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Updated: Jan 24, 2026

In vitro Enrichment of Ovarian Cancer Tumor-initiating Cells
Published on: February 18, 2015
Off to a Bad Start: Cancer Initiation by Pluripotency Regulator PRDM14
Lauren J Tracey1, Monica J Justice1
1Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, ONT, M5G 0A4, Canada; Department of Molecular Genetics, University of Toronto, Toronto, ONT, M5S 1A8, Canada.
Abstract:
Despite advances in chemotherapies that improve cancer survival, most patients who relapse succumb to the disease due to the presence of cancer stem cells (CSCs), which are highly chemoresistant. The pluripotency factor PR domain 14 (PRDM14) has a key role in initiating many types of cancer. Normally, PRDM14 uses epigenetic mechanisms to establish and maintain the pluripotency of embryonic cells, and its role in cancer is similar. This important link between cancer and induced pluripotency is a key revelation for how CSCs may form: pluripotency genes, such as PRDM14, can expand stem-like cells as they promote ongoing DNA damage. PRDM14 and its protein-binding partners, the ETO/CBFA2T family, are ideal candidates for eliminating CSCs from relevant cancers, preventing relapse and improving long-term survival.
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