bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract AP14: THERAPEUTIC TARGETING USING TUMOR SPECIFIC PEPTIDES INHIBITS LONG NON–CODING RNA HOTAIR ONCOGENIC ACTIVITY IN OVARIAN CANCER
Authors: Özeş Ali R. , Wang Yinu , Fang Fang , Nephew Kenneth P. 
Published: June 2017

Abstract
PURPOSE: Most women diagnosed with advanced-stage ovarian cancer develop chemo-resistant tumor recurrence, which is uniformly fatal. Long non-coding RNAs (lncRNAs) play key roles in human diseases, including cancer. Functional studies of the lncRNA HOTAIR (HOX transcript antisense RNA) provide compelling evidence for therapeutic targeting of HOTAIR in ovarian cancer to impact chemoresistance, but targeting lncRNAs in vivo has proven to be difficult.
EXPERIMENTAL DESIGN: In the current study, we describe a peptide nucleic acids (PNA)-based approach to effectively block the ability of HOTAIR to interact with EZH2 and subsequently inhibit oncogenic HOTAIR-EZH2 activity. In order to deliver the anti-lncRNA to the acidic (pH approximately 6) microenvironment of solid tumors in vivo, PNAs were conjugated to pH-low insertion peptide (pHLIP).
RESULTS: Treatment of HOTAIR-overexpressing ovarian cancer cell lines with PNAs decreased cancer cell invasion and increased chemotherapy sensitivity. The mechanism of action of the anti-lncRNA agent correlated with reduced nuclear factor-kappaB (NF-κB) activation and decreased expression of key NF-κB target genes including matrix metalloprotease 9 and interleukin 6. PNA treatment of ALDH1A1 positive/ovarian tumor initiating cells overexpressing HOTAIR markedly decreased ALDH1A1 activity and reduced the ovarian cancer stem cell population. In mice harboring ovarian tumor xerographs and treated with pHLIP-PNA constructs, HOTAIR oncogenic activity was suppressed, ovarian tumors were resensitized to platinum, and a significant (64%) survival improvement was observed.
CONCLUSIONS: Toward developing new therapeutic approaches against chemoresistant ovarian cancer, we designed a PNA-targeting strategy for HOTAIR that effectively blocks the ability of HOTAIR to interact with EZH2 and inhibits oncogenic HOTAIR-EZH2. This first report on pHLIP-PNA targeting HOTAIR in vivo offer pre-clinical proof-of-concept and represents a possible treatment alternative for chemotherapy-resistant ovarian cancer.
Citation Format: Ali R. Özeş, Yinu Wang, Fang Fang, and Kenneth P. Nephew. THERAPEUTIC TARGETING USING TUMOR SPECIFIC PEPTIDES INHIBITS LONG NON–CODING RNA HOTAIR ONCOGENIC ACTIVITY IN OVARIAN CANCER [abstract]. In: Proceedings of the 11th Biennial Ovarian Cancer Research Symposium; Sep 12-13, 2016; Seattle, WA. Philadelphia (PA): AACR; Clin Cancer Res 2017;23(11 Suppl):Abstract nr AP14.
Abstract AP21: LIPID DESATURATION IS A METABOLIC MARKER AND THERAPEUTIC TARGET OF OVARIAN CANCER STEM CELLS
Authors: Li Junjie , Condello Salvatore , Thomes-Pepin Jessica , Ma Xiaoxiao , Xia Yu , Hurley Thomas D. , Cheng Ji-Xin , Matei Daniela 
Published: June 2017

Abstract
OBJECTIVES: Lack of sensitive single-cell analysis tools has limited the characterization of the metabolic activity of cancer stem cells (CSCs). The objectives of this study were to identify and target metabolic pathways specifically deregulated in ovarian CSCs.
METHODS: We developed a new technique based on hyperspectral stimulated Raman scattering imaging of single living cells coupled with electrospray ionization mass spectrometry (ESI-MS) analysis of extracted lipids to identify unique metabolic spectra of ovarian CSCs. SiRNA knockdown and pharmacological inhibitors were used to block fatty acid desaturases and to measure effects on the ovarian CSCs charcateristics.
RESULTS: We report significantly increased levels of unsaturated lipids in flow-sorted ovarian CSCs (ALDH+CD133+) compared to non-CSCs (ALDH-CD133-). Higher lipid unsaturation levels were also detected in CSC-enriched spheroids compared to monolayer cultures of ovarian cancer cell lines or primary cells derived from human ovarian tumors. ESI-MS identified that the elevated unsaturation in lipid droplets involved an enhanced conversion from saturated fatty acids (18:0) to unsaturated fatty acids (18:1). Expression of fatty acid desaturases was increased in ovarian CSCs compared to non-CSCs. Pharmacological inhibition or siRNA knockdown of lipid desaturases Δ9 (SCD1) or Δ6 effectively eliminated CSCs, suppressed sphere formation in vitro, and blocked tumor initiation capacity in vivo, as measured by a tumor initiation dilution assay. Mechanistically, the lipid desaturase inhibitors suppressed ovarian cancer cell stemness by blocking the NF-κB survival pathway. Chromatin immunoprecipitation and overexpression of RelA demonstrated that NF-κB transcriptionally regulates SCD1 expression. Collectively, our data suggest that a positive feedback loop involving lipid desaturases, NF-κB, and the stem cell marker ALDH1 can be effectively blocked by SCD1 inhibitors, suppressing ovarian CSCs.
CONCLUSIONS: These results demonstrate that increased lipid unsaturation is a novel metabolic marker for ovarian CSCs and a target for CSC-specific therapy.
Citation Format: Junjie Li, Salvatore Condello, Jessica Thomes-Pepin, Xiaoxiao Ma, Yu Xia, Thomas D. Hurley, Ji-Xin Cheng, Daniela Matei. LIPID DESATURATION IS A METABOLIC MARKER AND THERAPEUTIC TARGET OF OVARIAN CANCER STEM CELLS [abstract]. In: Proceedings of the 11th Biennial Ovarian Cancer Research Symposium; Sep 12-13, 2016; Seattle, WA. Philadelphia (PA): AACR; Clin Cancer Res 2017;23(11 Suppl):Abstract nr AP21.
Abstract KP01: UNITED KINGDOM COLLABORATIVE TRIAL OF OVARIAN CANCER SCREENING – (UKCTOCS) – EXPLORING THE RESULTS
Authors: Menon Usha 
Published: June 2017

Abstract
The continued high case fatality ratio in ovarian cancer has underpinned efforts to develop a screening strategy that could impact on mortality. In the general population randomised control trial - United Kingdom Collaborative Trial of Ovarian Cancer Screening (UKCTOCS) two screening strategies (multimodal MMS and ultrasound USS) were compared to no screening (control C). Of 202,638 women randomised between April 2001-October 2005, 50,624 MMS; 50,623 USS; and 101,299 C were eligible for analysis. By the end of screening (December 2011) 345,570 MMS and 327,775 USS annual screens were performed. At censorship for the initial mortality analysis on 31st December 2014, there was an overall significant stage shift in invasive epithelial ovarian/tubal/peritoneal cancer in the MMS group compared to C in an ‘intention to screen’ analysis. More detailed analysis has shown this stage shift seen in the MMS group was limited to Type II (high grade serous) ovarian cancers. This was associated with a delayed but not yet statistically significant mortality reduction. Disease specific mortality rates in the C arm were continuing to rise while they appeared to have plateaued in the screen arms. Further follow-up is now underway to confirm the mortality reduction and determine its full extent. Meanwhile a focus on detecting low volume disease using cancer specific markers, novel biospecimens such as endocervical samples, targeted imaging and time series algorithms for interpreting marker profile suggest that a new era in ovarian cancer screening is underway.
Citation Format: Usha Menon. UNITED KINGDOM COLLABORATIVE TRIAL OF OVARIAN CANCER SCREENING – (UKCTOCS) – EXPLORING THE RESULTS [abstract]. In: Proceedings of the 11th Biennial Ovarian Cancer Research Symposium; Sep 12-13, 2016; Seattle, WA. Philadelphia (PA): AACR; Clin Cancer Res 2017;23(11 Suppl):Abstract nr KP01.
Abstract KP03: NOVEL IMMUNOTHERAPEUTICS FOR OVARIAN CANCER
Authors: Disis Mary L. 
Published: June 2017

Abstract
In the last decade we have seen significance advances in the understanding of how the immune system modulates the ovarian tumor microenvironment and cancer growth. A number of studies have shown that high levels of tumor infiltrating adaptive immune system cells (B-cells and T-cells) found in ovarian cancer are associated with a favorable prognosis, especially if there is evidence of reduced regulatory T-cells. Robust T-cell tumor infiltration (TIL) is associated with PD-L1 upregulation. Almost half of ovarian cancers demonstrate enhanced PD-L1 expression on tumor cells and/or tumor infiltrating immune system cells. Immune checkpoint inhibitor monoclonal antibodies block receptors such as PD-1 and PD-L1 which suppress T-cell function. The largest study of immune checkpoint inhibition in ovarian cancer evaluated the blockade of PD-L1 using avelumab. In this phase I/II study 124 patients with recurrent disease, considered chemotherapy refractory, were treated with 10mg/kg avelumab every 2 weeks (65% of patients with 3 or greater salvage regimens). The overall response rate was 10% with a stable disease rate of 44% resulting in a disease control rate of 54%. Overall survival at 12 months was 44%. Clinical response did not correlate with either PDL-1 expression on tumor or immune infiltrating cells or BRCA mutation status. A randomized trial of avelumab in combination with pegylated liposomal doxorubicin in cisplatin refractory ovarian cancer has been initiated. Pre-clinical studies have shown that clinical responses to immune checkpoint inhibitor therapy in ovarian cancer may be enhanced by increasing Type I T-cell infiltration concurrent with therapy. Clinical strategies aimed at increasing TIL include the use of vaccines immunizing against ovarian cancer antigens to stimulate T-cells trafficking to tumor. Specific chemotherapy may result in increased TIL as some cytotoxic agents have been shown to modulate both the level and phenotype of TIL in ovarian cancer. An alternate approach is to suppress alternate pathways of tumor immune escape such as depletion of macrophage or inhibition of the IDO pathway to enhance immune activation. Several promising combination immunotherapy strategies are currently being evaluated in ovarian cancer.
Citation Format: Mary L. Disis, MD. NOVEL IMMUNOTHERAPEUTICS FOR OVARIAN CANCER [abstract]. In: Proceedings of the 11th Biennial Ovarian Cancer Research Symposium; Sep 12-13, 2016; Seattle, WA. Philadelphia (PA): AACR; Clin Cancer Res 2017;23(11 Suppl):Abstract nr KP03.
Abstract MIP-047: INHIBITION OF POLY ADP–RIBOSE POLYMERASE (PARP) IN OVARIAN CANCER CELLS ENRICHES FOR CD133 AND CD117 POSITIVE POPULATIONS
Authors: Bellio Chiara , Foster Rosemary , Growdon Whitfield B. , Konstantinopoulos Panagiotis , Rueda Bo R. 
Published: June 2017

Abstract
Keywords: chemoresistance, cancer stem cells (CSC), DNA repair pathways, PARP inhibition
INTRODUCTION: Ovarian cancer (OvCa) is the most lethal gynecologic malignancy as women commonly present with metastatic disease that ultimately develops chemotherapy resistance. The development of OvCa has been linked to alterations in DNA repair pathways and the poly (adenosine diphosphate [ADP]–ribose) polymerase (PARP) inhibitor olaparib has demonstrated antitumor activity and is an FDA approved monotherapy for the treatment of recurrent OvCa in patients with a germline BRCA mutations. Despite promising response rates, not all patients derive benefit, and the majority develop resistance to this therapy that is poorly understood. We hypothesized that ultimate resistance to olaparib is in part mediated by small populations of cancer stem cells (CSCs) that are unaffected by olaparib therapy and may promote tumor resurgence.
METHODS: UWB1.289 (BRCA1 mutated), UWB1.289 (WT), OVCAR4 (WT), and OVCAR3 (WT) cell lines and primary cell lines derived from serous OvCa obtained with IRB approval were treated in vitro with 0.1 μM, 1 μM and 10 μM olaparib for 7 days. We assessed cell viability and CSC marker expression (CD133 and CD117) via flow cytometric analysis, and sphere forming capacity via extreme limiting dilution assay (ELDA).
RESULTS: Consecutive treatment over 7 days with olaparib decreased the viability of the non–sorted tumor cell population relative to the vehicle control treated cells. Despite the decrease in total cell number, the relative frequency of CD133+ and CD117+ cells increased (all lines p &lt;0.05) in response to treatment with olaparib. This shift was not observed in vehicle treated cells. The increase in CD133+ and CD117+ cell frequency in response to olaparib was not different in the BRCA1 mutant line when compared to the BRCA1 wild type lines. ELDA revealed an increase in the frequency of sphere formation following olaparib treatment relative to that observed with vehicle treated cells, though mutation status did not impact this frequency.
CONCLUSIONS: These results suggest that olaparib may enrich for CSC populations that could contribute to resistance and recurrence. These data expose a potential resistance mechanism to olaparib therapy that is in part independent of BRCA mutation status.
Citation Format: Chiara Bellio, Rosemary Foster, Whitfield B. Growdon Panagiotis Konstantinopoulos, and Bo R. Rueda. INHIBITION OF POLY ADP–RIBOSE POLYMERASE (PARP) IN OVARIAN CANCER CELLS ENRICHES FOR CD133 AND CD117 POSITIVE POPULATIONS [abstract]. In: Proceedings of the 11th Biennial Ovarian Cancer Research Symposium; Sep 12-13, 2016; Seattle, WA. Philadelphia (PA): AACR; Clin Cancer Res 2017;23(11 Suppl):Abstract nr MIP-047.
Abstract NTOC-101: INTRAPERITONEAL (IP) THERAPY FOR ADVANCED STAGE EPITHELIAL OVARIAN CANCER (EOC): THE CURRENT SPOTLIGHT IS ON CARBOPLATIN AND QUALITY OF LIFE
Authors: Muggia Franco , Wenzel Lari 
Published: June 2017

Abstract
PURPOSE: First-line treatments for (EOC) have been platinum-based for more than three decades; 16 years ago the landmark Gynecologic Oncology Group (GOG158) non-inferiority trial for optimal stage III patients led to the universal adoption of IV carboplatin/paclitaxel as the standard systemic regimen. However, IV cisplatin-based doublets were the comparators in the first 3 GOG studies assessing IP cisplatin-based regimens. Our purpose is to describe recent randomized trials that have assessed IP carboplatin and highlight quality of life (QOL) findings.
METHODS: Gynecology Oncology Group (GOG) studies comparing IP to IV cisplatin regimens formed the basis of the National Cancer Institute (NCI) 2005 Clinical Announcement that considered IP cisplatin-based therapy as a new standard for optimally debulked EOC. Recently, randomized trials with IV carboplatin/paclitaxel-based regimens as comparators have been part of preliminary reports: 1) GOG252 on March 2016 at the Society of Gynecologic Oncology (SGO), completing accrual in 2015, and 2) OV21/PETROC neoadjuvant randomized ‘pick the winner’ study at the June 2016 American Society of Clinical Oncology (ASCO). Beyond 2016, additional data is expected from the ongoing randomized study by the Japan GOG of IP versus IV carboplatin, --both with IV paclitaxel.
RESULTS: GOG252, the largest Phase III study of IV versus IP platinum-based therapy for the first line treatment of ovarian cancer, is the first IP GOG trial with a IV carboplatin-based control arm. None of the 3 arms differed in median progression-free survival. However, the companion QOL study, --contrary to prior GOG studies utilizing IV cisplatin-based controls—showed a clear advantage for the two non-cisplatin arms (not different whether IV or IP). In the OV21/PETROC trial, adverse toxicities coupled with no obvious therapeutic advantage led to dropping the IP cisplatin arm. With additional accrual in the two remaining arms, IP carboplatin was superior to IV carboplatin in time to progression.
CONCLUSIONS: Cisplatin has an unfavorable impact on QOL in women with ovarian cancer whether given IP or IV relative to carboplatin. With IV carboplatin as part of the comparator, unfavorable effects of cisplatin-based chemotherapy are further highlighted. IP carboplatin randomized studies and their final publications are awaited. On the other hand, revisiting the role of IP cisplatin at this time is not warranted.
Citation Format: Franco Muggia MD, Lari Wenzel, PhD. INTRAPERITONEAL (IP) THERAPY FOR ADVANCED STAGE EPITHELIAL OVARIAN CANCER (EOC): THE CURRENT SPOTLIGHT IS ON CARBOPLATIN AND QUALITY OF LIFE [abstract]. In: Proceedings of the 11th Biennial Ovarian Cancer Research Symposium; Sep 12-13, 2016; Seattle, WA. Philadelphia (PA): AACR; Clin Cancer Res 2017;23(11 Suppl):Abstract nr NTOC-101.
Abstract NTOC-105: RUXOLITINIB SENSITIZES OVARIAN CANCER CELLS TO LOW–DOSE PACLITAXEL THERAPY
Authors: Reeves Patrick , Abbaslou Mojgan , Poznansky Mark C. 
Published: June 2017

Abstract
In ovarian cancer chemotherapy initially reduces tumor burden; however, &gt;70% of patients experience tumor recurrence, creating a need for additional therapies. We evaluated the ability of Ruxolitinib, a FDA approved JAK 1/2 kinase inhibitor, as a potential adjunctive therapy for paclitaxel treatment of ovarian cancer. Using murine ID8 and human TOV-112D ovarian cancer cells we tested the ability of Ruxolitinib alone and in combination with low-dose paclitaxel to limit cell proliferation and colony formation in vitro. Additionally, using flow cytometry we assessed the capacity of paclitaxel to induce the expression of cell surface markers associated with stemness and the cellular stress response. We next determined if Ruxolitinib could reduce paclitaxel-induced expression of stemness and stress markers. Finally daily administration of Ruxolitinib, both alone and in combination with a single low-dose administration of paclitaxel, was tested for the capacity to reduce tumor growth and extend survival using the syngeneic ID8 luciferase-expressing model of ovarian cancer in C57Bl/6 mice.
Our in vitro data demonstrate that Ruxolitinib can sensitize both murine ID8 and human TOV-112D cells to low concentrations of paclitaxel, as evidenced by a significant reduction of cell proliferation and colony formation. We find that pre-incubation with Ruxolitinib is sufficient to sensitize cells to subsequent incubation with paclitaxel. Paclitaxel-induced expression of stemness and stress markers (SCA-1, GRP78 and CD133) is reduced by co-incubation with Ruxolitinib. In vivo, Ruxolitinib plus administration of a single low-dose paclitaxel treatment is sufficient to limit tumor growth and significantly extend median survival from in mice bearing ID8 ovarian cancer tumors (Control 59days vs Ruxolitinib-paclitaxel 77 days).
Together, these data indicate that Ruxolitinib can increase the susceptibility of both murine and human ovarian cancer cells to reduced concentrations paclitaxel chemotherapy in vitro and that combination therapy with Ruxolitinib and a single low-dose paclitaxel administration extends survival in mice. Our data provide important pre-clinical data to support the use of Ruxolitinib to enhance the efficacy of paclitaxel therapy for patients with ovarian cancer.
Citation Format: Patrick Reeves PhD, Mojgan Abbaslou MD, Mark C. Poznansky MD PHD. RUXOLITINIB SENSITIZES OVARIAN CANCER CELLS TO LOW–DOSE PACLITAXEL THERAPY [abstract]. In: Proceedings of the 11th Biennial Ovarian Cancer Research Symposium; Sep 12-13, 2016; Seattle, WA. Philadelphia (PA): AACR; Clin Cancer Res 2017;23(11 Suppl):Abstract nr NTOC-105.
Abstract NTOC-113: TGF–β SIGNALING INHIBITION AS A POTENTIAL APPROACH TO TARGET SUBOPTIMALLY DEBULKED OVARIAN TUMORS
Authors: Wei Wei , Birrer Michael J. 
Published: June 2017

Abstract
The current standard of care for all patients with high-grade, advanced-stage serous ovarian cancer is surgery followed by adjuvant chemotherapy. Resection of all visible residual disease to less than 1 cm is associated with a favorable prognosis, but this optimal debulking can only be achieved in ~70% of patients. Patients with suboptimal cytoreduction are presumed to have lower response rates to subsequent chemotherapy and are known to have a poor prognosis.
Recently, we performed a meta-analysis of 1,525 publicly available expression profiling assays and identified a 200-gene expression signature of primary ovarian tumors to predict the outcome of debulking surgery. The signature was validated using two independent sets of tumors. This debulking signature consists of transcripts positively regulated by TGF-β, indicating that hyperactivation of TGF-β signaling may be responsible of the aggressive biological and clinical behavior of suboptimally debulked tumors.
In this study, we evaluated the potential anti-tumor effect of TGF-β signaling blockade in ovarian cancer cells in vitro and in vivo. Integrated TGF-β signaling was observed in 8 of 10 ovarian cancer cell lines tested by a SMAD-binding element based luciferase assay. The potential anti-tumor effect of a small molecular TGFBR1 kinase inhibitor LY2157299 was further investigated in SKOV3 cell line, which presents both endogenous and inducible TGF-β signaling and is highly disseminative when inoculated into immunodeficient mice. Although imposing minimal effect on in vitro cellular proliferation, LY2157299 significantly inhibited tumor-dissemination related biological processes in SKOV3 cells including migration, invasion and mesothelial cell adhesion. In an interperitoneal SKOV3 xenograft model, administration of LY2157299 significantly increased cisplatin related cytotoxicity and tumor burden reduction. Taken together, our study has provided evidence for the potential clinical use of LY2157299 to improve the treatment and survival of women with suboptimal surgery.
Citation Format: Wei Wei and Michael J. Birrer. TGF–β SIGNALING INHIBITION AS A POTENTIAL APPROACH TO TARGET SUBOPTIMALLY DEBULKED OVARIAN TUMORS [abstract]. In: Proceedings of the 11th Biennial Ovarian Cancer Research Symposium; Sep 12-13, 2016; Seattle, WA. Philadelphia (PA): AACR; Clin Cancer Res 2017;23(11 Suppl):Abstract nr NTOC-113.
Abstract TMEM-027: TARGETING RGNEF (P190RHOGEF/ARHGEF28) IMPAIRS OVARIAN TUMOR INITIATION AND PROGRESSION
Authors: Kleinschmidt Elizabeth G. , Miller Nichol L.G. , Tancioni Isabelle , Connolly Denise C. , Schlaepfer David D. 
Published: June 2017

Abstract
Rho GTPase regulatory and integrin signaling pathways are associated with poor high-grade serous ovarian carcinoma (HGSOC) patient survival1. Focal adhesion kinase (FAK) transmits signals from integrins and promotes HGSOC tumor progression through mechanisms involving tumor-stromal cell interactions2. We previously found that the Rho guanine nucleotide exchange factor Rgnef (also named p190RhoGEF or Arhgef28) activates FAK as well as RhoA GTPase activity in mouse fibroblasts3. Here we find that Rgnef protein expression is elevated in Stage 3-4 HGSOC and that Rgnef knockout prevents spontaneous ovarian tumor formation in the MISIIR-T-antigen (TAg) induced C57BL/6 mouse model. At 17 weeks, Rgnef-/-;TAg ovarian tumors were significantly smaller (p&lt;0.001) than Rgnef+/+;TAg controls. Primary Rgnef-/-;TAg and Rgnef+/+;TAg tumor cells were isolated and expanded ex vivo. Although loss of Rgnef did not alter growth as 3D spheroids, Rgnef-/-;TAg orthotopic (ovarian bursa) and intraperitoneal tumors were significantly smaller (p&lt;0.01) than Rgnef+/+;TAg tumors in MISIIR-TAg-Low C57BL/6 syngeneic mice. Notably, FAK activation (as measured by FAK Y397 phosphorylation) was decreased in Rgnef-/-;TAg ascites-associated tumor cells. Together, these studies show that Rgnef loss impedes tumor growth independently of stromal Rgnef status and supports the notion that an Rgnef-FAK signaling linkage facilitates ovarian tumor initiation and progression.
1.Zhang, H., et al. Integrated Proteogenomic Characterization of Human High-Grade Serous Ovarian Cancer. Cell 166 (2016).
2.Sulzmaier, F.J., Jean, C. & Schlaepfer, D.D. FAK in cancer: mechanistic findings and clinical applications. Nat. Rev. Cancer 14, 598-610 (2014).
3.Miller, N.L., et al. A non-canonical role for Rgnef in promoting integrin-stimulated focal adhesion kinase activation. J. Cell Sci. 126, 5074-5085 (2013).
Citation Format: Elizabeth G. Kleinschmidt, Nichol L.G. Miller, Isabelle Tancioni, Denise C. Connolly, David D. Schlaepfer. TARGETING RGNEF (P190RHOGEF/ARHGEF28) IMPAIRS OVARIAN TUMOR INITIATION AND PROGRESSION [abstract]. In: Proceedings of the 11th Biennial Ovarian Cancer Research Symposium; Sep 12-13, 2016; Seattle, WA. Philadelphia (PA): AACR; Clin Cancer Res 2017;23(11 Suppl):Abstract nr TMEM-027.