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    An imbalance in progenitor cell populations reflects tumour progression in breast cancer primary culture models

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    Authors
    Donatello, Simona
    Hudson, Lance
    Cottell, David C
    Blanco, Alfonso
    Aurrekoetxea, Igor
    Shelly, Martin J
    Dervan, Peter A
    Kell, Malcolm R
    Stokes, Maurice
    Hill, Arnold DK
    Hopkins, Ann M
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    Issue Date
    2011-04-26
    
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    Citation
    Journal of Experimental & Clinical Cancer Research. 2011 Apr 26;30(1):45
    URI
    http://hdl.handle.net/10147/129536
    Abstract
    Abstract Background Many factors influence breast cancer progression, including the ability of progenitor cells to sustain or increase net tumour cell numbers. Our aim was to define whether alterations in putative progenitor populations could predict clinicopathological factors of prognostic importance for cancer progression. Methods Primary cultures were established from human breast tumour and adjacent non-tumour tissue. Putative progenitor cell populations were isolated based on co-expression or concomitant absence of the epithelial and myoepithelial markers EPCAM and CALLA respectively. Results Significant reductions in cellular senescence were observed in tumour versus non-tumour cultures, accompanied by a stepwise increase in proliferation:senescence ratios. A novel correlation between tumour aggressiveness and an imbalance of putative progenitor subpopulations was also observed. Specifically, an increased double-negative (DN) to double-positive (DP) ratio distinguished aggressive tumours of high grade, estrogen receptor-negativity or HER2-positivity. The DN:DP ratio was also higher in malignant MDA-MB-231 cells relative to non-tumourogenic MCF-10A cells. Ultrastructural analysis of the DN subpopulation in an invasive tumour culture revealed enrichment in lipofuscin bodies, markers of ageing or senescent cells. Conclusions Our results suggest that an imbalance in tumour progenitor subpopulations imbalances the functional relationship between proliferation and senescence, creating a microenvironment favouring tumour progression.
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    Journal Article
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