Journal article
Inhibition of the JAK2/STAT3 pathway in ovarian cancer results in the loss of cancer stem cell-like characteristics and a reduced tumor burden
K Abubaker, RB Luwor, H Zhu, O McNally, MA Quinn, CJ Burns, EW Thompson, JK Findlay, N Ahmed
BMC Cancer | Published : 2014
Abstract
Background: Current treatment of ovarian cancer patients with chemotherapy leaves behind a residual tumor which results in recurrent ovarian cancer within a short time frame. We have previously demonstrated that a single short-term treatment of ovarian cancer cells with chemotherapy in vitro resulted in a cancer stem cell (CSC)-like enriched residual population which generated significantly greater tumor burden compared to the tumor burden generated by control untreated cells. In this report we looked at the mechanisms of the enrichment of CSC-like residual cells in response to paclitaxel treatment.Methods: The mechanism of survival of paclitaxel-treated residual cells at a growth inhibitory..
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Awarded by Foundation for Women's Cancer
Funding Acknowledgements
The authors wish to thank Royal Women's Hospital Foundation, Women's Cancer Foundation, National Health and Medical Research Council of Australia (JKF, RegKey#441101) and the Victorian Government's Operational Infrastructure Support Program and National Breast Cancer Foundation (EWT) for supporting this work. KA is the recipient of Australian Postgraduate Award. RBL is a recipient of the Melbourne Brain Centre Post-Doctoral Research Fellowship from the University of Melbourne. The authors also wish to acknowledge the help of Dr Simon Nazaretian, Anatomical Pathology, and Royal Women's Hospital for the histological assessment of mouse xenografts.