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1,102 results on '"Drapkin, Ronny"'

2. Norepinephrine induces anoikis resistance in high-grade serous ovarian cancer precursor cells.

Author

Reavis, Hunter, Gysler, Stefan, McKenney, Grace, Knarr, Matthew, Lusk, Hannah, Rawat, Priyanka, Rendulich, Hannah, Mitchell, Marilyn, Berger, Dara, Moon, Jamie, Ryu, Suyeon, Mainigi, Monica, Iwanicki, Marcin, Hoon, Dave, Drapkin, Ronny, and Sanchez, Laura

Subjects
Cancer, Cell biology, Cell migration/adhesion, Obstetrics/gynecology, Oncology, Female, Humans, Ovarian Neoplasms, Cystadenocarcinoma, Serous, Fallopian Tubes, Anoikis, Norepinephrine, Tumor Microenvironment
Abstract

High-grade serous carcinoma (HGSC) is the most lethal gynecological malignancy in the United States. Late diagnosis and the emergence of chemoresistance have prompted studies into how the tumor microenvironment, and more recently tumor innervation, may be leveraged for HGSC prevention and interception. In addition to stess-induced sources, concentrations of the sympathetic neurotransmitter norepinephrine (NE) in the ovary increase during ovulation and after menopause. Importantly, NE exacerbates advanced HGSC progression. However, little is known about the role of NE in early disease pathogenesis. Here, we investigated the role of NE in instigating anchorage independence and micrometastasis of preneoplastic lesions from the fallopian tube epithelium (FTE) to the ovary, an essential step in HGSC onset. We found that in the presence of NE, FTE cell lines were able to survive in ultra-low-attachment (ULA) culture in a β-adrenergic receptor-dependent (β-AR-dependent) manner. Importantly, spheroid formation and cell viability conferred by treatment with physiological sources of NE were abrogated using the β-AR blocker propranolol. We have also identified that NE-mediated anoikis resistance may be attributable to downregulation of colony-stimulating factor 2. These findings provide mechanistic insight and identify targets that may be regulated by ovary-derived NE in early HGSC.

Published
2024

4. Molecular subclasses of clear cell ovarian carcinoma and their impact on disease behavior and outcomes

Author

Bolton, Kelly L, Chen, Denise, de la Fuente, Rosario I Corona, Fu, Zhuxuan, Murali, Rajmohan, K�bel, Martin, Tazi, Yanis, Cunningham, Julie M, Chan, Irenaeus CC, Wiley, Brian J, Moukarzel, Lea A, Winham, Stacey J, Armasu, Sebastian M, Lester, Jenny, Elishaev, Esther, Laslavic, Angela, Kennedy, Catherine J, Piskorz, Anna, Sekowska, Magdalena, Brand, Alison H, Chiew, Yoke-Eng, Pharoah, Paul, Elias, Kevin M, Drapkin, Ronny, Churchman, Michael, Gourley, Charlie, DeFazio, Anna, Karlan, Beth, Brenton, James D, Weigelt, Britta, Anglesio, Michael S, Huntsman, David, Gayther, Simon A, Konner, Jason, Modugno, Francesmary, Lawrenson, Kate, Goode, Ellen L, and Papaemmanuil, Elli

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Women's Health, Human Genome, Genetics, Rare Diseases, Cancer, Biotechnology, Cancer Genomics, Precision Medicine, Clinical Research, 2.1 Biological and endogenous factors, Good Health and Well Being, Female, Humans, Ovarian Neoplasms, Adenocarcinoma, Clear Cell, Mutation, Endometriosis, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

PurposeTo identify molecular subclasses of clear cell ovarian carcinoma (CCOC) and assess their impact on clinical presentation and outcomes.Experimental designWe profiled 421 primary CCOCs that passed quality control using a targeted deep sequencing panel of 163 putative CCOC driver genes and whole transcriptome sequencing of 211 of these tumors. Molecularly defined subgroups were identified and tested for association with clinical characteristics and overall survival.ResultsWe detected a putative somatic driver mutation in at least one candidate gene in 95% (401/421) of CCOC tumors including ARID1A (in 49% of tumors), PIK3CA (49%), TERT (20%), and TP53 (16%). Clustering of cancer driver mutations and RNA expression converged upon two distinct subclasses of CCOC. The first was dominated by ARID1A-mutated tumors with enriched expression of canonical CCOC genes and markers of platinum resistance; the second was largely comprised of tumors with TP53 mutations and enriched for the expression of genes involved in extracellular matrix organization and mesenchymal differentiation. Compared with the ARID1A-mutated group, women with TP53-mutated tumors were more likely to have advanced-stage disease, no antecedent history of endometriosis, and poorer survival, driven by their advanced stage at presentation. In women with ARID1A-mutated tumors, there was a trend toward a lower rate of response to first-line platinum-based therapy.ConclusionsOur study suggests that CCOC consists of two distinct molecular subclasses with distinct clinical presentation and outcomes, with potential relevance to both traditional and experimental therapy responsiveness. See related commentary by Lheureux, p. 4838.

Published
2022

7. LINE-1 ORF1p as a candidate biomarker in high grade serous ovarian carcinoma

Author

Sato, Sho, Gillette, Michael, de Santiago, Pamela R., Kuhn, Eric, Burgess, Michael, Doucette, Kristen, Feng, Yi, Mendez-Dorantes, Carlos, Ippoliti, Paul J., Hobday, Sara, Mitchell, Marilyn A., Doberstein, Kai, Gysler, Stefan M., Hirsch, Michelle S., Schwartz, Lauren, Birrer, Michael J., Skates, Steven J., Burns, Kathleen H., Carr, Steven A., and Drapkin, Ronny

Published
2023
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8. The transcription factor PAX8 promotes angiogenesis in ovarian cancer through interaction with SOX17.

Author

Chaves-Moreira, Daniele, Mitchell, Marilyn, Arruza, Cristina, Rawat, Priyanka, Sidoli, Simone, Nameki, Robbin, Reddy, Jessica, Corona, Rosario, Afeyan, Lena, Klein, Isaac, Ma, Sisi, Winterhoff, Boris, Konecny, Gottfried, Garcia, Benjamin, Brady, Donita, Lawrenson, Kate, Morin, Patrice, and Drapkin, Ronny

Subjects
Animals, Fallopian Tubes, Female, HMGB Proteins, Humans, Mice, Neoplasm Grading, Ovarian Neoplasms, PAX8 Transcription Factor, SOXF Transcription Factors, Transcription Factors
Abstract

PAX8 is a master transcription factor that is essential during embryogenesis and promotes neoplastic growth. It is expressed by the secretory cells lining the female reproductive tract, and its deletion during development results in atresia of reproductive tract organs. Nearly all ovarian carcinomas express PAX8, and its knockdown results in apoptosis of ovarian cancer cells. To explore the role of PAX8 in these tissues, we purified the PAX8 protein complex from nonmalignant fallopian tube cells and high-grade serous ovarian carcinoma cell lines. We found that PAX8 was a member of a large chromatin remodeling complex and preferentially interacted with SOX17, another developmental transcription factor. Depleting either PAX8 or SOX17 from cancer cells altered the expression of factors involved in angiogenesis and functionally disrupted tubule and capillary formation in cell culture and mouse models. PAX8 and SOX17 in ovarian cancer cells promoted the secretion of angiogenic factors by suppressing the expression of SERPINE1, which encodes a proteinase inhibitor with antiangiogenic effects. The findings reveal a non-cell-autonomous function of these transcription factors in regulating angiogenesis in ovarian cancer.

Published
2022

9. DNA Methylation Profiles of Ovarian Clear Cell Carcinoma

Author

Cunningham, Julie M, Winham, Stacey J, Wang, Chen, Weiglt, Britta, Fu, Zhuxuan, Armasu, Sebastian M, McCauley, Bryan M, Brand, Alison H, Chiew, Yoke-Eng, Elishaev, Esther, Gourley, Charlie, Kennedy, Catherine J, Laslavic, Angela, Lester, Jenny, Piskorz, Anna, Sekowska, Magdalena, Brenton, James D, Churchman, Michael, DeFazio, Anna, Drapkin, Ronny, Elias, Kevin M, Huntsman, David G, Karlan, Beth Y, Köbel, Martin, Konner, Jason, Lawrenson, Kate, Papaemmanuil, Elli, Bolton, Kelly L, Modugno, Francesmary, and Goode, Ellen L

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Ovarian Cancer, Rare Diseases, Human Genome, Genetics, 2.1 Biological and endogenous factors, Aetiology, Adenocarcinoma, Clear Cell, Adult, Aged, Aged, 80 and over, Aneuploidy, Class I Phosphatidylinositol 3-Kinases, CpG Islands, DNA Methylation, DNA-Binding Proteins, Disease Progression, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Humans, Middle Aged, Mutation, Neoplasm Staging, Ovarian Neoplasms, Prognosis, Transcription Factors, Tumor Suppressor Protein p53, Medical and Health Sciences, Epidemiology, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundOvarian clear cell carcinoma (OCCC) is a rare ovarian cancer histotype that tends to be resistant to standard platinum-based chemotherapeutics. We sought to better understand the role of DNA methylation in clinical and biological subclassification of OCCC.MethodsWe interrogated genome-wide methylation using DNA from fresh frozen tumors from 271 cases, applied nonsmooth nonnegative matrix factorization (nsNMF) clustering, and evaluated clinical associations and biological pathways.ResultsTwo approximately equally sized clusters that associated with several clinical features were identified. Compared with Cluster 2 (N = 137), Cluster 1 cases (N = 134) presented at a more advanced stage, were less likely to be of Asian ancestry, and tended to have poorer outcomes including macroscopic residual disease following primary debulking surgery (P < 0.10). Subset analyses of targeted tumor sequencing and IHC data revealed that Cluster 1 tumors showed TP53 mutation and abnormal p53 expression, and Cluster 2 tumors showed aneuploidy and ARID1A/PIK3CA mutation (P < 0.05). Cluster-defining CpGs included 1,388 CpGs residing within 200 bp of the transcription start sites of 977 genes; 38% of these genes (N = 369 genes) were differentially expressed across cluster in transcriptomic subset analysis (P < 10-4). Differentially expressed genes were enriched for six immune-related pathways, including IFNα and IFNγ responses (P < 10-6).ConclusionsDNA methylation clusters in OCCC correlate with disease features and gene expression patterns among immune pathways.ImpactThis work serves as a foundation for integrative analyses that better understand the complex biology of OCCC in an effort to improve potential for development of targeted therapeutics.

Published
2022

10. Predicting master transcription factors from pan-cancer expression data

Author

Reddy, Jessica, Fonseca, Marcos AS, Corona, Rosario I, Nameki, Robbin, Segato Dezem, Felipe, Klein, Isaac A, Chang, Heidi, Chaves-Moreira, Daniele, Afeyan, Lena K, Malta, Tathiane M, Lin, Xianzhi, Abbasi, Forough, Font-Tello, Alba, Sabedot, Thais, Cejas, Paloma, Rodríguez-Malavé, Norma, Seo, Ji-Heui, Lin, De-Chen, Matulonis, Ursula, Karlan, Beth Y, Gayther, Simon A, Pasaniuc, Bogdan, Gusev, Alexander, Noushmehr, Houtan, Long, Henry, Freedman, Matthew L, Drapkin, Ronny, Young, Richard A, Abraham, Brian J, and Lawrenson, Kate

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Rare Diseases, Genetics, Ovarian Cancer, Human Genome
Abstract

Critical developmental “master transcription factors” (MTFs) can be subverted during tumorigenesis to control oncogenic transcriptional programs. Current approaches to identifying MTFs rely on ChIP-seq data, which is unavailable for many cancers. We developed the CaCTS (Cancer Core Transcription factor Specificity) algorithm to prioritize candidate MTFs using pan-cancer RNA sequencing data. CaCTS identified candidate MTFs across 34 tumor types and 140 subtypes including predictions for cancer types/subtypes for which MTFs are unknown, including e.g. PAX8, SOX17, and MECOM as candidates in ovarian cancer (OvCa). In OvCa cells, consistent with known MTF properties, these factors are required for viability, lie proximal to superenhancers, co-occupy regulatory elements globally, co-bind loci encoding OvCa biomarkers, and are sensitive to pharmacologic inhibition of transcription. Our predictions of MTFs, especially for tumor types with limited understanding of transcriptional drivers, pave the way to therapeutic targeting of MTFs in a broad spectrum of cancers.

Published
2021

11. In vivo modeling of metastatic human high-grade serous ovarian cancer in mice.

Author

Kim, Olga, Park, Eun Young, Klinkebiel, David L, Pack, Svetlana D, Shin, Yong-Hyun, Abdullaev, Zied, Emerson, Robert E, Coffey, Donna M, Kwon, Sun Young, Creighton, Chad J, Kwon, Sanghoon, Chang, Edmund C, Chiang, Theodore, Yatsenko, Alexander N, Chien, Jeremy, Cheon, Dong-Joo, Yang-Hartwich, Yang, Nakshatri, Harikrishna, Nephew, Kenneth P, Behringer, Richard R, Fernández, Facundo M, Cho, Chi-Heum, Vanderhyden, Barbara, Drapkin, Ronny, Bast, Robert C, Miller, Kathy D, Karpf, Adam R, and Kim, Jaeyeon

Subjects
Cell Line, Tumor, Animals, Mice, Knockout, Humans, Mice, Cystadenocarcinoma, Serous, Peritoneal Neoplasms, Ovarian Neoplasms, Neoplasm Metastasis, Disease Models, Animal, Chromosomal Instability, Ribonuclease III, Antineoplastic Agents, Drug Screening Assays, Antitumor, Feasibility Studies, DNA Repair, Drug Resistance, Neoplasm, Mutation, Female, Tumor Suppressor Protein p53, PTEN Phosphohydrolase, DEAD-box RNA Helicases, Primary Cell Culture, Neoplasm Grading, Developmental Biology, Genetics
Abstract

Metastasis is responsible for 90% of human cancer mortality, yet it remains a challenge to model human cancer metastasis in vivo. Here we describe mouse models of high-grade serous ovarian cancer, also known as high-grade serous carcinoma (HGSC), the most common and deadliest human ovarian cancer type. Mice genetically engineered to harbor Dicer1 and Pten inactivation and mutant p53 robustly replicate the peritoneal metastases of human HGSC with complete penetrance. Arising from the fallopian tube, tumors spread to the ovary and metastasize throughout the pelvic and peritoneal cavities, invariably inducing hemorrhagic ascites. Widespread and abundant peritoneal metastases ultimately cause mouse deaths (100%). Besides the phenotypic and histopathological similarities, mouse HGSCs also display marked chromosomal instability, impaired DNA repair, and chemosensitivity. Faithfully recapitulating the clinical metastases as well as molecular and genomic features of human HGSC, this murine model will be valuable for elucidating the mechanisms underlying the development and progression of metastatic ovarian cancer and also for evaluating potential therapies.

Published
2020

12. A Study of High-Grade Serous Ovarian Cancer Origins Implicates the SOX18 Transcription Factor in Tumor Development

Author

Lawrenson, Kate, Fonseca, Marcos AS, Liu, Annie Y, Dezem, Felipe Segato, Lee, Janet M, Lin, Xianzhi, Corona, Rosario I, Abbasi, Forough, Vavra, Kevin C, Dinh, Huy Q, Gill, Navjot Kaur, Seo, Ji-Heui, Coetzee, Simon, Lin, Yvonne G, Pejovic, Tanja, Mhawech-Fauceglia, Paulette, Rowat, Amy C, Drapkin, Ronny, Karlan, Beth Y, Hazelett, Dennis J, Freedman, Matthew L, Gayther, Simon A, and Noushmehr, Houtan

Subjects
Biological Sciences, Rare Diseases, Ovarian Cancer, Cancer, Prevention, 2.1 Biological and endogenous factors, Aetiology, Adult, Aged, Cell Line, Cell Line, Tumor, Epithelial Cells, Epithelial-Mesenchymal Transition, Fallopian Tubes, Female, Gene Expression Regulation, Neoplastic, Humans, Machine Learning, Middle Aged, Ovarian Neoplasms, Ovary, RNA-Seq, SOXF Transcription Factors, Single-Cell Analysis, Transcriptome, RNA-seq, SOX18, dual origins, fallopian tube secretory epithelial cell, high-grade serous ovarian cancer, machine learning, one-class logistic regression models, ovarian surface epithelial cell, single-cell RNA-seq, super enhancers, transcription factors, Biochemistry and Cell Biology, Medical Physiology, Biological sciences
Abstract

Fallopian tube secretory epithelial cells (FTSECs) are likely the main precursor cell type of high-grade serous ovarian cancers (HGSOCs), but these tumors may also arise from ovarian surface epithelial cells (OSECs). We profiled global landscapes of gene expression and active chromatin to characterize molecular similarities between OSECs (n = 114), FTSECs (n = 74), and HGSOCs (n = 394). A one-class machine learning algorithm predicts that most HGSOCs derive from FTSECs, with particularly high FTSEC scores in mesenchymal-type HGSOCs (padj < 8 × 10-4). However, a subset of HGSOCs likely derive from OSECs, particularly HGSOCs of the proliferative type (padj < 2 × 10-4), suggesting a dualistic model for HGSOC origins. Super-enhancer (SE) landscapes were also more similar between FTSECs and HGSOCs than between OSECs and HGSOCs (p < 2.2 × 10-16). The SOX18 transcription factor (TF) coincided with a HGSOC-specific SE, and ectopic overexpression of SOX18 in FTSECs caused epithelial-to-mesenchymal transition, indicating that SOX18 plays a role in establishing the mesenchymal signature of fallopian-derived HGSOCs.

Published
2019

14. Nociceptor neurons affect cancer immunosurveillance

Author

Balood, Mohammad, Ahmadi, Maryam, Eichwald, Tuany, Ahmadi, Ali, Majdoubi, Abdelilah, Roversi, Karine, Roversi, Katiane, Lucido, Christopher T., Restaino, Anthony C., Huang, Siyi, Ji, Lexiang, Huang, Kai-Chih, Semerena, Elise, Thomas, Sini C., Trevino, Alexandro E., Merrison, Hannah, Parrin, Alexandre, Doyle, Benjamin, Vermeer, Daniel W., Spanos, William C., Williamson, Caitlin S., Seehus, Corey R., Foster, Simmie L., Dai, Hongyue, Shu, Chengyi J., Rangachari, Manu, Thibodeau, Jacques, V. Del Rincon, Sonia, Drapkin, Ronny, Rafei, Moutih, Ghasemlou, Nader, Vermeer, Paola D., Woolf, Clifford J., and Talbot, Sebastien

Published
2022
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15. Combination ATR and PARP Inhibitor (CAPRI): A phase 2 study of ceralasertib plus olaparib in patients with recurrent, platinum-sensitive epithelial ovarian cancer (cohort A).

Author

Simpkins, Fiona, primary, Nasioudis, Dimitrios, additional, Wethington, Stephanie L., additional, Martin, Lainie P., additional, Tanyi, Janos Laszlo, additional, Latif, Nawar A., additional, Torigian, Drew A., additional, Omran, Dalia K., additional, Rodriguez, Diego, additional, Smith, Simon, additional, Dean, Emma, additional, Domchek, Susan M., additional, Drapkin, Ronny, additional, Shih, Ie-Ming, additional, Brown, Eric J, additional, Hwang, Wei-Ting, additional, Armstrong, Deborah Kay, additional, Gaillard, Stephanie, additional, Giuntoli, Robert Lawrence, additional, and Liu, Joyce F., additional

Published
2024
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16. Early loss of Histone H2B monoubiquitylation alters chromatin accessibility and activates key immune pathways that facilitate progression of ovarian cancer

Author

Hooda, Jagmohan, Novak, Marián, Salomon, Matthew P, Matsuba, Chikako, Ramos, Romela I, MacDuffie, Emily, Song, Melissa, Hirsch, Michelle S, Lester, Jenny, Parkash, Vinita, Karlan, Beth Y, Oren, Moshe, Hoon, Dave S, and Drapkin, Ronny

Subjects
Ovarian Cancer, Rare Diseases, Prevention, Cancer, Aetiology, 2.1 Biological and endogenous factors, Apoptosis, Biomarkers, Tumor, Carcinoma, Ovarian Epithelial, Cell Proliferation, Chromatin, Cystadenocarcinoma, Serous, Disease Progression, Fallopian Tube Neoplasms, Female, Gene Expression Regulation, Neoplastic, Histones, Humans, Interleukin-6, Ovarian Neoplasms, Prognosis, Signal Transduction, Tumor Cells, Cultured, Ubiquitin-Protein Ligases, Ubiquitination, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Recent insights supporting the fallopian tube epithelium (FTE) and serous tubal intraepithelial carcinomas (STIC) as the tissue of origin and the precursor lesion, respectively, for the majority of high-grade serous ovarian carcinomas (HGSOC) provide the necessary context to study the mechanisms that drive the development and progression of HGSOC. Here, we investigate the role of the E3 ubiquitin ligase RNF20 and histone H2B monoubiquitylation (H2Bub1) in serous tumorigenesis and report that heterozygous loss of RNF20 defines the majority of HGSOC tumors. At the protein level, H2Bub1 was lost or downregulated in a large proportion of STIC and invasive HGSOC tumors, implicating RNF20/H2Bub1 loss as an early event in the development of serous ovarian carcinoma. Knockdown of RNF20, with concomitant loss of H2Bub1, was sufficient to enhance cell migration and clonogenic growth of FTE cells. To investigate the mechanisms underlying these effects, we performed ATAC-seq and RNA-seq in RNF20 knockdown FTE cell lines. Loss of RNF20 and H2Bub1 was associated with a more open chromatin conformation, leading to upregulation of immune signaling pathways, including IL6. IL6 was one of the key cytokines significantly upregulated in RNF20- and H2Bub1-depleted FTE cells and imparted upon these cells an enhanced migratory phenotype. These studies provide mechanistic insight into the observed oncogenic phenotypes triggered by the early loss of H2Bub1. SIGNIFICANCE: Loss of RNF20 and H2Bub1 contributes to transformation of the fallopian tube epithelium and plays a role in the initiation and progression of high-grade serous ovarian cancer.Graphical Abstract: http://cancerres.aacrjournals.org/content/canres/79/4/760/F1.large.jpg.

Published
2019

18. Repurposing colforsin daropate to treat MYC-driven high-grade serous ovarian carcinomas.

Author

Knarr, Matthew J., Moon, Jamie, Rawat, Priyanka, DiFeo, Analisa, Hoon, David S. B., and Drapkin, Ronny

Abstract

High-grade serous ovarian cancer (HGSOC) is one of the deadliest cancers for women, with a low survival rate, no early detection biomarkers, a high rate of recurrence, and few therapeutic options. Forskolin, an activator of cyclic AMP signaling, has several anticancer activities, including against HGSOC, but has limited use in vivo. Its water-soluble derivative, colforsin daropate, has the same mechanism of action as forskolin and is used to treat acute heart failure. Here, we investigated the potential of colforsin daropate as a treatment for HGSOC. We found that colforsin daropate induced cell cycle arrest and apoptosis in cultured HGSOC cells and spheroids but had negligible cytotoxicity in immortalized, nontumorigenic fallopian tube secretory cells and ovarian surface epithelial cells. Colforsin daropate also prevented HGSOC cells from invading ovarian surface epithelial cell layers in culture. In vivo, colforsin daropate reduced tumor growth, synergized with cisplatin (a standard chemotherapy in ovarian cancer care), and improved host survival in subcutaneous and intraperitoneal xenograft models. These antitumor effects of colforsin daropate were mediated in part by its reduction in the abundance and transcriptional activity of the oncoprotein c-MYC, which is often increased in HGSOC. Our findings demonstrate that colforsin daropate may be a promising therapeutic that could be combined with conventional therapies to treat HGSOC. Editor's summary: High-grade serous ovarian cancer (HGSOC) is aggressive and lacks durably effective treatments. Forskolin can suppress cancer cell proliferation but cannot be used clinically. Knarr et al. found that colforsin daropate, a forskolin derivative, specifically induced cell death in HGSOC cells but not normal fallopian or ovarian cells and inhibited HGSOC invasion in part by attenuating MYC signaling. Colforsin daropate synergized with cisplatin, a standard ovarian cancer chemotherapeutic, and resensitized cisplatin-resistant tumors in mice. Because colforsin daropate is already approved to treat acute heart failure, it could potentially be repurposed to treat HGSOC. —Leslie K. Ferrarelli [ABSTRACT FROM AUTHOR]

Published
2024
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19. Integrated Genomic, Epigenomic, and Expression Analyses of Ovarian Cancer Cell Lines.

Author

Papp, Eniko, Hallberg, Dorothy, Konecny, Gottfried, Bruhm, Daniel, Adleff, Vilmos, Noë, Michaël, Kagiampakis, Ioannis, Palsgrove, Doreen, Conklin, Dylan, Kinose, Yasuto, White, James, Press, Michael, Drapkin, Ronny, Easwaran, Hariharan, Baylin, Stephen, Slamon, Dennis, Velculescu, Victor, and Scharpf, Robert

Subjects
cancer cell lines, cancer genomics, drug response, gene fusions, ovarian cancer, structural variants, Cell Line, Tumor, CpG Islands, DNA Methylation, Drug Resistance, Neoplasm, Epigenomics, Female, Gene Expression Regulation, Neoplastic, Humans, Mutation, Ovarian Neoplasms, Protein Kinase Inhibitors
Abstract

To improve our understanding of ovarian cancer, we performed genome-wide analyses of 45 ovarian cancer cell lines. Given the challenges of genomic analyses of tumors without matched normal samples, we developed approaches for detection of somatic sequence and structural changes and integrated these with epigenetic and expression alterations. Alterations not previously implicated in ovarian cancer included amplification or overexpression of ASXL1 and H3F3B, deletion or underexpression of CDC73 and TGF-beta receptor pathway members, and rearrangements of YAP1-MAML2 and IKZF2-ERBB4. Dose-response analyses to targeted therapies revealed unique molecular dependencies, including increased sensitivity of tumors with PIK3CA and PPP2R1A alterations to PI3K inhibitor GNE-493, MYC amplifications to PARP inhibitor BMN673, and SMAD3/4 alterations to MEK inhibitor MEK162. Genome-wide rearrangements provided an improved measure of sensitivity to PARP inhibition. This study provides a comprehensive and broadly accessible resource of molecular information for the development of therapeutic avenues in ovarian cancer.

Published
2018

20. Stromal mediated DNA damage promotes high grade serous ovarian cancer initiation

Author

Garcia, Geyon L., primary, Orellana, Taylor, additional, Gorecki, Grace, additional, Frisbie, Leonard G., additional, Baruwal, Roja, additional, Goldfield, Ester, additional, Beddows, Ian, additional, MacFawn, Ian P., additional, Britt, Ananya K., additional, Hale, Macy M., additional, Shen, Hui, additional, Buckanovich, Ronald, additional, Finkel, Toren, additional, Drapkin, Ronny, additional, Soong, T. Rinda, additional, Bruno, Tullia C., additional, Atiya, Huda I., additional, and Coffman, Lan G., additional

Published
2024
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23. CCNE1 copy number is a biomarker for response to combination WEE1-ATR inhibition in ovarian and endometrial cancer models

Author

Xu, Haineng, George, Erin, Kinose, Yasuto, Kim, Hyoung, Shah, Jennifer B., Peake, Jasmine D., Ferman, Benjamin, Medvedev, Sergey, Murtha, Thomas, Barger, Carter J., Devins, Kyle M., D’Andrea, Kurt, Wubbenhorst, Bradley, Schwartz, Lauren E., Hwang, Wei-Ting, Mills, Gordon B., Nathanson, Katherine L., Karpf, Adam R., Drapkin, Ronny, Brown, Eric J., and Simpkins, Fiona

Published
2021
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26. Reprogramming of ovarian granulosa cells by YAP1 leads to development of high-grade cancer with mesenchymal lineage and serous features

Author

Lv, Xiangmin, He, Chunbo, Huang, Cong, Hua, Guohua, Chen, Xingcheng, Timm, Barbara K., Maclin, Victoria M., Haggerty, Abigail A., Aust, Shelly K., Golden, Denae M., Dave, Bhavana J., Tseng, Yun-An, Chen, Li, Wang, Hongbo, Chen, Peichao, Klinkebiel, David L., Karpf, Adam R., Dong, Jixin, Drapkin, Ronny I., Rueda, Bo R., Davis, John S., and Wang, Cheng

Published
2020
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27. Supplemental Table S5 from Aneuploidy Landscape in Precursors of Ovarian Cancer

Author

Wang, Yeh, primary, Douville, Christopher, primary, Chien, Yen-Wei, primary, Wang, Brant G., primary, Chen, Chi-Long, primary, Pinto, Andre, primary, Smith, Saron Ann, primary, Drapkin, Ronny, primary, Chui, M. Herman, primary, Numan, Tricia, primary, Vang, Russell, primary, Papadopoulos, Nickolas, primary, Wang, Tian-Li, primary, and Shih, Ie-Ming, primary

Published
2024
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28. Supplemental Figure S3 from Aneuploidy Landscape in Precursors of Ovarian Cancer

Author

Wang, Yeh, primary, Douville, Christopher, primary, Chien, Yen-Wei, primary, Wang, Brant G., primary, Chen, Chi-Long, primary, Pinto, Andre, primary, Smith, Saron Ann, primary, Drapkin, Ronny, primary, Chui, M. Herman, primary, Numan, Tricia, primary, Vang, Russell, primary, Papadopoulos, Nickolas, primary, Wang, Tian-Li, primary, and Shih, Ie-Ming, primary

Published
2024
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29. Data from Aneuploidy Landscape in Precursors of Ovarian Cancer

Author

Wang, Yeh, primary, Douville, Christopher, primary, Chien, Yen-Wei, primary, Wang, Brant G., primary, Chen, Chi-Long, primary, Pinto, Andre, primary, Smith, Saron Ann, primary, Drapkin, Ronny, primary, Chui, M. Herman, primary, Numan, Tricia, primary, Vang, Russell, primary, Papadopoulos, Nickolas, primary, Wang, Tian-Li, primary, and Shih, Ie-Ming, primary

Published
2024
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30. Supplementary Figure 6 from Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

Author

Taylor, Martin S., primary, Wu, Connie, primary, Fridy, Peter C., primary, Zhang, Stephanie J., primary, Senussi, Yasmeen, primary, Wolters, Justina C., primary, Cajuso, Tatiana, primary, Cheng, Wen-Chih, primary, Heaps, John D., primary, Miller, Bryant D., primary, Mori, Kei, primary, Cohen, Limor, primary, Jiang, Hua, primary, Molloy, Kelly R., primary, Chait, Brian T., primary, Goggins, Michael G., primary, Bhan, Irun, primary, Franses, Joseph W., primary, Yang, Xiaoyu, primary, Taplin, Mary-Ellen, primary, Wang, Xinan, primary, Christiani, David C., primary, Johnson, Bruce E., primary, Meyerson, Matthew, primary, Uppaluri, Ravindra, primary, Egloff, Ann Marie, primary, Denault, Elyssa N., primary, Spring, Laura M., primary, Wang, Tian-Li, primary, Shih, Ie-Ming, primary, Fairman, Jennifer E., primary, Jung, Euihye, primary, Arora, Kshitij S., primary, Yilmaz, Osman H., primary, Cohen, Sonia, primary, Sharova, Tatyana, primary, Chi, Gary, primary, Norden, Bryanna L., primary, Song, Yuhui, primary, Nieman, Linda T., primary, Pappas, Leontios, primary, Parikh, Aparna R., primary, Strickland, Matthew R., primary, Corcoran, Ryan B., primary, Mustelin, Tomas, primary, Eng, George, primary, Yilmaz, Ömer H., primary, Matulonis, Ursula A., primary, Chan, Andrew T., primary, Skates, Steven J., primary, Rueda, Bo R., primary, Drapkin, Ronny, primary, Klempner, Samuel J., primary, Deshpande, Vikram, primary, Ting, David T., primary, Rout, Michael P., primary, LaCava, John, primary, Walt, David R., primary, and Burns, Kathleen H., primary

Published
2024
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31. Supplementary Figure 24 from Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

Author

Taylor, Martin S., primary, Wu, Connie, primary, Fridy, Peter C., primary, Zhang, Stephanie J., primary, Senussi, Yasmeen, primary, Wolters, Justina C., primary, Cajuso, Tatiana, primary, Cheng, Wen-Chih, primary, Heaps, John D., primary, Miller, Bryant D., primary, Mori, Kei, primary, Cohen, Limor, primary, Jiang, Hua, primary, Molloy, Kelly R., primary, Chait, Brian T., primary, Goggins, Michael G., primary, Bhan, Irun, primary, Franses, Joseph W., primary, Yang, Xiaoyu, primary, Taplin, Mary-Ellen, primary, Wang, Xinan, primary, Christiani, David C., primary, Johnson, Bruce E., primary, Meyerson, Matthew, primary, Uppaluri, Ravindra, primary, Egloff, Ann Marie, primary, Denault, Elyssa N., primary, Spring, Laura M., primary, Wang, Tian-Li, primary, Shih, Ie-Ming, primary, Fairman, Jennifer E., primary, Jung, Euihye, primary, Arora, Kshitij S., primary, Yilmaz, Osman H., primary, Cohen, Sonia, primary, Sharova, Tatyana, primary, Chi, Gary, primary, Norden, Bryanna L., primary, Song, Yuhui, primary, Nieman, Linda T., primary, Pappas, Leontios, primary, Parikh, Aparna R., primary, Strickland, Matthew R., primary, Corcoran, Ryan B., primary, Mustelin, Tomas, primary, Eng, George, primary, Yilmaz, Ömer H., primary, Matulonis, Ursula A., primary, Chan, Andrew T., primary, Skates, Steven J., primary, Rueda, Bo R., primary, Drapkin, Ronny, primary, Klempner, Samuel J., primary, Deshpande, Vikram, primary, Ting, David T., primary, Rout, Michael P., primary, LaCava, John, primary, Walt, David R., primary, and Burns, Kathleen H., primary

Published
2024
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32. Supplementary Figure 5 from Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

Author

Taylor, Martin S., primary, Wu, Connie, primary, Fridy, Peter C., primary, Zhang, Stephanie J., primary, Senussi, Yasmeen, primary, Wolters, Justina C., primary, Cajuso, Tatiana, primary, Cheng, Wen-Chih, primary, Heaps, John D., primary, Miller, Bryant D., primary, Mori, Kei, primary, Cohen, Limor, primary, Jiang, Hua, primary, Molloy, Kelly R., primary, Chait, Brian T., primary, Goggins, Michael G., primary, Bhan, Irun, primary, Franses, Joseph W., primary, Yang, Xiaoyu, primary, Taplin, Mary-Ellen, primary, Wang, Xinan, primary, Christiani, David C., primary, Johnson, Bruce E., primary, Meyerson, Matthew, primary, Uppaluri, Ravindra, primary, Egloff, Ann Marie, primary, Denault, Elyssa N., primary, Spring, Laura M., primary, Wang, Tian-Li, primary, Shih, Ie-Ming, primary, Fairman, Jennifer E., primary, Jung, Euihye, primary, Arora, Kshitij S., primary, Yilmaz, Osman H., primary, Cohen, Sonia, primary, Sharova, Tatyana, primary, Chi, Gary, primary, Norden, Bryanna L., primary, Song, Yuhui, primary, Nieman, Linda T., primary, Pappas, Leontios, primary, Parikh, Aparna R., primary, Strickland, Matthew R., primary, Corcoran, Ryan B., primary, Mustelin, Tomas, primary, Eng, George, primary, Yilmaz, Ömer H., primary, Matulonis, Ursula A., primary, Chan, Andrew T., primary, Skates, Steven J., primary, Rueda, Bo R., primary, Drapkin, Ronny, primary, Klempner, Samuel J., primary, Deshpande, Vikram, primary, Ting, David T., primary, Rout, Michael P., primary, LaCava, John, primary, Walt, David R., primary, and Burns, Kathleen H., primary

Published
2024
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33. Supplementary Figure 17 from Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

Author

Taylor, Martin S., primary, Wu, Connie, primary, Fridy, Peter C., primary, Zhang, Stephanie J., primary, Senussi, Yasmeen, primary, Wolters, Justina C., primary, Cajuso, Tatiana, primary, Cheng, Wen-Chih, primary, Heaps, John D., primary, Miller, Bryant D., primary, Mori, Kei, primary, Cohen, Limor, primary, Jiang, Hua, primary, Molloy, Kelly R., primary, Chait, Brian T., primary, Goggins, Michael G., primary, Bhan, Irun, primary, Franses, Joseph W., primary, Yang, Xiaoyu, primary, Taplin, Mary-Ellen, primary, Wang, Xinan, primary, Christiani, David C., primary, Johnson, Bruce E., primary, Meyerson, Matthew, primary, Uppaluri, Ravindra, primary, Egloff, Ann Marie, primary, Denault, Elyssa N., primary, Spring, Laura M., primary, Wang, Tian-Li, primary, Shih, Ie-Ming, primary, Fairman, Jennifer E., primary, Jung, Euihye, primary, Arora, Kshitij S., primary, Yilmaz, Osman H., primary, Cohen, Sonia, primary, Sharova, Tatyana, primary, Chi, Gary, primary, Norden, Bryanna L., primary, Song, Yuhui, primary, Nieman, Linda T., primary, Pappas, Leontios, primary, Parikh, Aparna R., primary, Strickland, Matthew R., primary, Corcoran, Ryan B., primary, Mustelin, Tomas, primary, Eng, George, primary, Yilmaz, Ömer H., primary, Matulonis, Ursula A., primary, Chan, Andrew T., primary, Skates, Steven J., primary, Rueda, Bo R., primary, Drapkin, Ronny, primary, Klempner, Samuel J., primary, Deshpande, Vikram, primary, Ting, David T., primary, Rout, Michael P., primary, LaCava, John, primary, Walt, David R., primary, and Burns, Kathleen H., primary

Published
2024
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34. Supplementary Tables S1-S12 from Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

Author

Taylor, Martin S., primary, Wu, Connie, primary, Fridy, Peter C., primary, Zhang, Stephanie J., primary, Senussi, Yasmeen, primary, Wolters, Justina C., primary, Cajuso, Tatiana, primary, Cheng, Wen-Chih, primary, Heaps, John D., primary, Miller, Bryant D., primary, Mori, Kei, primary, Cohen, Limor, primary, Jiang, Hua, primary, Molloy, Kelly R., primary, Chait, Brian T., primary, Goggins, Michael G., primary, Bhan, Irun, primary, Franses, Joseph W., primary, Yang, Xiaoyu, primary, Taplin, Mary-Ellen, primary, Wang, Xinan, primary, Christiani, David C., primary, Johnson, Bruce E., primary, Meyerson, Matthew, primary, Uppaluri, Ravindra, primary, Egloff, Ann Marie, primary, Denault, Elyssa N., primary, Spring, Laura M., primary, Wang, Tian-Li, primary, Shih, Ie-Ming, primary, Fairman, Jennifer E., primary, Jung, Euihye, primary, Arora, Kshitij S., primary, Yilmaz, Osman H., primary, Cohen, Sonia, primary, Sharova, Tatyana, primary, Chi, Gary, primary, Norden, Bryanna L., primary, Song, Yuhui, primary, Nieman, Linda T., primary, Pappas, Leontios, primary, Parikh, Aparna R., primary, Strickland, Matthew R., primary, Corcoran, Ryan B., primary, Mustelin, Tomas, primary, Eng, George, primary, Yilmaz, Ömer H., primary, Matulonis, Ursula A., primary, Chan, Andrew T., primary, Skates, Steven J., primary, Rueda, Bo R., primary, Drapkin, Ronny, primary, Klempner, Samuel J., primary, Deshpande, Vikram, primary, Ting, David T., primary, Rout, Michael P., primary, LaCava, John, primary, Walt, David R., primary, and Burns, Kathleen H., primary

Published
2024
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35. Supplementary Figure 9 from Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

Author

Taylor, Martin S., primary, Wu, Connie, primary, Fridy, Peter C., primary, Zhang, Stephanie J., primary, Senussi, Yasmeen, primary, Wolters, Justina C., primary, Cajuso, Tatiana, primary, Cheng, Wen-Chih, primary, Heaps, John D., primary, Miller, Bryant D., primary, Mori, Kei, primary, Cohen, Limor, primary, Jiang, Hua, primary, Molloy, Kelly R., primary, Chait, Brian T., primary, Goggins, Michael G., primary, Bhan, Irun, primary, Franses, Joseph W., primary, Yang, Xiaoyu, primary, Taplin, Mary-Ellen, primary, Wang, Xinan, primary, Christiani, David C., primary, Johnson, Bruce E., primary, Meyerson, Matthew, primary, Uppaluri, Ravindra, primary, Egloff, Ann Marie, primary, Denault, Elyssa N., primary, Spring, Laura M., primary, Wang, Tian-Li, primary, Shih, Ie-Ming, primary, Fairman, Jennifer E., primary, Jung, Euihye, primary, Arora, Kshitij S., primary, Yilmaz, Osman H., primary, Cohen, Sonia, primary, Sharova, Tatyana, primary, Chi, Gary, primary, Norden, Bryanna L., primary, Song, Yuhui, primary, Nieman, Linda T., primary, Pappas, Leontios, primary, Parikh, Aparna R., primary, Strickland, Matthew R., primary, Corcoran, Ryan B., primary, Mustelin, Tomas, primary, Eng, George, primary, Yilmaz, Ömer H., primary, Matulonis, Ursula A., primary, Chan, Andrew T., primary, Skates, Steven J., primary, Rueda, Bo R., primary, Drapkin, Ronny, primary, Klempner, Samuel J., primary, Deshpande, Vikram, primary, Ting, David T., primary, Rout, Michael P., primary, LaCava, John, primary, Walt, David R., primary, and Burns, Kathleen H., primary

Published
2024
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36. Supplementary Figure 7 from Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

Author

Taylor, Martin S., primary, Wu, Connie, primary, Fridy, Peter C., primary, Zhang, Stephanie J., primary, Senussi, Yasmeen, primary, Wolters, Justina C., primary, Cajuso, Tatiana, primary, Cheng, Wen-Chih, primary, Heaps, John D., primary, Miller, Bryant D., primary, Mori, Kei, primary, Cohen, Limor, primary, Jiang, Hua, primary, Molloy, Kelly R., primary, Chait, Brian T., primary, Goggins, Michael G., primary, Bhan, Irun, primary, Franses, Joseph W., primary, Yang, Xiaoyu, primary, Taplin, Mary-Ellen, primary, Wang, Xinan, primary, Christiani, David C., primary, Johnson, Bruce E., primary, Meyerson, Matthew, primary, Uppaluri, Ravindra, primary, Egloff, Ann Marie, primary, Denault, Elyssa N., primary, Spring, Laura M., primary, Wang, Tian-Li, primary, Shih, Ie-Ming, primary, Fairman, Jennifer E., primary, Jung, Euihye, primary, Arora, Kshitij S., primary, Yilmaz, Osman H., primary, Cohen, Sonia, primary, Sharova, Tatyana, primary, Chi, Gary, primary, Norden, Bryanna L., primary, Song, Yuhui, primary, Nieman, Linda T., primary, Pappas, Leontios, primary, Parikh, Aparna R., primary, Strickland, Matthew R., primary, Corcoran, Ryan B., primary, Mustelin, Tomas, primary, Eng, George, primary, Yilmaz, Ömer H., primary, Matulonis, Ursula A., primary, Chan, Andrew T., primary, Skates, Steven J., primary, Rueda, Bo R., primary, Drapkin, Ronny, primary, Klempner, Samuel J., primary, Deshpande, Vikram, primary, Ting, David T., primary, Rout, Michael P., primary, LaCava, John, primary, Walt, David R., primary, and Burns, Kathleen H., primary

Published
2024
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37. Supplementary Data 1 from Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

Author

Taylor, Martin S., primary, Wu, Connie, primary, Fridy, Peter C., primary, Zhang, Stephanie J., primary, Senussi, Yasmeen, primary, Wolters, Justina C., primary, Cajuso, Tatiana, primary, Cheng, Wen-Chih, primary, Heaps, John D., primary, Miller, Bryant D., primary, Mori, Kei, primary, Cohen, Limor, primary, Jiang, Hua, primary, Molloy, Kelly R., primary, Chait, Brian T., primary, Goggins, Michael G., primary, Bhan, Irun, primary, Franses, Joseph W., primary, Yang, Xiaoyu, primary, Taplin, Mary-Ellen, primary, Wang, Xinan, primary, Christiani, David C., primary, Johnson, Bruce E., primary, Meyerson, Matthew, primary, Uppaluri, Ravindra, primary, Egloff, Ann Marie, primary, Denault, Elyssa N., primary, Spring, Laura M., primary, Wang, Tian-Li, primary, Shih, Ie-Ming, primary, Fairman, Jennifer E., primary, Jung, Euihye, primary, Arora, Kshitij S., primary, Yilmaz, Osman H., primary, Cohen, Sonia, primary, Sharova, Tatyana, primary, Chi, Gary, primary, Norden, Bryanna L., primary, Song, Yuhui, primary, Nieman, Linda T., primary, Pappas, Leontios, primary, Parikh, Aparna R., primary, Strickland, Matthew R., primary, Corcoran, Ryan B., primary, Mustelin, Tomas, primary, Eng, George, primary, Yilmaz, Ömer H., primary, Matulonis, Ursula A., primary, Chan, Andrew T., primary, Skates, Steven J., primary, Rueda, Bo R., primary, Drapkin, Ronny, primary, Klempner, Samuel J., primary, Deshpande, Vikram, primary, Ting, David T., primary, Rout, Michael P., primary, LaCava, John, primary, Walt, David R., primary, and Burns, Kathleen H., primary

Published
2024
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38. Data from Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

Author

Taylor, Martin S., primary, Wu, Connie, primary, Fridy, Peter C., primary, Zhang, Stephanie J., primary, Senussi, Yasmeen, primary, Wolters, Justina C., primary, Cajuso, Tatiana, primary, Cheng, Wen-Chih, primary, Heaps, John D., primary, Miller, Bryant D., primary, Mori, Kei, primary, Cohen, Limor, primary, Jiang, Hua, primary, Molloy, Kelly R., primary, Chait, Brian T., primary, Goggins, Michael G., primary, Bhan, Irun, primary, Franses, Joseph W., primary, Yang, Xiaoyu, primary, Taplin, Mary-Ellen, primary, Wang, Xinan, primary, Christiani, David C., primary, Johnson, Bruce E., primary, Meyerson, Matthew, primary, Uppaluri, Ravindra, primary, Egloff, Ann Marie, primary, Denault, Elyssa N., primary, Spring, Laura M., primary, Wang, Tian-Li, primary, Shih, Ie-Ming, primary, Fairman, Jennifer E., primary, Jung, Euihye, primary, Arora, Kshitij S., primary, Yilmaz, Osman H., primary, Cohen, Sonia, primary, Sharova, Tatyana, primary, Chi, Gary, primary, Norden, Bryanna L., primary, Song, Yuhui, primary, Nieman, Linda T., primary, Pappas, Leontios, primary, Parikh, Aparna R., primary, Strickland, Matthew R., primary, Corcoran, Ryan B., primary, Mustelin, Tomas, primary, Eng, George, primary, Yilmaz, Ömer H., primary, Matulonis, Ursula A., primary, Chan, Andrew T., primary, Skates, Steven J., primary, Rueda, Bo R., primary, Drapkin, Ronny, primary, Klempner, Samuel J., primary, Deshpande, Vikram, primary, Ting, David T., primary, Rout, Michael P., primary, LaCava, John, primary, Walt, David R., primary, and Burns, Kathleen H., primary

Published
2024
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39. Supplementary Figure 4 from Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

Author

Taylor, Martin S., primary, Wu, Connie, primary, Fridy, Peter C., primary, Zhang, Stephanie J., primary, Senussi, Yasmeen, primary, Wolters, Justina C., primary, Cajuso, Tatiana, primary, Cheng, Wen-Chih, primary, Heaps, John D., primary, Miller, Bryant D., primary, Mori, Kei, primary, Cohen, Limor, primary, Jiang, Hua, primary, Molloy, Kelly R., primary, Chait, Brian T., primary, Goggins, Michael G., primary, Bhan, Irun, primary, Franses, Joseph W., primary, Yang, Xiaoyu, primary, Taplin, Mary-Ellen, primary, Wang, Xinan, primary, Christiani, David C., primary, Johnson, Bruce E., primary, Meyerson, Matthew, primary, Uppaluri, Ravindra, primary, Egloff, Ann Marie, primary, Denault, Elyssa N., primary, Spring, Laura M., primary, Wang, Tian-Li, primary, Shih, Ie-Ming, primary, Fairman, Jennifer E., primary, Jung, Euihye, primary, Arora, Kshitij S., primary, Yilmaz, Osman H., primary, Cohen, Sonia, primary, Sharova, Tatyana, primary, Chi, Gary, primary, Norden, Bryanna L., primary, Song, Yuhui, primary, Nieman, Linda T., primary, Pappas, Leontios, primary, Parikh, Aparna R., primary, Strickland, Matthew R., primary, Corcoran, Ryan B., primary, Mustelin, Tomas, primary, Eng, George, primary, Yilmaz, Ömer H., primary, Matulonis, Ursula A., primary, Chan, Andrew T., primary, Skates, Steven J., primary, Rueda, Bo R., primary, Drapkin, Ronny, primary, Klempner, Samuel J., primary, Deshpande, Vikram, primary, Ting, David T., primary, Rout, Michael P., primary, LaCava, John, primary, Walt, David R., primary, and Burns, Kathleen H., primary

Published
2024
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40. Supplementary Data 2 from Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

Author

Taylor, Martin S., primary, Wu, Connie, primary, Fridy, Peter C., primary, Zhang, Stephanie J., primary, Senussi, Yasmeen, primary, Wolters, Justina C., primary, Cajuso, Tatiana, primary, Cheng, Wen-Chih, primary, Heaps, John D., primary, Miller, Bryant D., primary, Mori, Kei, primary, Cohen, Limor, primary, Jiang, Hua, primary, Molloy, Kelly R., primary, Chait, Brian T., primary, Goggins, Michael G., primary, Bhan, Irun, primary, Franses, Joseph W., primary, Yang, Xiaoyu, primary, Taplin, Mary-Ellen, primary, Wang, Xinan, primary, Christiani, David C., primary, Johnson, Bruce E., primary, Meyerson, Matthew, primary, Uppaluri, Ravindra, primary, Egloff, Ann Marie, primary, Denault, Elyssa N., primary, Spring, Laura M., primary, Wang, Tian-Li, primary, Shih, Ie-Ming, primary, Fairman, Jennifer E., primary, Jung, Euihye, primary, Arora, Kshitij S., primary, Yilmaz, Osman H., primary, Cohen, Sonia, primary, Sharova, Tatyana, primary, Chi, Gary, primary, Norden, Bryanna L., primary, Song, Yuhui, primary, Nieman, Linda T., primary, Pappas, Leontios, primary, Parikh, Aparna R., primary, Strickland, Matthew R., primary, Corcoran, Ryan B., primary, Mustelin, Tomas, primary, Eng, George, primary, Yilmaz, Ömer H., primary, Matulonis, Ursula A., primary, Chan, Andrew T., primary, Skates, Steven J., primary, Rueda, Bo R., primary, Drapkin, Ronny, primary, Klempner, Samuel J., primary, Deshpande, Vikram, primary, Ting, David T., primary, Rout, Michael P., primary, LaCava, John, primary, Walt, David R., primary, and Burns, Kathleen H., primary

Published
2024
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41. Supplementary Figure 8 from Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

Author

Taylor, Martin S., primary, Wu, Connie, primary, Fridy, Peter C., primary, Zhang, Stephanie J., primary, Senussi, Yasmeen, primary, Wolters, Justina C., primary, Cajuso, Tatiana, primary, Cheng, Wen-Chih, primary, Heaps, John D., primary, Miller, Bryant D., primary, Mori, Kei, primary, Cohen, Limor, primary, Jiang, Hua, primary, Molloy, Kelly R., primary, Chait, Brian T., primary, Goggins, Michael G., primary, Bhan, Irun, primary, Franses, Joseph W., primary, Yang, Xiaoyu, primary, Taplin, Mary-Ellen, primary, Wang, Xinan, primary, Christiani, David C., primary, Johnson, Bruce E., primary, Meyerson, Matthew, primary, Uppaluri, Ravindra, primary, Egloff, Ann Marie, primary, Denault, Elyssa N., primary, Spring, Laura M., primary, Wang, Tian-Li, primary, Shih, Ie-Ming, primary, Fairman, Jennifer E., primary, Jung, Euihye, primary, Arora, Kshitij S., primary, Yilmaz, Osman H., primary, Cohen, Sonia, primary, Sharova, Tatyana, primary, Chi, Gary, primary, Norden, Bryanna L., primary, Song, Yuhui, primary, Nieman, Linda T., primary, Pappas, Leontios, primary, Parikh, Aparna R., primary, Strickland, Matthew R., primary, Corcoran, Ryan B., primary, Mustelin, Tomas, primary, Eng, George, primary, Yilmaz, Ömer H., primary, Matulonis, Ursula A., primary, Chan, Andrew T., primary, Skates, Steven J., primary, Rueda, Bo R., primary, Drapkin, Ronny, primary, Klempner, Samuel J., primary, Deshpande, Vikram, primary, Ting, David T., primary, Rout, Michael P., primary, LaCava, John, primary, Walt, David R., primary, and Burns, Kathleen H., primary

Published
2024
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42. Supplementary Figure 3 from Ultrasensitive Detection of Circulating LINE-1 ORF1p as a Specific Multicancer Biomarker

Author

Taylor, Martin S., primary, Wu, Connie, primary, Fridy, Peter C., primary, Zhang, Stephanie J., primary, Senussi, Yasmeen, primary, Wolters, Justina C., primary, Cajuso, Tatiana, primary, Cheng, Wen-Chih, primary, Heaps, John D., primary, Miller, Bryant D., primary, Mori, Kei, primary, Cohen, Limor, primary, Jiang, Hua, primary, Molloy, Kelly R., primary, Chait, Brian T., primary, Goggins, Michael G., primary, Bhan, Irun, primary, Franses, Joseph W., primary, Yang, Xiaoyu, primary, Taplin, Mary-Ellen, primary, Wang, Xinan, primary, Christiani, David C., primary, Johnson, Bruce E., primary, Meyerson, Matthew, primary, Uppaluri, Ravindra, primary, Egloff, Ann Marie, primary, Denault, Elyssa N., primary, Spring, Laura M., primary, Wang, Tian-Li, primary, Shih, Ie-Ming, primary, Fairman, Jennifer E., primary, Jung, Euihye, primary, Arora, Kshitij S., primary, Yilmaz, Osman H., primary, Cohen, Sonia, primary, Sharova, Tatyana, primary, Chi, Gary, primary, Norden, Bryanna L., primary, Song, Yuhui, primary, Nieman, Linda T., primary, Pappas, Leontios, primary, Parikh, Aparna R., primary, Strickland, Matthew R., primary, Corcoran, Ryan B., primary, Mustelin, Tomas, primary, Eng, George, primary, Yilmaz, Ömer H., primary, Matulonis, Ursula A., primary, Chan, Andrew T., primary, Skates, Steven J., primary, Rueda, Bo R., primary, Drapkin, Ronny, primary, Klempner, Samuel J., primary, Deshpande, Vikram, primary, Ting, David T., primary, Rout, Michael P., primary, LaCava, John, primary, Walt, David R., primary, and Burns, Kathleen H., primary

Published
2024
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43. Targeting glutamine dependence through GLS1 inhibition suppresses ARID1A-inactivated clear cell ovarian carcinoma

Author

Wu, Shuai, Fukumoto, Takeshi, Lin, Jianhuang, Nacarelli, Timothy, Wang, Yemin, Ong, Dionzie, Liu, Heng, Fatkhutdinov, Nail, Zundell, Joseph A., Karakashev, Sergey, Zhou, Wei, Schwartz, Lauren E., Tang, Hsin-Yao, Drapkin, Ronny, Liu, Qin, Huntsman, David G., Kossenkov, Andrew V., Speicher, David W., Schug, Zachary T., Van Dang, Chi, and Zhang, Rugang

Published
2021
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44. Rethinking ovarian cancer II: reducing mortality from high-grade serous ovarian cancer

Author

Bowtell, David D, Böhm, Steffen, Ahmed, Ahmed A, Aspuria, Paul-Joseph, Bast, Robert C, Beral, Valerie, Berek, Jonathan S, Birrer, Michael J, Blagden, Sarah, Bookman, Michael A, Brenton, James D, Chiappinelli, Katherine B, Martins, Filipe Correia, Coukos, George, Drapkin, Ronny, Edmondson, Richard, Fotopoulou, Christina, Gabra, Hani, Galon, Jérôme, Gourley, Charlie, Heong, Valerie, Huntsman, David G, Iwanicki, Marcin, Karlan, Beth Y, Kaye, Allyson, Lengyel, Ernst, Levine, Douglas A, Lu, Karen H, McNeish, Iain A, Menon, Usha, Narod, Steven A, Nelson, Brad H, Nephew, Kenneth P, Pharoah, Paul, Powell, Daniel J, Ramos, Pilar, Romero, Iris L, Scott, Clare L, Sood, Anil K, Stronach, Euan A, and Balkwill, Frances R

Subjects
Cancer, Ovarian Cancer, Prevention, Rare Diseases, Good Health and Well Being, Cystadenocarcinoma, Serous, Female, Humans, Neoplasm Grading, Ovarian Neoplasms, Prognosis, Survival Rate, Medical and Health Sciences, Oncology & Carcinogenesis
Abstract

High-grade serous ovarian cancer (HGSOC) accounts for 70-80% of ovarian cancer deaths, and overall survival has not changed significantly for several decades. In this Opinion article, we outline a set of research priorities that we believe will reduce incidence and improve outcomes for women with this disease. This 'roadmap' for HGSOC was determined after extensive discussions at an Ovarian Cancer Action meeting in January 2015.

Published
2015

45. Beyond genomics: Critical evaluation of cell line utility for ovarian cancer research

Author

Elias, Kevin M, Emori, Megan M, Papp, Eniko, MacDuffie, Emily, Konecny, Gottfried E, Velculescu, Victor E, and Drapkin, Ronny

Subjects
Human Genome, Biotechnology, Ovarian Cancer, Genetic Testing, Genetics, Rare Diseases, Cancer, Good Health and Well Being, Animals, Cell Line, Tumor, Female, Heterografts, Humans, Mice, Mice, Nude, Mice, SCID, Ovarian Neoplasms, Ovarian cancer, Cell line model, Xenograft, Genomics, Oncology and Carcinogenesis, Paediatrics and Reproductive Medicine, Oncology & Carcinogenesis
Abstract

ObjectiveComparisons of The Cancer Genome Atlas (TCGA) with high grade serous ovarian cancer (HGSOC) cell lines used in research reveal that many common experimental models lack defining genomic characteristics seen in patient tumors. As cell lines exist with higher genomic fidelity to TCGA, this study aimed to evaluate the utility of these cell lines as tools for preclinical investigation.MethodsWe compared two HGSOC cell lines with supposed high genomic fidelity to TCGA, KURAMOCHI and OVSAHO, with the most commonly cited ovarian cancer cell line, SKOV3, which has poor genomic fidelity to TCGA. The lines were analyzed for genomic alterations, in vitro performance, and growth in murine xenografts.ResultsUsing targeted next generation sequencing analyses, we determined that each line had a distinct mutation profile, including alterations in TP53, and copy number variation of specific genes. KURAMOCHI and OVSAHO better recapitulated serous carcinoma morphology than SKOV3. All lines expressed PAX8 and stathmin, but KURAMOCHI and OVSAHO did not express CK7. KURAMOCHI was significantly more platinum sensitive than OVSAHO and SKOV3. Unlike SKOV3, KURAMOCHI and OVSAHO engrafted poorly in subcutaneous xenografts. KURAMOCHI and OVSAHO grew best after intraperitoneal injection in SCID mice and recapitulated miliary disease while SKOV3 grew in all murine systems and formed oligometastatic disease.ConclusionsThe research utility of HGSOC cell line models requires a comprehensive assessment of genomic as well as in vitro and in vivo properties. Cell lines with closer genomic fidelity to human tumors may have limitations in performance for preclinical investigation.

Published
2015

46. Stathmin 1 and p16INK4A are sensitive adjunct biomarkers for serous tubal intraepithelial carcinoma

Author

Novak, Marián, Lester, Jenny, Karst, Alison M, Parkash, Vinita, Hirsch, Michelle S, Crum, Christopher P, Karlan, Beth Y, and Drapkin, Ronny

Subjects
Cancer, Biomarkers, Tumor, Cell Line, Tumor, Cyclin-Dependent Kinase Inhibitor p16, Cystadenocarcinoma, Serous, Fallopian Tube Neoplasms, Female, Gene Knockdown Techniques, Humans, Immunohistochemistry, Ki-67 Antigen, Mutation, Neoplasm Proteins, Ovarian Neoplasms, Stathmin, Tumor Suppressor Protein p53, Ovarian, Serous, Fallopian tube, STIC, p16, Oncology and Carcinogenesis, Paediatrics and Reproductive Medicine, Oncology & Carcinogenesis
Abstract

ObjectiveTo credential Stathmin 1 (STMN1) and p16(INK4A) (p16) as adjunct markers for the diagnosis of serous tubal intraepithelial carcinoma (STIC), and to compare STMN1 and p16 expression in p53-positive and p53-negative STIC and invasive high-grade serous carcinoma (HGSC).MethodsImmunohistochemistry (IHC) was used to examine STMN1 and p16 expression in fallopian tube specimens (n=31) containing p53-positive and p53-negative STICs, invasive HGSCs, and morphologically normal FTE (fallopian tube epithelium). STMN1 and p16 expression was scored semiquantitatively by four individuals. The semiquantitative scores were dichotomized, and reported as positive or negative. Pooled siRNA was used to knockdown p53 in a panel of cell lines derived from immortalized FTE and HGSC.ResultsSTMN1 and p16 were expressed in the majority of p53-positive and p53-negative STICs and concomitant invasive HGSCs, but only scattered positive cells were present in morphologically normal FTE. Both proteins were expressed consistently across multiple STICs from the same patient and in concomitant invasive HGSC. Knockdown of p53 in immortalized FTE cells and in four HGSC-derived cell lines expressing different missense p53 mutations did not affect STMN1 protein levels.ConclusionsThis study demonstrates that STMN1 and p16 are sensitive and specific adjunct biomarkers that, when used with p53 and Ki-67, improve the diagnostic accuracy of STIC. The addition of STMN1 and p16 helps to compensate for practical limitations of p53 and Ki-67 that complicate the diagnosis in up to one third of STICs.

Published
2015

47. Cis-eQTL analysis and functional validation of candidate susceptibility genes for high-grade serous ovarian cancer.

Author

Lawrenson, Kate, Li, Qiyuan, Kar, Siddhartha, Seo, Ji-Heui, Tyrer, Jonathan, Spindler, Tassja J, Lee, Janet, Chen, Yibu, Karst, Alison, Drapkin, Ronny, Aben, Katja KH, Anton-Culver, Hoda, Antonenkova, Natalia, Australian Ovarian Cancer Study Group, Baker, Helen, Bandera, Elisa V, Bean, Yukie, Beckmann, Matthias W, Berchuck, Andrew, Bisogna, Maria, Bjorge, Line, Bogdanova, Natalia, Brinton, Louise A, Brooks-Wilson, Angela, Bruinsma, Fiona, Butzow, Ralf, Campbell, Ian G, Carty, Karen, Chang-Claude, Jenny, Chenevix-Trench, Georgia, Chen, Anne, Chen, Zhihua, Cook, Linda S, Cramer, Daniel W, Cunningham, Julie M, Cybulski, Cezary, Dansonka-Mieszkowska, Agnieszka, Dennis, Joe, Dicks, Ed, Doherty, Jennifer A, Dörk, Thilo, du Bois, Andreas, Dürst, Matthias, Eccles, Diana, Easton, Douglas T, Edwards, Robert P, Eilber, Ursula, Ekici, Arif B, Fasching, Peter A, Fridley, Brooke L, Gao, Yu-Tang, Gentry-Maharaj, Aleksandra, Giles, Graham G, Glasspool, Rosalind, Goode, Ellen L, Goodman, Marc T, Grownwald, Jacek, Harrington, Patricia, Harter, Philipp, Hasmad, Hanis Nazihah, Hein, Alexander, Heitz, Florian, Hildebrandt, Michelle AT, Hillemanns, Peter, Hogdall, Estrid, Hogdall, Claus, Hosono, Satoyo, Iversen, Edwin S, Jakubowska, Anna, James, Paul, Jensen, Allan, Ji, Bu-Tian, Karlan, Beth Y, Kruger Kjaer, Susanne, Kelemen, Linda E, Kellar, Melissa, Kelley, Joseph L, Kiemeney, Lambertus A, Krakstad, Camilla, Kupryjanczyk, Jolanta, Lambrechts, Diether, Lambrechts, Sandrina, Le, Nhu D, Lee, Alice W, Lele, Shashi, Leminen, Arto, Lester, Jenny, Levine, Douglas A, Liang, Dong, Lissowska, Jolanta, Lu, Karen, Lubinski, Jan, Lundvall, Lene, Massuger, Leon FAG, Matsuo, Keitaro, McGuire, Valerie, McLaughlin, John R, Nevanlinna, Heli, McNeish, Ian, and Menon, Usha

Subjects
Australian Ovarian Cancer Study Group, Cell Line, Tumor, Humans, Neoplasms, Glandular and Epithelial, Ovarian Neoplasms, Genetic Predisposition to Disease, Homeodomain Proteins, Neoplasm Proteins, Gene Expression Regulation, Neoplastic, Protein Binding, Quantitative Trait Loci, Female, Nuchal Cord, Genetic Association Studies, Carcinoma, Ovarian Epithelial, Cell Line, Tumor, Neoplasms, Glandular and Epithelial, Gene Expression Regulation, Neoplastic, Carcinoma, Ovarian Epithelial, Rare Diseases, Prevention, Ovarian Cancer, Biotechnology, Human Genome, Cancer, Genetics, 2.1 Biological and endogenous factors
Abstract

Genome-wide association studies have reported 11 regions conferring risk of high-grade serous epithelial ovarian cancer (HGSOC). Expression quantitative trait locus (eQTL) analyses can identify candidate susceptibility genes at risk loci. Here we evaluate cis-eQTL associations at 47 regions associated with HGSOC risk (P≤10(-5)). For three cis-eQTL associations (P

Published
2015

48. Cell-type-specific enrichment of risk-associated regulatory elements at ovarian cancer susceptibility loci

Author

Coetzee, Simon G, Shen, Howard C, Hazelett, Dennis J, Lawrenson, Kate, Kuchenbaecker, Karoline, Tyrer, Jonathan, Rhie, Suhn K, Levanon, Keren, Karst, Alison, Drapkin, Ronny, Ramus, Susan J, Consortium, The Consortium of Investigators of Modifiers of BRCA1 2 The Ovarian Cancer Association, Couch, Fergus J, Offit, Kenneth, Chenevix-Trench, Georgia, Monteiro, Alvaro NA, Antoniou, Antonis, Freedman, Matthew, Coetzee, Gerhard A, Pharoah, Paul DP, Noushmehr, Houtan, Gayther, Simon A, Anton-Culver, Hoda, Antonenkova, Natalia, Baker, Helen, Bandera, Elisa V, Bean, Yukie, Beckmann, Matthias W, Berchuck, Andrew, Bisogna, Maria, Bjorge, Line, Bogdanova, Natalia, Brinton, Louise A, Brooks-Wilson, Angela, Bruinsma, Fiona, Butzow, Ralf, Campbell, Ian G, Carty, Karen, Chang-Claude, Jenny, Chen, Ann, Chen, Zhihua, Cook, Linda S, Cramer, Daniel W, Cunningham, Julie M, Cybulski, Cezary, Dansonka-Mieszkowska, Agnieszka, Dennis, Joe, Dicks, Ed, Doherty, Jennifer A, Dörk, Thilo, du Bois, Andreas, Dürst, Matthias, Eccles, Diana, Easton, Douglas F, Edwards, Robert P, Eilber, Ursula, Ekici, Arif B, Fasching, Peter A, Fridley, Brooke L, Gao, Yu-Tang, Gentry-Maharaj, Aleksandra, Giles, Graham G, Glasspool, Rosalind, Goode, Ellen L, Goodman, Marc T, Grownwald, Jacek, Harrington, Patricia, Harter, Philipp, Hasmad, Hanis Nazihah, Hein, Alexander, Heitz, Florian, Hildebrandt, Michelle AT, Hillemanns, Peter, Hogdall, Estrid, Hogdall, Claus, Hosono, Satoyo, Iversen, Edwin S, Jakubowska, Anna, James, Paul, Jensen, Allan, Ji, Bu-Tian, Karlan, Beth Y, Kjaer, Susanne Kruger, Kelemen, Linda E, Kellar, Melissa, Kelley, Joseph L, Kiemeney, Lambertus A, Krakstad, Camilla, Kupryjanczyk, Jolanta, Lambrechts, Diether, Lambrechts, Sandrina, Le, Nhu D, Lele, Shashi, Leminen, Arto, Lester, Jenny, Levine, Douglas A, Liang, Dong, and Lissowska, Jolanta

Subjects
Biological Sciences, Genetics, Rare Diseases, Prevention, Human Genome, Ovarian Cancer, Biotechnology, Cancer, 2.1 Biological and endogenous factors, Underpinning research, Aetiology, 1.1 Normal biological development and functioning, Chromatin, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Histones, Humans, Organ Specificity, Ovarian Neoplasms, Polymorphism, Single Nucleotide, Regulatory Sequences, Nucleic Acid, Ovarian Cancer Association Consortium, The Consortium of Investigators of Modifiers of BRCA1/2, Ovarian Cancer Association Consortium The Consortium of Investigators of Modifiers of BRCA1/2, Medical and Health Sciences, Genetics & Heredity
Abstract

Understanding the regulatory landscape of the human genome is a central question in complex trait genetics. Most single-nucleotide polymorphisms (SNPs) associated with cancer risk lie in non-protein-coding regions, implicating regulatory DNA elements as functional targets of susceptibility variants. Here, we describe genome-wide annotation of regions of open chromatin and histone modification in fallopian tube and ovarian surface epithelial cells (FTSECs, OSECs), the debated cellular origins of high-grade serous ovarian cancers (HGSOCs) and in endometriosis epithelial cells (EECs), the likely precursor of clear cell ovarian carcinomas (CCOCs). The regulatory architecture of these cell types was compared with normal human mammary epithelial cells and LNCaP prostate cancer cells. We observed similar positional patterns of global enhancer signatures across the three different ovarian cancer precursor cell types, and evidence of tissue-specific regulatory signatures compared to non-gynecological cell types. We found significant enrichment for risk-associated SNPs intersecting regulatory biofeatures at 17 known HGSOC susceptibility loci in FTSECs (P = 3.8 × 10(-30)), OSECs (P = 2.4 × 10(-23)) and HMECs (P = 6.7 × 10(-15)) but not for EECs (P = 0.45) or LNCaP cells (P = 0.88). Hierarchical clustering of risk SNPs conditioned on the six different cell types indicates FTSECs and OSECs are highly related (96% of samples using multi-scale bootstrapping) suggesting both cell types may be precursors of HGSOC. These data represent the first description of regulatory catalogues of normal precursor cells for different ovarian cancer subtypes, and provide unique insights into the tissue specific regulatory variation with respect to the likely functional targets of germline genetic susceptibility variants for ovarian cancer.

Published
2015

49. Flower lose, a cell fitness marker, predicts COVID‐19 prognosis

Author

Yekelchyk, Michail, Madan, Esha, Wilhelm, Jochen, Short, Kirsty R, Palma, António M, Liao, Linbu, Camacho, Denise, Nkadori, Everlyne, Winters, Michael T, Rice, Emily S, Rolim, Inês, Cruz‐Duarte, Raquel, Pelham, Christopher J, Nagane, Masaki, Gupta, Kartik, Chaudhary, Sahil, Braun, Thomas, Pillappa, Raghavendra, Parker, Mark S, Menter, Thomas, Matter, Matthias, Haslbauer, Jasmin Dionne, Tolnay, Markus, Galior, Kornelia D, Matkwoskyj, Kristina A, McGregor, Stephanie M, Muller, Laura K, Rakha, Emad A, Lopez‐Beltran, Antonio, Drapkin, Ronny, Ackermann, Maximilian, Fisher, Paul B, Grossman, Steven R, Godwin, Andrew K, Kulasinghe, Arutha, Martinez, Ivan, Marsh, Clay B, Tang, Benjamin, Wicha, Max S, Won, Kyoung Jae, Tzankov, Alexandar, Moreno, Eduardo, and Gogna, Rajan

Published
2021
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50. Defining the molecular evolution of extrauterine high grade serous carcinoma

Author

Beirne, James P., McArt, Darragh G., Roddy, Aideen, McDermott, Clara, Ferris, Jennifer, Buckley, Niamh E., Coulter, Paula, McCabe, Nuala, Eddie, Sharon L., Dunne, Philip D., O'Reilly, Paul, Gilmore, Alan, Feeney, Laura, Ewing, David Lyons, Drapkin, Ronny I., Salto-Tellez, Manuel, Kennedy, Richard D., Harley, Ian J.G., McCluggage, W. Glenn, and Mullan, Paul B.

Published
2019
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