Abstract
Ovarian cancer is the most lethal gynecological malignancy. Poor overall survival, particularly for patients with high grade serous (HGS) ovarian cancer, is often attributed to late stage at diagnosis and relapse following chemotherapy. HGS ovarian cancer is a heterogenous disease in that few genes are consistently mutated between patients. Additionally, HGS ovarian cancer is characterized by high genomic instability. For these reasons, personalized approaches may be necessary for effective treatment and cure. Understanding the molecular mechanisms that contribute to tumor metastasis and chemoresistance are essential to improve survival rates. One favored model for tumor metastasis and chemoresistance is the cancer stem cell (CSC) model. CSCs are cells with enhanced self-renewal properties that are enriched following chemotherapy. Elimination of this cell population is thought to be a mechanism to increase therapeutic response. Therefore, accurate identification of stem cell populations that are most clinically relevant is necessary. While many CSC identifiers (ALDH, OCT4, CD133, and side population) have been established, it is still not clear which population(s) will be most beneficial to target in patients. Therefore, there is a critical need to characterize CSCs with reliable markers and find their weaknesses that will make the CSCs amenable to therapy. Many signaling pathways are implicated for their roles in CSC initiation and maintenance. Therapeutically targeting pathways needed for CSC initiation or maintenance may be an effective way of treating HGS ovarian cancer patients. In conclusion, the prognosis for HGS ovarian cancer may be improved by combining CSC phenotyping with targeted therapies for pathways involved in CSC maintenance.
Highlights
In the United States, ovarian cancer is the fifth leading cause of cancer death in women [1].The American Cancer Society (ACS) estimates that this year approximately 22,240 women will be newly diagnosed with ovarian cancer, and ~14,075 women will die as a result of the disease, making it the most lethal gynecologic malignancy (ACS Facts and Figures 2018)
The prognosis for high grade serous (HGS) ovarian cancer may be improved by combining CSC phenotyping with targeted therapies for pathways involved in Keywords: ovarian cancer; cancer stem cells; signaling; chemoresistance; metastasis
We will discuss how CSC properties contribute to chemoresistance and how investigating these properties may lead to novel therapeutics to eliminate ovarian cancer and prevent relapse
Summary
In the United States, ovarian cancer is the fifth leading cause of cancer death in women [1]. Mutational and gene expression heterogeneity is found in different subpopulations within a single tumor. The lack of consistent mutations or mis-expressed genes makes developing novel targeted therapeutics difficult. The presence of microscopic tumors left behind during surgical debulking and the limitations of current chemotherapeutics contribute to the likelihood of relapse. The presence or enrichment of cancer stem cells (CSCs), which are defined as tumor cells that survive and/or accumulate after chemotherapy, have activation of self-renewing signaling pathways, and exhibit increased tumor-initiating properties, may contribute to relapse [11,12,13]. We will discuss how CSC properties contribute to chemoresistance and how investigating these properties may lead to novel therapeutics to eliminate ovarian cancer and prevent relapse
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