in this review. Highlighting such limitations or weaknesses is required to properly evaluate data and broaden our interpretation of potential mechanisms that might be contributing to the pathogenesis of ovarian cancer.

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“…Kulkarni-Datar showed that CD133/Sca-1 cells persist in tumors treated with carboplatin and paclitaxel treatment, and maintain their tumor-initiating properties (34). Steg et al measured expression of stem cell markers in a cohort of matched primary and recurrent tumor patient samples, on the premise that if CSCs are an important population to target, they should represent a denser population within recurrent chemoresistant tumors (35).…”

Section: Clinical Significance Of Cancer Stem Cellsmentioning

confidence: 99%

Ovarian cancer stem cells: Are they real and why are they important?

Shah

Landen

2014

Gynecologic Oncology

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The cancer stem cell hypothesis has been put forward as a paradigm to describe varying levels of aggressiveness in heterogeneous tumors. Specifically, many subpopulations have been clearly demonstrated to possess increased tumorigenicity in mice, broad differentiating capacity, and resistance to therapy. However, it is still not clear the extent to which these experimental findings are potentially clinically significant. This review will describe the principles of this emerging hypothesis, ways in which it may be appropriate in ovarian cancer based on the clinical course of the disease, and how we might exploit it to improve outcomes in ovarian cancer patients.

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Ovarian tumor initiating cell populations persist following paclitaxel and carboplatin chemotherapy treatment in vivo

Cited by 26 publications

References 57 publications

NFκB Promotes Ovarian Tumorigenesis via Classical Pathways That Support Proliferative Cancer Cells and Alternative Pathways That Support ALDH+ Cancer Stem–like Cells

NFκB Promotes Ovarian Tumorigenesis via Classical Pathways That Support Proliferative Cancer Cells and Alternative Pathways That Support ALDH+ Cancer Stem–like Cells

Epithelial ovarian cancer stem cells: underlying complexity of a simple paradigm

Ovarian cancer stem cells: Are they real and why are they important?

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