Cancer Growth and Metastasis 2013:6 15-21
Perspective
Published on 18 Feb 2013
DOI: 10.4137/CGM.S11333
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The high mortality rate caused by ovarian cancer has not changed for the past thirty years. Although most patients diagnosed with this disease respond to cytoreductive surgery and platinum-based chemotherapy and undergo remission, foci of cells almost always escape therapy, manage to survive, and acquire the capacity to repopulate the tumor. Repopulation of ovarian cancer cells that escape front-line chemotherapy, however, is a poorly understood phenomenon. Here I analyze cancer-initiating cells, transitory senescence, reverse ploidy, and cellular dormancy as putative players in ovarian cancer cell repopulation. As part of the standard of care, ovarian cancer patients do not receive treatment between primary cytotoxic therapy and clinical relapse. Understanding the mechanisms driving cellular escape from chemotherapy should lead to the development of low toxicity, chronic treatment approaches that can be initiated right after primary therapy to interrupt cell repopulation and disease relapse by keeping it dormant and, therefore, subclinical.
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