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Emori, Megan Marie

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Emori

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Megan Marie

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Emori, Megan Marie

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2014 - 20152

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Author's Publications: search.filters.isAuthorOfPublication.523608f8-a952-4a84-953c-d39608d7f03c

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    The hormonal composition of follicular fluid and its implications for ovarian cancer pathogenesis
    (BioMed Central, 2014) Emori, Megan Marie; Drapkin, Ronny
    Ovulation has long been associated with an increased risk in ovarian cancer, yet the underlying molecular mechanisms remain obscure. Two aspects of ovulation have been linked to ovarian cancer pathogenesis. The first is the impact of repetitive tissue injury and repair that occurs with each ovulatory event. The second is the release of follicular fluid that accompanies the follicular rupture and its effect on the ovarian and fallopian tube epithelial cells. Hormones are an important component of follicular fluid, which transiently bathes the ovarian surface and fallopian tube epithelium during ovulation. Much work has been done exploring the role of hormones in fertility, but some, such as estrogen, have also been implicated in the pathogenesis of ovarian and other cancers. Understanding the role of hormones within follicular fluid, as well as how they are altered in disorders which increase ovarian cancer risk, will enhance our ability to assess risk and develop preventative strategies. This review provides an in depth discussion of the logistics of using and studying follicular fluid in ovarian cancer research, and discusses the fluctuations in follicular fluid hormone levels during normal physiological processes versus conditions that increase ovarian cancer risk.
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    Evolving Models of Ovarian Cancer: Defining the Role of PAX8 in Fallopian Tube Tumorigenesis
    (2015-08-07) Emori, Megan Marie; Drapkin, Ronny; Frank, David; McAllister, Sandra; Bass, Adam; Hammond, Paula
    Ovarian cancer is the most deadly gynecological malignancy in the US. Once thought to be a single disease arising from the ovarian surface epithelium, we now understand that it is in fact a heterogenous disease with origins across the female reproductive tract. Ovarian cancers can be broken down into type I and type II tumors. While type I tumors are typically slow growing and arise from the ovary, type II tumors are highly aggressive, particularly the most common and deadliest subtype, High Grade Serous Ovarian Cancer (HGSOC), which arises from the fallopian tube epithelium. While our understanding of the complexity of ovarian cancer has evolved significantly over the last few decades, ovarian cancer is still primarily modeled by a few historical and robust cell lines which poorly recapitulate the genetics of HGSOC patient tumors. Here we characterize less studied cell lines with high genomic fidelity to HGSOC, KURAMOCHI and OVSAHO. Through in vivo xenograft experiments, we determined that these two cell lines form more diffuse tumors which better represent the HGSOC phenotype. In vitro, these lines are tractable to a variety of standard molecular biology techniques, but only express a subset of common markers of HGSOC, including PAX8 and stabilized TP53, while others were absent. These results indicate that it is important to take both molecular and genetic relevance into consideration when selecting cell lines for laboratory studies. PAX8 is a nuclear transcription factor critical to the development of the female reproductive tract, including the fallopian tube, and is conserved in both the adult fallopian tube and HGSOC. Recent studies have identified PAX8 as a differentially expressed, essential gene to ovarian cancer, making it a promising drug target for HGSOC. Here, we identify a subset of ovarian cancers that exhibit decreased proliferation when PAX8 expression is decreased, and determine that in KURAMOCHI cells this defect appears to be driven by cell cycle arrest. We also characterized the similarities and differences of PAX8 DNA binding and gene regulation through ChIPseq and RNAseq, respectively, in the context of the fallopian tube and HGSOC. We determined that while a small subset of PAX8 binding sites are conserved across the fallopian tube and ovarian cancer, there is a significant gain of novel binding sites in ovarian cancer that is unique to each cancer cell line. In contrast, different fallopian tube derived lines have very similar PAX8 binding sites and many of these are uniformly lost in the context of cancer. Understanding how the role of PAX8 changes from the fallopian tube to cancer is an important step to drug development targeting PAX8. Ultimately, this body of research seeks to improve ovarian cancer modeling techniques and to better understand fallopian tube pathogenesis, leading to more effective translation of ovarian cancer research from bench to bedside.