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1. Genome-wide association analyses of ovarian cancer patients undergoing primary debulking surgery identify candidate genes for residual disease

Author

Dhanya Ramachandran, Jonathan P. Tyrer, Stefan Kommoss, Anna DeFazio, Marjorie J. Riggan, AOCS Group, Penelope M. Webb, Peter A. Fasching, Diether Lambrechts, María J. García, Cristina Rodríguez-Antona, Marc T. Goodman, Francesmary Modugno, Kirsten B. Moysich, Beth Y. Karlan, Jenny Lester, Susanne K. Kjaer, Allan Jensen, Estrid Høgdall, Ellen L. Goode, William A. Cliby, Amanika Kumar, Chen Wang, Julie M. Cunningham, Stacey J. Winham, Alvaro N. Monteiro, Joellen M. Schildkraut, Daniel W. Cramer, Kathryn L. Terry, Linda Titus, Line Bjorge, Liv Cecilie Vestrheim Thomsen, OPAL Study Group, Tanja Pejovic, Claus K. Høgdall, Iain A. McNeish, Taymaa May, David G. Huntsman, Jacobus Pfisterer, Ulrich Canzler, Tjoung-Won Park-Simon, Willibald Schröder, Antje Belau, Lars Hanker, Philipp Harter, Jalid Sehouli, Rainer Kimmig, Nikolaus de Gregorio, Barbara Schmalfeldt, Klaus Baumann, Felix Hilpert, Alexander Burges, Boris Winterhoff, Peter Schürmann, Lisa-Marie Speith, Peter Hillemanns, Andrew Berchuck, Sharon E. Johnatty, Susan J. Ramus, Georgia Chenevix-Trench, Paul D. P. Pharoah, Thilo Dörk, and Florian Heitz

Subjects
Medicine, Genetics, QH426-470
Abstract

Abstract Survival from ovarian cancer depends on the resection status after primary surgery. We performed genome-wide association analyses for resection status of 7705 ovarian cancer patients, including 4954 with high-grade serous carcinoma (HGSOC), to identify variants associated with residual disease. The most significant association with resection status was observed for rs72845444, upstream of MGMT, in HGSOC (p = 3.9 × 10−8). In gene-based analyses, PPP2R5C was the most strongly associated gene in HGSOC after stage adjustment. In an independent set of 378 ovarian tumours from the AGO-OVAR 11 study, variants near MGMT and PPP2R5C correlated with methylation and transcript levels, and PPP2R5C mRNA levels predicted progression-free survival in patients with residual disease. MGMT encodes a DNA repair enzyme, and PPP2R5C encodes the B56γ subunit of the PP2A tumour suppressor. Our results link heritable variation at these two loci with resection status in HGSOC.

Published
2024
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2. Maternal use of hormonal contraception and rare cancer types in children: A nationwide PECH cohort study

Author

Caroline H. Hemmingsen, Susanne K. Kjaer, Jeanette F. Winther, Kjeld Schmiegelow, Lina S. Mørch, and Marie Hargreave

Subjects
contraception, epidemiology, maternal medicine, oncology, pediatrics, Reproduction, QH471-489, Women. Feminism, HQ1101-2030.7
Abstract

Abstract Background Maternal hormonal contraception use has been associated with an increased risk of leukaemia and central nervous system (CNS) tumours in children. However, little is known about the association with other, less common childhood cancer types. We assessed associations between maternal hormonal contraceptive use and all main types of childhood cancer, excluding leukaemia and CNS tumours. Methods In this nationwide PECH cohort study, we followed all Danish children liveborn in 1996–2014 (n = 1 185 063) from birth until 2018. Registry information was extracted on maternal filled prescriptions of hormonal contraception and childhood cancer diagnoses (age at diagnosis

Published
2024
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3. Social inequality in cancer survivorship: Educational differences in health‐related quality of life among 27,857 cancer survivors in Denmark

Author

Anne Katrine Graudal Levinsen, Trille Kristina Kjaer, Lau Caspar Thygesen, Thomas Maltesen, Erik Jakobsen, Ismail Gögenur, Michael Borre, Peer Christiansen, Robert Zachariae, Peter Christensen, Søren Laurberg, Peter deNully Brown, Lisbet Rosenkrantz Hölmich, Christoffer Johansen, Susanne K. Kjær, Lonneke van dePoll‐Franse, Lena Saltbæk, and Susanne Oksbjerg Dalton

Subjects
cancer survivorship, health‐related quality of life, social inequality, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background With a growing population of cancer survivors in Denmark, the evaluation of health‐related quality of life (HRQoL) has become increasingly important. We describe variations in HRQoL between educational groups in a national population of cancer survivors. Methods We conducted a cross‐sectional questionnaire study among breast, prostate, lung, and colon cancer survivors diagnosed in 2010–2019 in Denmark. We used the EORTC QLQ‐C30 to assess HRQoL including physical, role, emotional, cognitive, social functioning, and symptoms (fatigue, nausea and vomiting, pain, dyspnea, insomnia, appetite loss, constipation, diarrhea, and financial difficulties). Information on educational level and clinical data were extracted from national registers and clinical databases. Levels of impaired functioning and severe symptoms were identified using newly established thresholds for clinical importance. Multivariate logistic regression was used to examine associations between education and HRQoL. All statistical tests were 2‐sided. Results In total, 27,857 (42%) participated in the study. Up to 72% and 75% of cancer survivors with short education (≤9 years) reported impaired functioning and severe symptoms, respectively. Cancer survivors with short compared to long education (>12 years) were more likely to report impaired functioning and severe symptoms, with for example significantly higher odds ratios (ORs) for impaired physical function (breast OR = 2.41, 99% CI = 2.01–2.89; prostate OR = 1.81, 99% CI = 1.48–2.21; lung OR = 2.97, 99% CI = 1.95–4.57; and colon cancer OR = 1.69, 99% CI = 1.28–2.24). Conclusions Cancer survivors with short education are at greater risk of impaired HRQoL than survivors with long education 2–12 years after diagnosis. This underscores the need for systematic screening and symptom management in cancer aftercare, in order to reach all cancer survivors, also cancer survivors with short education.

Published
2023
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4. Educational differences in healthcare use among survivors after breast, prostate, lung, and colon cancer – a SEQUEL cohort study

Author

Anne Katrine Graudal Levinsen, Trille Kristina Kjaer, Thomas Maltesen, Erik Jakobsen, Ismail Gögenur, Michael Borre, Peer Christiansen, Robert Zachariae, Søren Laurberg, Peter Christensen, Niels Kroman, Signe Benzon Larsen, Thea Helene Degett, Lisbet Rosenkrantz Hölmich, Peter de Nully Brown, Christoffer Johansen, Susanne K. Kjær, Lau Caspar Thygesen, and Susanne Oksbjerg Dalton

Subjects
Healthcare use, Social inequality, Survivorship, Breast cancer, Prostate cancer, Lung cancer, Public aspects of medicine, RA1-1270
Abstract

Abstract Background Many cancer survivors experience late effects after cancer. Comorbidity, health literacy, late effects, and help-seeking behavior may affect healthcare use and may differ among socioeconomic groups. We examined healthcare use among cancer survivors, compared with cancer-free individuals, and investigated educational differences in healthcare use among cancer survivors. Methods A Danish cohort of 127,472 breast, prostate, lung, and colon cancer survivors from the national cancer databases, and 637,258 age- and sex-matched cancer-free individuals was established. Date of entry was 12 months after diagnosis/index date (for cancer-free individuals). Follow-up ended at death, emigration, new primary cancer, December 31st, 2018, or up to 10 years. Information about education and healthcare use, defined as the number of consultations with general practitioner (GP), private practicing specialists (PPS), hospital, and acute healthcare contacts 1–9 years after diagnosis/index date, was extracted from national registers. We used Poisson regression models to compare healthcare use between cancer survivors and cancer-free individuals, and to investigate the association between education and healthcare use among cancer survivors. Results Cancer survivors had more GP, hospital, and acute healthcare contacts than cancer-free individuals, while the use of PPS were alike. One-to-four-year survivors with short compared to long education had more GP consultations (breast, rate ratios (RR) = 1.28, 95% CI = 1.25–1.30; prostate, RR = 1.14, 95% CI = 1.10–1.18; lung, RR = 1.18, 95% CI = 1.13–1.23; and colon cancer, RR = 1.17, 95% CI = 1.13–1.22) and acute contacts (breast, RR = 1.35, 95% CI = 1.26–1.45; prostate, RR = 1.26, 95% CI = 1.15–1.38; lung, RR = 1.24, 95% CI = 1.16–1.33; and colon cancer, RR = 1.35, 95% CI = 1.14–1.60), even after adjusting for comorbidity. One-to-four-year survivors with short compared to long education had less consultations with PPS, while no association was observed for hospital contacts. Conclusion Cancer survivors used more healthcare than cancer-free individuals. Cancer survivors with short education had more GP and acute healthcare contacts than survivors with long education. To optimize healthcare use after cancer, we need to better understand survivors’ healthcare-seeking behaviors and their specific needs, especially among survivors with short education.

Published
2023
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5. Knowledge on human papilloma virus and experience of getting positive results: a qualitative study among women in Kilimanjaro, Tanzania

Author

Patricia Swai, Melina Mgongo, Beatrice J. Leyaro, Julius Mwaiselage, Bariki L. Mchome, Susanne K. Kjaer, Vibeke Rasch, Rachel Manongi, and Sia E. Msuya

Subjects
HR-HPV, HPV results, HPV screening, Screening, Reaction, Tanzania, Gynecology and obstetrics, RG1-991, Public aspects of medicine, RA1-1270
Abstract

Abstract Background Human papilloma virus (HPV) is a sexually transmitted infection causing more than 80% of cervical cancers. WHO recommends using of sensitive screening methods like HPV-testing to timely prevent future morbidity and mortality from cervical cancer. Pilot studies have shown that HPV-testing is feasible and can be scaled in developing country like Tanzania. However, there is limited information on women understanding, reactions and psychological challenges following diagnosis of high risk HPV (HR-HPV). This study explored the knowledge of women on HPV and their experience after HPV positive results in Kilimanjaro, Tanzania. Methods The study was part of a larger study that assessed incidence and persistence of HR-HPV among women aged 18 years and above in Kilimanjaro. This was a cross sectional study conducted in Moshi municipal council among women who had HR-HPV positive results at enrollment. In-depth interviews were conducted with 13 randomly selected women who were attending for follow-up after enrollment. Interviews were conducted at the health facility and Atlas.ti.8 was used to analyze the data using thematic framework analysis. Results Women had knowledge on HPV infection but they had different reactions following receiving positive HPV results. Reaction toward the positive HPV results had two extremes; some women had psychological effect (hopeless, death sentence, having cancer, being shocked, failure to disclose and psychosexual effects) while others women explained positive results is good as they are identified earlier, will be followed up and it has made them plan to continue with cervical cancer screening in future. Conclusion Women had knowledge on HPV, but positive results lead to negative and positive experiences by women. Clinicians and programs need to develop interventions and good strategies to minimize the psychological and social burden of testing positive for HPV.

Published
2023
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6. Persistence and risk factors of high-risk human papillomavirus infection among HIV positive and HIV negative tanzanian women: a cohort study

Author

Patricia Swai, Vibeke Rasch, Ditte S. Linde, Bariki Mchome, Rachel Manongi, Chun Sen Wu, Marianne Waldstrom, Thomas Iftner, Julius Mwaiselage, and Susanne K. Kjaer

Subjects
HR HPV, Persistence, Risk factors, HIV status, Tanzania, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282, Infectious and parasitic diseases, RC109-216
Abstract

Abstract Background High-risk (HR) human papillomavirus (HPV) persistence is the most important risk factor for cervical cancer. We have assessed the type-specific HR HPV persistence among HIV positive and HIV negative Tanzanian women and factors associated with HR HPV persistence. Methods In a cohort study including 4080 Tanzanian women, 3074 attended follow-up examination (up to 32 months after enrollment). Cervical samples were obtained for liquid-based cytology and HPV DNA testing using Hybrid Capture 2 and Inno-Lipa Extra II. Information on lifestyle factors was collected through a personal interview. The probability of HR HPV persistence at a given time point since enrollment was estimated non-parametrically using the EMICM algorithm. Results Among the 462 women HR HPV positive at enrollment, 158 had at least one identical type detected at follow-up. The probability of persistence at 18 months after enrollment was 34.2 (95% CI 29.0–39.4). Stratifying by HIV status, the persistence probability was 42.9% (95% CI 33.5–51.9) among HIV positive, and 28.0% (95% CI 22.1–34.2) among HIV negative. Overall, HR HPV persistence was most common for HPV58, 35, 16, 31, and 52. Among HIV positive women it was HPV45, and HPV16, followed by HPV58 and HPV18, and among HIV negative women it was HPV31, HPV33 and HPV58. Risk factors associated with persistence of HR HPV were older age, longer interval between enrollment and follow-up, binge drinking, and HIV status. Conclusions HR HPV persistence was common in Tanzania, and most common among HIV positive women. Overall, persistence was most frequent for HPV 58, 35, 16, 31 and 52. The nonavalent HPV vaccine should be considered.

Published
2022
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7. Concordance in HPV Detection Between Self-Collected and Health Provider–Collected Cervicovaginal Samples Using careHPV in Tanzanian Women

Author

Johnson J. Katanga, Vibeke Rasch, Rachel Manongi, Andrea B. Pembe, Julius D. Mwaiselage, and Susanne K. Kjaer

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

PURPOSECervical cancer screening is one of the strategies to prevent the disease among women at risk. Human papillomavirus (HPV) DNA testing is increasingly used as the cervical cancer screening method because of its high sensitivity. Self-collection of cervical specimens has the potential to improve participation. However, there is only limited information on comparison between self-collected and provider-collected samples with regard to detection of high-risk HPV using the careHPV method. The study aimed to compare HPV detection by careHPV in self-collected and provider-collected cervical samples and to assess the acceptability of self-collection techniques.MATERIAL AND METHODSWomen attending cervical cancer screening clinics at Ocean Road Cancer Institute, Kilimanjaro Christian Medical Centre or Mawenzi Hospital in Tanzania were included in the study. They underwent a face-to-face interview, HIV testing, and collected a self-sample using Evalyn Brush. Subsequently, they had a cervical sample taken by a health provider. Both samples were tested for high-risk HPV DNA using careHPV.RESULTSOverall, 464 women participated in the study. The high-risk HPV prevalence was 19.0% (95% CI, 15.6 to 22.9) in the health provider samples, but lower (13.8%; 95% CI, 10.9 to 17.3) in the self-collected samples. There was a good overall agreement 90.5% (95% CI, 87.5 to 93.0) and concordance (κ = 0.66; 95% CI, 0.56 to 0.75) between the two sets of samples. Sensitivity and specificity were 61.4% (95% CI, 50.4 to 71.6) and 97.3% (95% CI, 95.2 to 98.7), respectively, varying with age. Most women preferred self-collection (79.8%).CONCLUSIONOverall, self-sampling seems to be a reliable alternative to health-provider collection and is acceptable to the majority of women. However, instructions on proper procedures for sample collection to the women are important.

Published
2021
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8. Effects of early maternal cancer and fertility treatment on the risk of adverse birth outcomes

Author

Cathrine Everhøj, Filippa Nyboe Norsker, Catherine Rechnitzer, Sofie de Fine Licht, Thomas T Nielsen, Susanne K. Kjær, Allan Jensen, Marie Hargreave, Jane Christensen, Federica Belmonte, Stine Kjaer Urhoj, Katrine Strandberg-Larsen, Jeanette F Winther, and Line Kenborg

Subjects
Early onset cancer, Survivorship, Fertility treatment, Birth outcomes, Population-based, Cohort study, Medicine (General), R5-920
Abstract

Summary: Background: Early maternal cancer and fertility treatment each increase the risk for adverse birth outcomes, but the joint effect of these outcomes has not yet been reported. Thus, the aim was to assess the individual and joint effect of maternal cancer and fertility treatment on the risk for adverse birth outcomes. Methods: This population-based cohort study included 5487 live-born singletons identified in the Danish Medical Birth Register (1994–2016) of mothers with previous cancer (

Published
2022
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10. Spontaneous preterm birth risk among <scp>HPV</scp> ‐vaccinated and ‐unvaccinated women: a nationwide retrospective cohort study of over 240 000 singleton births

Author

Elisabeth McClymont, Mette T. Faber, Federica Belmonte, and Susanne K. Kjaer

Subjects
Obstetrics and Gynecology
Abstract

To determine if prior HPV vaccination contributes to preterm birth risk.Population-based retrospective cohort study.Denmark.243 136 primiparous females born 1961-2004 who had a singleton delivery at22 weeks' gestation occurring in October 2006 to December 2018.High-quality nationwide registries were linked to provide information on demographics, birth outcomes, HPV vaccination status, smoking, BMI, and cervical lesions and treatment history.We assessed the association between HPV vaccination status and spontaneous preterm birth using logistic regression. To address age at vaccination, we performed a stratified analysis by vaccination before and after 17 years old.In age-adjusted and fully-adjusted models, there was a non-significant difference in the odds of spontaneous preterm birth between vaccinated and unvaccinated women (OR: 1.05 [95% CI: 0.99-1.12] and 1.04 [95% CI: 0.98-1.10], respectively). There was no difference in the odds of spontaneous preterm birth in relation to time between vaccination and pregnancy. In contrast, compared to unvaccinated women, the odds of preterm birth were lower among women vaccinated before age 17 (fully-adjusted OR: 0.87, 95% CI: 0.75-1.00). This association was not present for women vaccinated at age17.In this large, population-based cohort, we found reduced odds of spontaneous preterm birth among women HPV vaccinated at an early age compared to those unvaccinated. It seems conceivable that HPV vaccination may not only reduce the incidence of cervical cancer and severe precursors, but also the risk of preterm birth related to HPV infection.

Published
2022

11. Time trends in prevalence of p16 positivity and combined HPV/p16 positivity in a large cohort of Danish vulvar cancer patients

Author

Christina Louise Rasmussen, Louise T. Thomsen, Louise Baandrup, Maria Benedicte Franzmann, Alexander K. Kjær, Lise Grupe Larsen, Else Mejlgaard Madsen, Nadia Margeth Villena Salinas, Doris Schledermann, Birgitte Hjelm Winberg, Dorthe Ørnskov, Marianne Waldstrøm, and Susanne K. Kjær

Subjects
time trends, Cancer Research, HPV, vulvar cancer, Oncology, p16
Abstract

Vulvar cancer is rare, but causes substantial morbidity in affected patients. A subset of vulvar cancers is caused by high-risk human papillomavirus (hrHPV), which primarily exerts its oncogenic effect through upregulation of tumor suppressor protein p16. Tumors positive for both hrHPV and p16 (double positive) are assumed to be HPV-driven, but only few large studies have investigated the combined prevalence of hrHPV and p16 positivity in vulvar cancer over time. In this Danish cross-sectional study, we assessed the prevalence of p16 positivity and double positivity for hrHPV and p16 in a large sample of vulvar squamous cell carcinomas (VSCCs) diagnosed during 1990 to 2017. In a nationwide register, we identified VSCCs from 13 hospitals across Denmark, and collected archival tumor tissue for hrHPV testing with INNO-LiPA and immunohistochemical p16 staining. We calculated the prevalence of hrHPV, p16 positivity and double positivity according to time, age and histological subtype and evaluated time trends through estimated annual percentage changes. We included 1278 VSCCs. Overall, 35.0% (95% confidence interval [CI]: 32.4-37.6) were positive for p16 and 31.0% (95% CI: 28.4-33.5) were positive for both hrHPV and p16. The prevalence of p16 positivity and double positivity increased over time, both in women aged ≤59 and ≥60 years. The double positive prevalence was higher in nonkeratinizing (60.7%) and warty/basaloid VSCCs (67.5%) than in keratinizing (16.1%) and verrucous VSCCs (5.0%). These results indicate that approximately one-third of vulvar cancers were caused by hrHPV infection, supporting a substantial preventive potential of the HPV vaccine.

Published
2023

12. Tumors of the central nervous system among women treated with fertility drugs: a population-based cohort study

Author

Clarissa L. B. Frandsen, Allan Jensen, Frantz R. Poulsen, Maria Møller, Sofie Lindquist, Vanna Albieri, Bugge Nøhr, and Susanne K. Kjær

Subjects
Central Nervous System Neoplasms, Cohort Studies, Cancer Research, Oncology, Risk Factors, Denmark, Meningeal Neoplasms, Humans, Female, Meningioma, Infertility, Female, Fertility Agents
Abstract

To investigate the association between fertility drugs and tumors of the central nervous system (CNS).This cohort study was based on The Danish Infertility Cohort and included 148,016 infertile women living in Denmark (1995-2017). The study cohort was linked to national registers to obtain information on use of specific fertility drugs, cancer diagnoses, covariates, emigration, and vital status. Cox proportional hazard regression models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for all CNS tumors and separately for gliomas, meningiomas and diverse benign tumors of the brain and other parts of the CNS.During a median 11.3 years of follow-up, 328 women were diagnosed with CNS tumors. No marked associations were observed between use of the fertility drugs clomiphene citrate, gonadotropins, gonadotropin-releasing hormone receptor modulators and progesterone and CNS tumors. However, use of human chorionic gonadotropin was associated with a decreased rate of meningiomas (HR 0.49 95% CI 0.28-0.87). No clear associations with CNS tumors were observed according to time since first use or cumulative dose for any of the fertility drugs.No associations between use of most types of fertility drugs and CNS tumors were observed. However, our findings only apply to premenopausal women and additional studies with longer follow-up time are necessary.

Published
2022

14. Data from A Pooled Analysis of Continued Prophylactic Efficacy of Quadrivalent Human Papillomavirus (Types 6/11/16/18) Vaccine against High-grade Cervical and External Genital Lesions

Author

Richard M. Haupt, Eliav Barr, Alfred Saah, Teresa M. Hesley, Scott Vuocolo, Shuang Lu, Roger Maansson, Janine Bryan, Amha Tadesse, Christine Roberts, Frank J. Taddeo, Luisa L. Villa, Evan R. Myers, Nubia Muñoz, Slawomir Majewski, Elmar A. Joura, Joakim Dillner, F. Xavier Bosch, Marc Steben, Matti Lehtinen, Jorma Paavonen, Daron G. Ferris, Grace W.K. Tang, Sven-Eric Olsson, Sepp Leodolter, Suzanne M. Garland, Kevin A. Ault, Patricia García, Eng Hseon Tay, Laura A. Koutsky, Darron R. Brown, Gonzalo Perez, Cosette M. Wheeler, Mauricio Hernandez-Avila, Ole-Erik Iversen, Kristján Sigurdsson, and Susanne K. Kjaer

Abstract

Quadrivalent human papillomavirus (HPV) vaccine has been shown to provide protection from HPV 6/11/16/18–related cervical, vaginal, and vulvar disease through 3 years. We provide an update on the efficacy of the quadrivalent HPV vaccine against high-grade cervical, vaginal, and vulvar lesions based on end-of-study data from three clinical trials. Additionally, we stratify vaccine efficacy by several baseline characteristics, including age, smoking status, and Papanicolaou (Pap) test results. A total of 18,174 females ages 16 to 26 years were randomized and allocated into one of three clinical trials (protocols 007, 013, and 015). Vaccine or placebo was given at baseline, month 2, and month 6. Pap testing was conducted at regular intervals. Cervical and anogenital swabs were collected for HPV DNA testing. Examination for the presence of vulvar and vaginal lesions was also done. Endpoints included high-grade cervical, vulvar, or vaginal lesions (CIN 2/3, VIN 2/3, or VaIN 2/3). Mean follow-up time was 42 months post dose 1. Vaccine efficacy against HPV 6/11/16/18–related high-grade cervical lesions in the per-protocol and intention-to-treat populations was 98.2% [95% confidence interval (95% CI), 93.3-99.8] and 51.5% (95% CI, 40.6-60.6), respectively. Vaccine efficacy against HPV 6/11/16/18–related high-grade vulvar and vaginal lesions in the per-protocol and intention-to-treat populations was 100.0% (95% CI, 82.6-100.0) and 79.0% (95% CI, 56.4-91.0), respectively. Efficacy in the intention-to-treat population tended to be lower in older women, women with more partners, and women with abnormal Pap test results. The efficacy of quadrivalent HPV vaccine against high-grade cervical and external anogenital neoplasia remains high through 42 months post vaccination.

Published
2023

15. Supplementary Tables 1-2 from A Pooled Analysis of Continued Prophylactic Efficacy of Quadrivalent Human Papillomavirus (Types 6/11/16/18) Vaccine against High-grade Cervical and External Genital Lesions

Author

Richard M. Haupt, Eliav Barr, Alfred Saah, Teresa M. Hesley, Scott Vuocolo, Shuang Lu, Roger Maansson, Janine Bryan, Amha Tadesse, Christine Roberts, Frank J. Taddeo, Luisa L. Villa, Evan R. Myers, Nubia Muñoz, Slawomir Majewski, Elmar A. Joura, Joakim Dillner, F. Xavier Bosch, Marc Steben, Matti Lehtinen, Jorma Paavonen, Daron G. Ferris, Grace W.K. Tang, Sven-Eric Olsson, Sepp Leodolter, Suzanne M. Garland, Kevin A. Ault, Patricia García, Eng Hseon Tay, Laura A. Koutsky, Darron R. Brown, Gonzalo Perez, Cosette M. Wheeler, Mauricio Hernandez-Avila, Ole-Erik Iversen, Kristján Sigurdsson, and Susanne K. Kjaer

Abstract

PDF file - 284K

Published
2023

16. Supplementary Tables 1 - 4 from Large-Scale Evaluation of Common Variation in Regulatory T Cell–Related Genes and Ovarian Cancer Outcome

Author

Ellen L. Goode, Keith L. Knutson, Lara E. Sucheston, Kunle Odunsi, Roberta B. Ness, Simon A. Gayther, Paul D.P. Pharoah, Georgia Chenevix-Trench, Mary Anne Rossing, Daniel W. Cramer, Celeste Leigh Pearce, Joellen M. Schildkraut, Usha Menon, Susanne K. Kjaer, Douglas A. Levine, Jacek Gronwald, Hoda Anton Culver, Alice S. Whittemore, Beth Y. Karlan, Diether Lambrechts, Nicolas Wentzensen, Jolanta Kupryjanczyk, Jenny Chang-Claude, Elisa V. Bandera, Estrid Hogdall, Florian Heitz, Stanley B. Kaye, Gottfried Konecny, Peter A. Fasching, Ian Campbell, Marc T. Goodman, Tanja Pejovic, Yukie T. Bean, Laura E. Hays, Galina Lurie, Diana Eccles, Alexander Hein, Matthias W. Beckmann, Arif B. Ekici, James Paul, Robert Brown, James M. Flanagan, Philipp Harter, Andreas du Bois, Ira Schwaab, Claus K. Hogdall, Sara H. Olson, Lene Lundvall, Irene Orlow, Lisa E. Paddock, Anja Rudolph, Petra Seibold, Agnieszka Dansonka-Mieszkowska, Iwona K. Rzepecka, Beata Spiewankiewicz, Louise A. Brinton, Hannah Yang, Montserrat Garcia-Closas, Evelyn Despierre, Sandrina Lambrechts, Ignace Vergote, Christine Walsh, Jenny Lester, Weiva Sieh, Valerie McGuire, Joseph H. Rothstein, Argyrios Ziogas, Jan Lubiński, Cezary Cybulski, Janusz Menkiszak, Allan Jensen, Howard Shen, Brenda Diergaarde, Susan J. Ramus, Aleksandra Gentry-Maharaj, Andrew Berchuck, Anna H. Wu, Malcolm C. Pike, David Van Den Berg, Kathryn L. Terry, Allison F. Vitonis, Starr M. Ramirez, Thomas A. Sellers, Catherine M. Phelan, Jennifer A. Doherty, Sharon E. Johnatty, Anna deFazio, Honglin Song, Jonathan Tyrer, Chen Wang, Kate Lawrenson, Lynn C. Hartmann, Claudia Preston, David N. Rider, Julie M. Cunningham, Brooke L. Fridley, Krista M. Goergen, Matthew J. Maurer, Matthew S. Block, Zachary C. Fogarty, Robert A. Vierkant, Ann L. Oberg, Kimberly R. Kalli, Kirsten B. Moysich, and Bridget Charbonneau

Abstract

PDF file - 157K, Supplemental Table 1. Regulatory T cell genes included in this study (N=25). Supplemental Table 2. Regulatory T cell SNPs included in this study. Supplemental Table 3. Participating invasive epithelial ovarian cancer studies. Supplemental Table 4. Association between clinical variables and overall survival.

Published
2023

17. Data from Large-Scale Evaluation of Common Variation in Regulatory T Cell–Related Genes and Ovarian Cancer Outcome

Author

Ellen L. Goode, Keith L. Knutson, Lara E. Sucheston, Kunle Odunsi, Roberta B. Ness, Simon A. Gayther, Paul D.P. Pharoah, Georgia Chenevix-Trench, Mary Anne Rossing, Daniel W. Cramer, Celeste Leigh Pearce, Joellen M. Schildkraut, Usha Menon, Susanne K. Kjaer, Douglas A. Levine, Jacek Gronwald, Hoda Anton Culver, Alice S. Whittemore, Beth Y. Karlan, Diether Lambrechts, Nicolas Wentzensen, Jolanta Kupryjanczyk, Jenny Chang-Claude, Elisa V. Bandera, Estrid Hogdall, Florian Heitz, Stanley B. Kaye, Gottfried Konecny, Peter A. Fasching, Ian Campbell, Marc T. Goodman, Tanja Pejovic, Yukie T. Bean, Laura E. Hays, Galina Lurie, Diana Eccles, Alexander Hein, Matthias W. Beckmann, Arif B. Ekici, James Paul, Robert Brown, James M. Flanagan, Philipp Harter, Andreas du Bois, Ira Schwaab, Claus K. Hogdall, Sara H. Olson, Lene Lundvall, Irene Orlow, Lisa E. Paddock, Anja Rudolph, Petra Seibold, Agnieszka Dansonka-Mieszkowska, Iwona K. Rzepecka, Beata Spiewankiewicz, Louise A. Brinton, Hannah Yang, Montserrat Garcia-Closas, Evelyn Despierre, Sandrina Lambrechts, Ignace Vergote, Christine Walsh, Jenny Lester, Weiva Sieh, Valerie McGuire, Joseph H. Rothstein, Argyrios Ziogas, Jan Lubiński, Cezary Cybulski, Janusz Menkiszak, Allan Jensen, Howard Shen, Brenda Diergaarde, Susan J. Ramus, Aleksandra Gentry-Maharaj, Andrew Berchuck, Anna H. Wu, Malcolm C. Pike, David Van Den Berg, Kathryn L. Terry, Allison F. Vitonis, Starr M. Ramirez, Thomas A. Sellers, Catherine M. Phelan, Jennifer A. Doherty, Sharon E. Johnatty, Anna deFazio, Honglin Song, Jonathan Tyrer, Chen Wang, Kate Lawrenson, Lynn C. Hartmann, Claudia Preston, David N. Rider, Julie M. Cunningham, Brooke L. Fridley, Krista M. Goergen, Matthew J. Maurer, Matthew S. Block, Zachary C. Fogarty, Robert A. Vierkant, Ann L. Oberg, Kimberly R. Kalli, Kirsten B. Moysich, and Bridget Charbonneau

Abstract

The presence of regulatory T cells (Treg) in solid tumors is known to play a role in patient survival in ovarian cancer and other malignancies. We assessed inherited genetic variations via 749 tag single-nucleotide polymorphisms (SNP) in 25 Treg-associated genes (CD28, CTLA4, FOXP3, IDO1, IL10, IL10RA, IL15, 1L17RA, IL23A, IL23R, IL2RA, IL6, IL6R, IL8, LGALS1, LGALS9, MAP3K8, STAT5A, STAT5B, TGFB1, TGFB2, TGFB3, TGFBR1, TGRBR2, and TGFBR3) in relation to ovarian cancer survival. We analyzed genotype and overall survival in 10,084 women with invasive epithelial ovarian cancer, including 5,248 high-grade serous, 1,452 endometrioid, 795 clear cell, and 661 mucinous carcinoma cases of European descent across 28 studies from the Ovarian Cancer Association Consortium (OCAC). The strongest associations were found for endometrioid carcinoma and IL2RA SNPs rs11256497 [HR, 1.42; 95% confidence interval (CI), 1.22–1.64; P = 5.7 × 10−6], rs791587 (HR, 1.36; 95% CI, 1.17–1.57; P = 6.2 × 10−5), rs2476491 (HR, = 1.40; 95% CI, 1.19–1.64; P = 5.6 × 10−5), and rs10795763 (HR, 1.35; 95% CI, 1.17–1.57; P = 7.9 × 10−5), and for clear cell carcinoma and CTLA4 SNP rs231775 (HR, 0.67; 95% CI, 0.54–0.82; P = 9.3 × 10−5) after adjustment for age, study site, population stratification, stage, grade, and oral contraceptive use. The rs231775 allele associated with improved survival in our study also results in an amino acid change in CTLA4 and previously has been reported to be associated with autoimmune conditions. Thus, we found evidence that SNPs in genes related to Tregs seem to play a role in ovarian cancer survival, particularly in patients with clear cell and endometrioid epithelial ovarian cancer. Cancer Immunol Res; 2(4); 332–40. ©2014 AACR.

Published
2023

18. Table S8 from A Transcriptome-Wide Association Study Among 97,898 Women to Identify Candidate Susceptibility Genes for Epithelial Ovarian Cancer Risk

Author

Jirong Long, Wei Zheng, Paul D.P. Pharoah, Thomas A. Sellers, Georgia Chenevix-Trench, Ellen L. Goode, Andrew Berchuck, Antonis C. Antoniou, Simon A. Gayther, Kristin K. Zorn, Drakoulis Yannoukakos, Anna H. Wu, Alicja Wolk, Emily White, Nicolas Wentzensen, Jeffrey N. Weitzel, Penelope M. Webb, Digna Velez Edwards, Ana Vega, Adriaan Vanderstichele, Elizabeth J. van Rensburg, Shelley S. Tworoger, Nadine Tung, Antonia Trichopoulou, Amanda E. Toland, Marc Tischkowitz, Mads Thomassen, Soo H. Teo, Manuel R. Teixeira, Anthony J. Swerdlow, Rebecca Sutphen, Amanda B. Spurdle, Melissa C. Southey, Honglin Song, Christian F. Singer, Jacques Simard, Weiva Sieh, Priyanka Sharma, Veronica W. Setiawan, Rita K. Schmutzler, Dale P. Sandler, Iwona K. Rzepecka, Mary Anne Rossing, Matti A. Rookus, Isabelle Romieu, Cristina Rodríguez-Antona, Gustavo C. Rodriguez, Harvey Risch, Gad Rennert, Susan J. Ramus, Miquel Angel Pujana, Catherine M. Phelan, Paolo Peterlongo, Tanja Pejovic, Petra H.M. Peeters, Michael T. Parsons, Sue K. Park, Ana Osorio, Håkan Olsson, Sara H. Olson, Olufunmilayo I. Olopade, Edith Olah, Kenneth Offit, Robert L. Nussbaum, Liene Nikitina-Zake, Finn C. Nielsen, Heli Nevanlinna, Susan L. Neuhausen, Marco Montagna, Francesmary Modugno, Melissa A. Merritt, Iain A. McNeish, Lesley McGuffog, Taymaa May, Amalia Mattiello, Douglas A. Levine, Fabienne Lesueur, Goska Leslie, Nhu D. Le, Ava Kwong, Susanne K. Kjaer, Lambertus A. Kiemeney, Linda E. Kelemen, Beth Y. Karlan, Paul James, Anna Jakubowska, Claudine Isaacs, Evgeny N. Imyanitov, David G. Huntsman, Peter J. Hulick, Antoinette Hollestelle, Claus K. Høgdall, Michelle A.T. Hildebrandt, Florian Heitz, Ute Hamann, Jacek Gronwald, Mark H. Greene, Marc T. Goodman, David E. Goldgar, Andrew K. Godwin, Graham G. Giles, Judy Garber, Patricia A. Ganz, Eitan Friedman, George Fountzilas, Renée T. Fortner, Peter A. Fasching, Diana M. Eccles, Douglas F. Easton, Thilo Dörk, Susan M. Domchek, Orland Diez, Joe Dennis, Anna deFazio, Mary B. Daly, Daniel W. Cramer, Fergus J. Couch, Kathleen B.M. Claes, Jenny Chang-Claude, Ian Campbell, Maria A. Caligo, Trinidad Caldes, Ralf Butzow, James Brenton, Line Bjorge, Javier Benitez, Daniel R. Barnes, Rosa B. Barkardottir, Elisa V. Bandera, Banu K. Arun, Hoda Anton-Culver, Irene L. Andrulis, Kirsten B. Moysich, Jamie K. Teer, Brett M. Reid, Jennifer B. Permuth, Yian A. Chen, Hae Kyung Im, Joellen M. Schildkraut, Bingshan Li, Xingyi Guo, Lang Wu, Alicia Beeghly-Fadiel, and Yingchang Lu

Abstract

Association results between minor alleles of 467 variants incorportated in cross tissue gene expression prediction model for the gene of CRHR1.

Published
2023

19. Data from Network-Based Integration of GWAS and Gene Expression Identifies a HOX-Centric Network Associated with Serous Ovarian Cancer Risk

Author

Paul D.P. Pharoah, Simon A. Gayther, Matthew L. Freedman, Alvaro N.A. Monteiro, Thomas A. Sellers, Argyrios Ziogas, Wei Zheng, Hannah Yang, Anna Wu, Xifeng Wu, Yin-Ling Woo, Lynne R. Wilkens, Kristine G. Wicklund, Alice S. Whittemore, Nicolas Wentzensen, Christine Walsh, Shan Wang-Gohrke, Robert A. Vierkant, Ignace Vergote, Els Van Nieuwenhuysen, Anne M. van Altena, Shelley S. Tworoger, Ya-Yu Tsai, Agnieszka Timorek, Pamela J. Thompson, Kathryn L. Terry, Soo-Hwang Teo, Ingvild L. Tangen, Lara E. Sucheston-Campbell, Melissa C. Southey, Honglin Song, Weiva Sieh, Nadeem Siddiqui, Yurii B. Shvetsov, Xiao-Ou Shu, Ira Schwaab, Joellen M. Schildkraut, Helga B. Salvesen, Iwona K. Rzepecka, Ingo B. Runnebaum, Anja Rudolph, Joseph H. Rothstein, Mary Anne Rossing, Barry Rosen, Harvey A. Risch, Susan J. Ramus, Elizabeth M. Poole, Malcolm C. Pike, Catherine M. Phelan, Jennifer Permuth-Wey, Liisa M. Pelttari, Tanja Pejovic, Celeste Leigh Pearce, Rachel Palmieri Weber, Sandra Orsulic, Irene Orlow, Sara H. Olson, Kunle Odunsi, Heli Nevanlinna, Roberta B. Ness, Lotte Nedergaard, Steven A. Narod, Kirsten B. Moysich, Francesmary Modugno, Usha Menon, Iain A. McNeish, John R. McLaughlin, Valerie McGuire, Keitaro Matsuo, Leon Massuger, Lene Lundvall, Jan Lubinski, Karen Lu, Jolanta Lissowska, Dong Liang, Douglas A. Levine, Jenny Lester, Arto Leminen, Shashi Lele, Alice W. Lee, Nhu D. Le, Sandrina Lambrechts, Diether Lambrechts, Jolanta Kupryjanczyk, Camilla Krakstad, Lambertus A. Kiemeney, Joseph Kelley, Melissa Kellar, Linda E. Kelemen, Susanne K. Kjaer, Beth Y. Karlan, Bu-Tian Ji, Allan Jensen, James Paul, Anna Jakubowska, Edwin S. Iversen, Satoyo Hosono, Claus K. Hogdall, Estrid Hogdall, Peter Hillemanns, Michelle A.T. Hildebrandt, Florian Heitz, Alexander Hein, Philipp Harter, Patricia Harrington, Jacek Grownwald, Marc T. Goodman, Ellen L. Goode, Rosalind Glasspool, Graham G. Giles, Aleksandra Gentry-Maharaj, Yu-Tang Gao, Brooke L. Fridley, Peter A. Fasching, Arif B. Ekici, Robert P. Edwards, Douglas F. Easton, Diana Eccles, Matthias Dürst, Andreas du Bois, Thilo Dörk, Jennifer A. Doherty, Ed Dicks, Joe Dennis, Agnieszka Dansonka-Mieszkowska, Cezary Cybulski, Julie M. Cunningham, Daniel Cramer, Linda S. Cook, Zhihua Chen, Yian Ann Chen, Jenny Chang-Claude, Karen Carty, Ian Campbell, Ralf Butzow, Angela Brooks-Wilson, Louise Brinton, Natalia Bogdanova, Line Bjørge, Maria Bisogna, Andrew Berchuck, Matthias W. Beckmann, Yukie T. Bean, Elisa V. Bandera, Helen Baker, Georgia Chenevix-Trench, Natalia Antonenkova, Hoda Anton-Culver, Katja K.H. Aben, Kate Lawrenson, Qiyuan Li, Jonathan P. Tyrer, and Siddhartha P. Kar

Abstract

Background: Genome-wide association studies (GWAS) have so far reported 12 loci associated with serous epithelial ovarian cancer (EOC) risk. We hypothesized that some of these loci function through nearby transcription factor (TF) genes and that putative target genes of these TFs as identified by coexpression may also be enriched for additional EOC risk associations.Methods: We selected TF genes within 1 Mb of the top signal at the 12 genome-wide significant risk loci. Mutual information, a form of correlation, was used to build networks of genes strongly coexpressed with each selected TF gene in the unified microarray dataset of 489 serous EOC tumors from The Cancer Genome Atlas. Genes represented in this dataset were subsequently ranked using a gene-level test based on results for germline SNPs from a serous EOC GWAS meta-analysis (2,196 cases/4,396 controls).Results: Gene set enrichment analysis identified six networks centered on TF genes (HOXB2, HOXB5, HOXB6, HOXB7 at 17q21.32 and HOXD1, HOXD3 at 2q31) that were significantly enriched for genes from the risk-associated end of the ranked list (P < 0.05 and FDR < 0.05). These results were replicated (P < 0.05) using an independent association study (7,035 cases/21,693 controls). Genes underlying enrichment in the six networks were pooled into a combined network.Conclusion: We identified a HOX-centric network associated with serous EOC risk containing several genes with known or emerging roles in serous EOC development.Impact: Network analysis integrating large, context-specific datasets has the potential to offer mechanistic insights into cancer susceptibility and prioritize genes for experimental characterization. Cancer Epidemiol Biomarkers Prev; 24(10); 1574–84. ©2015 AACR.

Published
2023

20. Figure S3 from Investigation of Exomic Variants Associated with Overall Survival in Ovarian Cancer

Author

Ellen L. Goode, Thomas A. Sellers, Brooke L. Fridley, Paul D.P. Pharoah, Catherine M. Phelan, Jennifer Permuth-Wey, Joellen M. Schildkraut, Andrew Berchuck, Argyrios Ziogas, Hannah Yang, Anna H. Wu, Lynne R. Wilkens, Christine Walsh, Allison F. Vitonis, Robert A. Vierkant, David J. van den Berg, Jonathan P. Tyrer, Pamela J. Thompson, Kathryn L. Terry, Honglin Song, Susan J. Ramus, Malcolm C. Pike, Irene Orlow, Kirsten B. Moysich, Francesmary Modugno, Janusz Menkiszak, Jan Lubinski, Jolanta Lissowska, Hui-Yi Lin, Jenny Lester, Sharon E. Johnatty, Allan Jensen, Edwin S. Iversen, Martin Gore, Aleksandra Gentry-Maharaj, Simon A. Gayther, Robert P. Edwards, Ed M. Dicks, Anna deFazio, Cezary Cybulski, Julie M. Cunningham, Michael E. Carney, Louise A. Brinton, Maria Bisogna, Yukie T. Bean, Nicolas Wentzensen, Mary Anne Rossing, Tanja Pejovic, Celeste L. Pearce, Roberta B. Ness, Usha Menon, Douglas A. Levine, Susanne K. Kjaer, Beth Y. Karlan, Jacek Gronwald, Marc T. Goodman, Jennifer A. Doherty, Daniel Cramer, Elisa V. Bandera, Hoda Anton-Culver, Madalene A. Earp, Zachary C. Fogarty, Melissa C. Larson, Yian Ann Chen, Ailith Pirie, and Stacey J. Winham

Abstract

Supplemental Figure S 3

Published
2023

21. Supplementary Figure S2 from The BRCA1-Δ11q Alternative Splice Isoform Bypasses Germline Mutations and Promotes Therapeutic Resistance to PARP Inhibition and Cisplatin

Author

Neil Johnson, Violeta Serra, Judith Balmaña, Jos Jonkers, Peter Bouwman, Elizabeth M. Swisher, Mary B. Daly, Denise C. Connolly, David L. Wiest, Geoffrey I. Shapiro, Alan D. D'Andrea, Susanne K. Kjaer, Simon A. Gayther, Siegal Sadetzki, Robert Nussbaum, Martin Gore, Mark H. Greene, Javier J. Benitez, Håkan Olsson, Georgia Chenevix-Trench, Diether Lambrechts, Charlie Gourley, Beth Karlan, Paul D. P. Pharoah, Francisco J. Candido Dos Reis, Shawn F. Johnson, Maribel I. Harrell, Yong Zhang, Shane W. O'Brien, Ingrid van der Heijden, Hanneke van der Gulden, Suraj Peri, Emmanuelle Nicolas, Joseph Nacson, John J. Krais, Cristina Cruz, Andrea J. Bernhardy, and Yifan Wang

Abstract

Genetic analyses of BRCA1 mutant cell lines and PDX models.

Published
2023

22. Data from The BRCA1-Δ11q Alternative Splice Isoform Bypasses Germline Mutations and Promotes Therapeutic Resistance to PARP Inhibition and Cisplatin

Author

Neil Johnson, Violeta Serra, Judith Balmaña, Jos Jonkers, Peter Bouwman, Elizabeth M. Swisher, Mary B. Daly, Denise C. Connolly, David L. Wiest, Geoffrey I. Shapiro, Alan D. D'Andrea, Susanne K. Kjaer, Simon A. Gayther, Siegal Sadetzki, Robert Nussbaum, Martin Gore, Mark H. Greene, Javier J. Benitez, Håkan Olsson, Georgia Chenevix-Trench, Diether Lambrechts, Charlie Gourley, Beth Karlan, Paul D. P. Pharoah, Francisco J. Candido Dos Reis, Shawn F. Johnson, Maribel I. Harrell, Yong Zhang, Shane W. O'Brien, Ingrid van der Heijden, Hanneke van der Gulden, Suraj Peri, Emmanuelle Nicolas, Joseph Nacson, John J. Krais, Cristina Cruz, Andrea J. Bernhardy, and Yifan Wang

Abstract

Breast and ovarian cancer patients harboring BRCA1/2 germline mutations have clinically benefitted from therapy with PARP inhibitor (PARPi) or platinum compounds, but acquired resistance limits clinical impact. In this study, we investigated the impact of mutations on BRCA1 isoform expression and therapeutic response. Cancer cell lines and tumors harboring mutations in exon 11 of BRCA1 express a BRCA1-Δ11q splice variant lacking the majority of exon 11. The introduction of frameshift mutations to exon 11 resulted in nonsense-mediated mRNA decay of full-length, but not the BRCA1-Δ11q isoform. CRISPR/Cas9 gene editing as well as overexpression experiments revealed that the BRCA1-Δ11q protein was capable of promoting partial PARPi and cisplatin resistance relative to full-length BRCA1, both in vitro and in vivo. Furthermore, spliceosome inhibitors reduced BRCA1-Δ11q levels and sensitized cells carrying exon 11 mutations to PARPi treatment. Taken together, our results provided evidence that cancer cells employ a strategy to remove deleterious germline BRCA1 mutations through alternative mRNA splicing, giving rise to isoforms that retain residual activity and contribute to therapeutic resistance. Cancer Res; 76(9); 2778–90. ©2016 AACR.

Published
2023

23. Supplementary Figures 1-3 from Platinum Sensitivity–Related Germline Polymorphism Discovered via a Cell-Based Approach and Analysis of Its Association with Outcome in Ovarian Cancer Patients

Author

M. Eileen Dolan, Georgia Chenevix-Trench, Anna deFazio, Beth Y. Karlan, Jenny Gross, Ignace Vergote, Evelyn Despierre, Diether Lambrechts, Jim Paul, Robert Brown, Kunle Odunsi, Matthew Grasela, Kirsten B. Moysich, Allan Jensen, Susanne K. Kjaer, Estrid Hogdall, Brooke L. Fridley, Robert A. Vierkant, Ellen L. Goode, Stuart MacGregor, Yi Lu, Nancy J. Cox, Soma Das, Yarden S. Fraiman, Peter H. O'Donnell, Shuangli Mi, Jonathan Beesley, Peixian Chen, Emily O. Kistner, Wei Zhang, Shiwei Duan, Dana Ziliak, Hae Kyung Im, Eric R. Gamazon, Sharon E. Johnatty, and R. Stephanie Huang

Abstract

PDF file - 263K

Published
2023

24. Supplementary Figure Legends from The BRCA1-Δ11q Alternative Splice Isoform Bypasses Germline Mutations and Promotes Therapeutic Resistance to PARP Inhibition and Cisplatin

Author

Neil Johnson, Violeta Serra, Judith Balmaña, Jos Jonkers, Peter Bouwman, Elizabeth M. Swisher, Mary B. Daly, Denise C. Connolly, David L. Wiest, Geoffrey I. Shapiro, Alan D. D'Andrea, Susanne K. Kjaer, Simon A. Gayther, Siegal Sadetzki, Robert Nussbaum, Martin Gore, Mark H. Greene, Javier J. Benitez, Håkan Olsson, Georgia Chenevix-Trench, Diether Lambrechts, Charlie Gourley, Beth Karlan, Paul D. P. Pharoah, Francisco J. Candido Dos Reis, Shawn F. Johnson, Maribel I. Harrell, Yong Zhang, Shane W. O'Brien, Ingrid van der Heijden, Hanneke van der Gulden, Suraj Peri, Emmanuelle Nicolas, Joseph Nacson, John J. Krais, Cristina Cruz, Andrea J. Bernhardy, and Yifan Wang

Abstract

Legend for Supplementary Figures S1-S6.

Published
2023

25. Data from Investigation of Exomic Variants Associated with Overall Survival in Ovarian Cancer

Author

Ellen L. Goode, Thomas A. Sellers, Brooke L. Fridley, Paul D.P. Pharoah, Catherine M. Phelan, Jennifer Permuth-Wey, Joellen M. Schildkraut, Andrew Berchuck, Argyrios Ziogas, Hannah Yang, Anna H. Wu, Lynne R. Wilkens, Christine Walsh, Allison F. Vitonis, Robert A. Vierkant, David J. van den Berg, Jonathan P. Tyrer, Pamela J. Thompson, Kathryn L. Terry, Honglin Song, Susan J. Ramus, Malcolm C. Pike, Irene Orlow, Kirsten B. Moysich, Francesmary Modugno, Janusz Menkiszak, Jan Lubinski, Jolanta Lissowska, Hui-Yi Lin, Jenny Lester, Sharon E. Johnatty, Allan Jensen, Edwin S. Iversen, Martin Gore, Aleksandra Gentry-Maharaj, Simon A. Gayther, Robert P. Edwards, Ed M. Dicks, Anna deFazio, Cezary Cybulski, Julie M. Cunningham, Michael E. Carney, Louise A. Brinton, Maria Bisogna, Yukie T. Bean, Nicolas Wentzensen, Mary Anne Rossing, Tanja Pejovic, Celeste L. Pearce, Roberta B. Ness, Usha Menon, Douglas A. Levine, Susanne K. Kjaer, Beth Y. Karlan, Jacek Gronwald, Marc T. Goodman, Jennifer A. Doherty, Daniel Cramer, Elisa V. Bandera, Hoda Anton-Culver, Madalene A. Earp, Zachary C. Fogarty, Melissa C. Larson, Yian Ann Chen, Ailith Pirie, and Stacey J. Winham

Abstract

Background: While numerous susceptibility loci for epithelial ovarian cancer (EOC) have been identified, few associations have been reported with overall survival. In the absence of common prognostic genetic markers, we hypothesize that rare coding variants may be associated with overall EOC survival and assessed their contribution in two exome-based genotyping projects of the Ovarian Cancer Association Consortium (OCAC).Methods: The primary patient set (Set 1) included 14 independent EOC studies (4,293 patients) and 227,892 variants, and a secondary patient set (Set 2) included six additional EOC studies (1,744 patients) and 114,620 variants. Because power to detect rare variants individually is reduced, gene-level tests were conducted. Sets were analyzed separately at individual variants and by gene, and then combined with meta-analyses (73,203 variants and 13,163 genes overlapped).Results: No individual variant reached genome-wide statistical significance. A SNP previously implicated to be associated with EOC risk and, to a lesser extent, survival, rs8170, showed the strongest evidence of association with survival and similar effect size estimates across sets (Pmeta = 1.1E−6, HRSet1 = 1.17, HRSet2 = 1.14). Rare variants in ATG2B, an autophagy gene important for apoptosis, were significantly associated with survival after multiple testing correction (Pmeta = 1.1E−6; Pcorrected = 0.01).Conclusions: Common variant rs8170 and rare variants in ATG2B may be associated with EOC overall survival, although further study is needed.Impact: This study represents the first exome-wide association study of EOC survival to include rare variant analyses, and suggests that complementary single variant and gene-level analyses in large studies are needed to identify rare variants that warrant follow-up study. Cancer Epidemiol Biomarkers Prev; 25(3); 446–54. ©2016 AACR.

Published
2023

26. Data from Chronic Recreational Physical Inactivity and Epithelial Ovarian Cancer Risk: Evidence from the Ovarian Cancer Association Consortium

Author

Kirsten B. Moysich, Linda E. Kelemen, Kathryn L. Terry, Joellen M. Schildkraut, Francesmary Modugno, Anna H. Wu, Stacey J. Winham, Kristine G. Wicklund, Nicolas Wentzensen, Penelope M. Webb, Robert A. Vierkant, Chiu-Chen Tseng, Pamela J. Thompson, Elizabeth A. Szamreta, Mary Anne Rossing, Malcolm C. Pike, Celeste Leigh Pearce, Sara H. Olson, Catherine M. Olsen, Roberta B. Ness, Keitaro Matsuo, Susanne K. Kjaer, Susan Jordan, Allan Jensen, Satoyo Hosono, Estrid Hogdall, Marc T. Goodman, Ellen L. Goode, Brooke L. Fridley, Robert P. Edwards, Jennifer A. Doherty, Daniel Cramer, Andrew Berchuck, Elisa V. Bandera, Gary R. Zirpoli, Albina N. Minlikeeva, Emily Gower, Ruediger Klapdor, Barbara Schmalfeldt, Jenny Chang-Claude, J. Brian Szender, Kevin H. Eng, Lara E. Sucheston-Campbell, Chi-Chen Hong, Harvey A. Risch, Michael J. LaMonte, and Rikki Cannioto

Abstract

Background: Despite a large body of literature evaluating the association between recreational physical activity and epithelial ovarian cancer (EOC) risk, the extant evidence is inconclusive, and little is known about the independent association between recreational physical inactivity and EOC risk. We conducted a pooled analysis of nine studies from the Ovarian Cancer Association Consortium to investigate the association between chronic recreational physical inactivity and EOC risk.Methods: In accordance with the 2008 Physical Activity Guidelines for Americans, women reporting no regular, weekly recreational physical activity were classified as inactive. Multivariable logistic regression was utilized to estimate the ORs and 95% confidence intervals (CI) for the association between inactivity and EOC risk overall and by subgroups based upon histotype, menopausal status, race, and body mass index.Results: The current analysis included data from 8,309 EOC patients and 12,612 controls. We observed a significant positive association between inactivity and EOC risk (OR = 1.34; 95% CI, 1.14–1.57), and similar associations were observed for each histotype.Conclusions: In this large pooled analysis examining the association between recreational physical inactivity and EOC risk, we observed consistent evidence of an association between chronic inactivity and all EOC histotypes.Impact: These data add to the growing body of evidence suggesting that inactivity is an independent risk factor for cancer. If the apparent association between inactivity and EOC risk is substantiated, additional work via targeted interventions should be pursued to characterize the dose of activity required to mitigate the risk of this highly fatal disease. Cancer Epidemiol Biomarkers Prev; 25(7); 1114–24. ©2016 AACR.

Published
2023

27. Data from Platinum Sensitivity–Related Germline Polymorphism Discovered via a Cell-Based Approach and Analysis of Its Association with Outcome in Ovarian Cancer Patients

Author

M. Eileen Dolan, Georgia Chenevix-Trench, Anna deFazio, Beth Y. Karlan, Jenny Gross, Ignace Vergote, Evelyn Despierre, Diether Lambrechts, Jim Paul, Robert Brown, Kunle Odunsi, Matthew Grasela, Kirsten B. Moysich, Allan Jensen, Susanne K. Kjaer, Estrid Hogdall, Brooke L. Fridley, Robert A. Vierkant, Ellen L. Goode, Stuart MacGregor, Yi Lu, Nancy J. Cox, Soma Das, Yarden S. Fraiman, Peter H. O'Donnell, Shuangli Mi, Jonathan Beesley, Peixian Chen, Emily O. Kistner, Wei Zhang, Shiwei Duan, Dana Ziliak, Hae Kyung Im, Eric R. Gamazon, Sharon E. Johnatty, and R. Stephanie Huang

Abstract

Purpose: Cell-based approaches were used to identify genetic markers predictive of patients' risk for poor response prior to chemotherapy.Experimental Design: We conducted genome-wide association studies (GWAS) to identify single-nucleotide polymorphisms (SNP) associated with cellular sensitivity to carboplatin through their effects on mRNA expression using International HapMap lymphoblastoid cell lines (LCL) and replicated them in additional LCLs. SNPs passing both stages of the cell-based study were tested for association with progression-free survival (PFS) in patients. Phase 1 validation was based on 377 ovarian cancer patients receiving at least four cycles of carboplatin and paclitaxel from the Australian Ovarian Cancer Study (AOCS). Positive associations were then assessed in phase 2 validation analysis of 1,326 patients from the Ovarian Cancer Association Consortium and The Cancer Genome Atlas.Results: In the initial GWAS, 342 SNPs were associated with carboplatin-induced cytotoxicity, of which 18 unique SNPs were retained after assessing their association with gene expression. One SNP (rs1649942) was replicated in an independent LCL set (Bonferroni adjusted P < 0.05). It was found to be significantly associated with decreased PFS in phase 1 AOCS patients (Pper-allele = 2 × 10−2), with a stronger effect in the subset of women with optimally debulked tumors (Pper-allele = 4 × 10−3). rs1649942 was also associated with poorer overall survival in women with optimally debulked tumors (Pper-allele = 9 × 10−3). However, this SNP was not significant in phase 2 validation analysis with patients from numerous cohorts.Conclusion: This study shows the potential of cell-based, genome-wide approaches to identify germline predictors of treatment outcome and highlights the need for extensive validation in patients to assess their clinical effect. Clin Cancer Res; 17(16); 5490–500. ©2011 AACR.

Published
2023

28. Supplemental Figure 1 from Assessment of Multifactor Gene–Environment Interactions and Ovarian Cancer Risk: Candidate Genes, Obesity, and Hormone-Related Risk Factors

Author

Brooke L. Fridley, Ellen L. Goode, Paul Pharoah, Joellen M. Schildkraut, Celeste Leigh Pearce, Hannah Yang, Anna H. Wu, Lynne R. Wilkens, Alice S. Whittemore, Nicolas Wentzensen, Shan Wang-Gohrke, Robert A. Vierkant, David J. van den Berg, Pamela J. Thompson, Honglin Song, Joseph Rothstein, Mary Anne Rossing, Susan J. Ramus, Malcolm C. Pike, Roberta B. Ness, Kirsten B. Moysich, Francesmary Modugno, Usha Menon, Leon Massuger, Galina Lurie, Melissa C. Larson, Susanne K. Kjaer, Lambertus A. Kiemeney, Sharon E. Johnatty, Allan Jensen, Estrid Høgdall, Marc T. Goodman, Aleksandra Gentry-Maharaj, Simon A. Gayther, Robert P. Edwards, Jennifer A. Doherty, Anna DeFazio, Julie M. Cunningham, Louise Brinton, Andrew Berchuck, Hoda Anton-Culver, Anja Rudolph, Jenny Chang-Claude, Penelope Webb, Weiva Sieh, Valerie McGuire, Jonathan P. Tyrer, Rama Raghavan, and Joseph L. Usset

Abstract

Potential hormonal mechanism to motivate investigation of multi-factor obesity-hormone related risk factors - SNP interactions.

Published
2023

29. Data from Assessment of Multifactor Gene–Environment Interactions and Ovarian Cancer Risk: Candidate Genes, Obesity, and Hormone-Related Risk Factors

Author

Brooke L. Fridley, Ellen L. Goode, Paul Pharoah, Joellen M. Schildkraut, Celeste Leigh Pearce, Hannah Yang, Anna H. Wu, Lynne R. Wilkens, Alice S. Whittemore, Nicolas Wentzensen, Shan Wang-Gohrke, Robert A. Vierkant, David J. van den Berg, Pamela J. Thompson, Honglin Song, Joseph Rothstein, Mary Anne Rossing, Susan J. Ramus, Malcolm C. Pike, Roberta B. Ness, Kirsten B. Moysich, Francesmary Modugno, Usha Menon, Leon Massuger, Galina Lurie, Melissa C. Larson, Susanne K. Kjaer, Lambertus A. Kiemeney, Sharon E. Johnatty, Allan Jensen, Estrid Høgdall, Marc T. Goodman, Aleksandra Gentry-Maharaj, Simon A. Gayther, Robert P. Edwards, Jennifer A. Doherty, Anna DeFazio, Julie M. Cunningham, Louise Brinton, Andrew Berchuck, Hoda Anton-Culver, Anja Rudolph, Jenny Chang-Claude, Penelope Webb, Weiva Sieh, Valerie McGuire, Jonathan P. Tyrer, Rama Raghavan, and Joseph L. Usset

Abstract

Background: Many epithelial ovarian cancer (EOC) risk factors relate to hormone exposure and elevated estrogen levels are associated with obesity in postmenopausal women. Therefore, we hypothesized that gene–environment interactions related to hormone-related risk factors could differ between obese and non-obese women.Methods: We considered interactions between 11,441 SNPs within 80 candidate genes related to hormone biosynthesis and metabolism and insulin-like growth factors with six hormone-related factors (oral contraceptive use, parity, endometriosis, tubal ligation, hormone replacement therapy, and estrogen use) and assessed whether these interactions differed between obese and non-obese women. Interactions were assessed using logistic regression models and data from 14 case–control studies (6,247 cases; 10,379 controls). Histotype-specific analyses were also completed.Results: SNPs in the following candidate genes showed notable interaction: IGF1R (rs41497346, estrogen plus progesterone hormone therapy, histology = all, P = 4.9 × 10−6) and ESR1 (rs12661437, endometriosis, histology = all, P = 1.5 × 10−5). The most notable obesity–gene–hormone risk factor interaction was within INSR (rs113759408, parity, histology = endometrioid, P = 8.8 × 10−6).Conclusions: We have demonstrated the feasibility of assessing multifactor interactions in large genetic epidemiology studies. Follow-up studies are necessary to assess the robustness of our findings for ESR1, CYP11A1, IGF1R, CYP11B1, INSR, and IGFBP2. Future work is needed to develop powerful statistical methods able to detect these complex interactions.Impact: Assessment of multifactor interaction is feasible, and, here, suggests that the relationship between genetic variants within candidate genes and hormone-related risk factors may vary EOC susceptibility. Cancer Epidemiol Biomarkers Prev; 25(5); 780–90. ©2016 AACR.

Published
2023

31. Online Supplementary Materials from A Transcriptome-Wide Association Study Among 97,898 Women to Identify Candidate Susceptibility Genes for Epithelial Ovarian Cancer Risk

Author

Jirong Long, Wei Zheng, Paul D.P. Pharoah, Thomas A. Sellers, Georgia Chenevix-Trench, Ellen L. Goode, Andrew Berchuck, Antonis C. Antoniou, Simon A. Gayther, Kristin K. Zorn, Drakoulis Yannoukakos, Anna H. Wu, Alicja Wolk, Emily White, Nicolas Wentzensen, Jeffrey N. Weitzel, Penelope M. Webb, Digna Velez Edwards, Ana Vega, Adriaan Vanderstichele, Elizabeth J. van Rensburg, Shelley S. Tworoger, Nadine Tung, Antonia Trichopoulou, Amanda E. Toland, Marc Tischkowitz, Mads Thomassen, Soo H. Teo, Manuel R. Teixeira, Anthony J. Swerdlow, Rebecca Sutphen, Amanda B. Spurdle, Melissa C. Southey, Honglin Song, Christian F. Singer, Jacques Simard, Weiva Sieh, Priyanka Sharma, Veronica W. Setiawan, Rita K. Schmutzler, Dale P. Sandler, Iwona K. Rzepecka, Mary Anne Rossing, Matti A. Rookus, Isabelle Romieu, Cristina Rodríguez-Antona, Gustavo C. Rodriguez, Harvey Risch, Gad Rennert, Susan J. Ramus, Miquel Angel Pujana, Catherine M. Phelan, Paolo Peterlongo, Tanja Pejovic, Petra H.M. Peeters, Michael T. Parsons, Sue K. Park, Ana Osorio, Håkan Olsson, Sara H. Olson, Olufunmilayo I. Olopade, Edith Olah, Kenneth Offit, Robert L. Nussbaum, Liene Nikitina-Zake, Finn C. Nielsen, Heli Nevanlinna, Susan L. Neuhausen, Marco Montagna, Francesmary Modugno, Melissa A. Merritt, Iain A. McNeish, Lesley McGuffog, Taymaa May, Amalia Mattiello, Douglas A. Levine, Fabienne Lesueur, Goska Leslie, Nhu D. Le, Ava Kwong, Susanne K. Kjaer, Lambertus A. Kiemeney, Linda E. Kelemen, Beth Y. Karlan, Paul James, Anna Jakubowska, Claudine Isaacs, Evgeny N. Imyanitov, David G. Huntsman, Peter J. Hulick, Antoinette Hollestelle, Claus K. Høgdall, Michelle A.T. Hildebrandt, Florian Heitz, Ute Hamann, Jacek Gronwald, Mark H. Greene, Marc T. Goodman, David E. Goldgar, Andrew K. Godwin, Graham G. Giles, Judy Garber, Patricia A. Ganz, Eitan Friedman, George Fountzilas, Renée T. Fortner, Peter A. Fasching, Diana M. Eccles, Douglas F. Easton, Thilo Dörk, Susan M. Domchek, Orland Diez, Joe Dennis, Anna deFazio, Mary B. Daly, Daniel W. Cramer, Fergus J. Couch, Kathleen B.M. Claes, Jenny Chang-Claude, Ian Campbell, Maria A. Caligo, Trinidad Caldes, Ralf Butzow, James Brenton, Line Bjorge, Javier Benitez, Daniel R. Barnes, Rosa B. Barkardottir, Elisa V. Bandera, Banu K. Arun, Hoda Anton-Culver, Irene L. Andrulis, Kirsten B. Moysich, Jamie K. Teer, Brett M. Reid, Jennifer B. Permuth, Yian A. Chen, Hae Kyung Im, Joellen M. Schildkraut, Bingshan Li, Xingyi Guo, Lang Wu, Alicia Beeghly-Fadiel, and Yingchang Lu

Abstract

Online Supplementary Documents

Published
2023

32. Supplementary Tables 1, 2 and 4 from Platinum Sensitivity–Related Germline Polymorphism Discovered via a Cell-Based Approach and Analysis of Its Association with Outcome in Ovarian Cancer Patients

Author

M. Eileen Dolan, Georgia Chenevix-Trench, Anna deFazio, Beth Y. Karlan, Jenny Gross, Ignace Vergote, Evelyn Despierre, Diether Lambrechts, Jim Paul, Robert Brown, Kunle Odunsi, Matthew Grasela, Kirsten B. Moysich, Allan Jensen, Susanne K. Kjaer, Estrid Hogdall, Brooke L. Fridley, Robert A. Vierkant, Ellen L. Goode, Stuart MacGregor, Yi Lu, Nancy J. Cox, Soma Das, Yarden S. Fraiman, Peter H. O'Donnell, Shuangli Mi, Jonathan Beesley, Peixian Chen, Emily O. Kistner, Wei Zhang, Shiwei Duan, Dana Ziliak, Hae Kyung Im, Eric R. Gamazon, Sharon E. Johnatty, and R. Stephanie Huang

Abstract

PDF file - 115K

Published
2023

33. Data from Variation in NF-κB Signaling Pathways and Survival in Invasive Epithelial Ovarian Cancer

Author

Ellen L. Goode, Julie M. Cunningham, Brooke L. Fridley, Kimberly R. Kalli, Jonathan Tyrer, Honglin Song, Anna deFazio, Sharon E. Johnatty, Jennifer A. Doherty, Catherine M. Phelan, Thomas A. Sellers, Keith L. Knutson, David N. Rider, Starr M. Ramirez, Allison F. Vitonis, Kathryn L. Terry, David Van Den Berg, Malcolm C. Pike, Anna H. Wu, Andrew Berchuck, Aleksandra Gentry-Maharaj, Susan J. Ramus, Simon A. Gayther, Allan Jensen, Janusz Menkiszak, Cezary Cybulski, Jan Lubiński, Argyrios Ziogas, Joseph H. Rothstein, Valerie McGuire, Weiva Sieh, Jenny Lester, Christine S. Walsh, Ignace Vergote, Sandrina Lambrechts, Evelyn Despierre, Montserrat Garcia-Closas, Hannah Yang, Louise A. Brinton, Izabela Ziolkowska-Seta, Iwona K. Rzepecka, Agnieszka Dansonka-Mieszkowska, Ursula Eilber, Anja Rudolph, Lisa E. Paddock, Irene Orlow, Sara H. Olson, Lene Lundvall, Claus K. Hogdall, Ira Schwaab, Andreas du Bois, Philipp Harter, James M. Flanagan, Robert Brown, James Paul, Arif B. Ekici, Matthias W. Beckmann, Alexander Hein, Diana Eccles, Galina Lurie, Laura E. Hays, Yukie T. Bean, Tanja Pejovic, Marc T. Goodman, Ian Campbell, Peter A. Fasching, Stanley B. Kaye, Florian Heitz, Estrid Hogdall, Elisa V. Bandera, Jenny Chang-Claude, Jolanta Kupryjanczyk, Nicolas Wentzensen, Diether Lambrechts, Beth Y. Karlan, Alice S. Whittemore, Hoda Anton Culver, Jacek Gronwald, Douglas A. Levine, Susanne K. Kjaer, Usha Menon, Joellen Schildkraut, Celeste Leigh Pearce, Daniel Cramer, Mary Anne Rossing, Paul D.P. Pharoah, William R. Bamlet, Zachary Fogarty, Robert A. Vierkant, Bridget Charbonneau, and Matthew S. Block

Abstract

Survival in epithelial ovarian cancer (EOC) is influenced by the host immune response, yet the key genetic determinants of inflammation and immunity that affect prognosis are not known. The nuclear factor-κB (NF-κB) transcription factor family plays an important role in many immune and inflammatory responses, including the response to cancer. We studied common inherited variation in 210 genes in the NF-κB family in 10,084 patients with invasive EOC (5,248 high-grade serous, 1,452 endometrioid, 795 clear cell, and 661 mucinous) from the Ovarian Cancer Association Consortium. Associations between genotype and overall survival were assessed using Cox regression for all patients and by major histology, adjusting for known prognostic factors and correcting for multiple testing (threshold for statistical significance, P < 2.5 × 10−5). Results were statistically significant when assessed for patients of a single histology. Key associations were with caspase recruitment domain family, member 11 (CARD11) rs41324349 in patients with mucinous EOC [HR, 1.82; 95% confidence interval (CI), 1.41–2.35; P = 4.13 × 10−6] and tumor necrosis factor receptor superfamily, member 13B (TNFRSF13B) rs7501462 in patients with endometrioid EOC (HR, 0.68; 95% CI, 0.56–0.82; P = 2.33 × 10−5). Other associations of note included TNF receptor–associated factor 2 (TRAF2) rs17250239 in patients with high-grade serous EOC (HR, 0.84; 95% CI, 0.77–0.92; P = 6.49 × 10−5) and phospholipase C, gamma 1 (PLCG1) rs11696662 in patients with clear cell EOC (HR, 0.43; 95% CI, 0.26–0.73; P = 4.56 × 10−4). These associations highlight the potential importance of genes associated with host inflammation and immunity in modulating clinical outcomes in distinct EOC histologies. Cancer Epidemiol Biomarkers Prev; 23(7); 1421–7. ©2014 AACR.

Published
2023

34. Supplementary Tables S1-S4 from The BRCA1-Δ11q Alternative Splice Isoform Bypasses Germline Mutations and Promotes Therapeutic Resistance to PARP Inhibition and Cisplatin

Author

Neil Johnson, Violeta Serra, Judith Balmaña, Jos Jonkers, Peter Bouwman, Elizabeth M. Swisher, Mary B. Daly, Denise C. Connolly, David L. Wiest, Geoffrey I. Shapiro, Alan D. D'Andrea, Susanne K. Kjaer, Simon A. Gayther, Siegal Sadetzki, Robert Nussbaum, Martin Gore, Mark H. Greene, Javier J. Benitez, Håkan Olsson, Georgia Chenevix-Trench, Diether Lambrechts, Charlie Gourley, Beth Karlan, Paul D. P. Pharoah, Francisco J. Candido Dos Reis, Shawn F. Johnson, Maribel I. Harrell, Yong Zhang, Shane W. O'Brien, Ingrid van der Heijden, Hanneke van der Gulden, Suraj Peri, Emmanuelle Nicolas, Joseph Nacson, John J. Krais, Cristina Cruz, Andrea J. Bernhardy, and Yifan Wang

Abstract

RNA-seq analyses of global exon splicing events (S1); Cell line therapy sensitivities (S2); Hazard ratios for survival of patients with serous ovarian carcinomas associated with BRCA1 mutation, age at diagnosis and stage (S3); Characteristics of studies included in survival analysis from Fig. 5A (S4).

Published
2023

35. Data from History of Comorbidities and Survival of Ovarian Cancer Patients, Results from the Ovarian Cancer Association Consortium

Author

Kirsten B. Moysich, Penelope M. Webb, Allan Jensen, Jolanta Kupryjanczyk, Anna H. Wu, Celeste L. Pearce, Aleksandra Gentry-Maharaj, Susan J. Ramus, Simon A. Gayther, Usha Menon, Argyrios Ziogas, Hoda Anton-Culver, Rebecca Sutphen, Leon F.A.G. Massuger, Lambertus A. Kiemeney, Lisa E. Paddock, Elisa V. Bandera, Daniel W. Cramer, Kathryn L. Terry, Joellen M. Schildkraut, Estrid Høgdall, Susanne K. Kjær, Ellen L. Goode, Beth Y. Karlan, Mika Mizuno, Keitaro Matsuo, Roberta B. Ness, Francesmary Modugno, Robert Edwards, Thilo Dörk, Marc T. Goodman, Jenny Chang-Claude, Jennifer A. Doherty, Mary Anne Rossing, Harvey A. Risch, Matthias W. Beckmann, Peter A. Fasching, Susan J. Jordan, Anna deFazio, Helen Steed, Martin Köbel, Linda E. Kelemen, Emese Zsiros, Brenda Diergaarde, Paul Mayor, Kunle Odunsi, Brahm Segal, J. Brian Szender, Grace Friel, Rikki A. Cannioto, Kevin H. Eng, Jo L. Freudenheim, and Albina N. Minlikeeva

Abstract

Background: Comorbidities can affect survival of ovarian cancer patients by influencing treatment efficacy. However, little evidence exists on the association between individual concurrent comorbidities and prognosis in ovarian cancer patients.Methods: Among patients diagnosed with invasive ovarian carcinoma who participated in 23 studies included in the Ovarian Cancer Association Consortium, we explored associations between histories of endometriosis; asthma; depression; osteoporosis; and autoimmune, gallbladder, kidney, liver, and neurological diseases and overall and progression-free survival. Using Cox proportional hazards regression models adjusted for age at diagnosis, stage of disease, histology, and study site, we estimated pooled HRs and 95% confidence intervals to assess associations between each comorbidity and ovarian cancer outcomes.Results: None of the comorbidities were associated with ovarian cancer outcome in the overall sample nor in strata defined by histologic subtype, weight status, age at diagnosis, or stage of disease (local/regional vs. advanced).Conclusions: Histories of endometriosis; asthma; depression; osteoporosis; and autoimmune, gallbladder, kidney, liver, or neurologic diseases were not associated with ovarian cancer overall or progression-free survival.Impact: These previously diagnosed chronic diseases do not appear to affect ovarian cancer prognosis. Cancer Epidemiol Biomarkers Prev; 26(9); 1470–3. ©2017 AACR.

Published
2023

36. Data from Attribution of 12 High-Risk Human Papillomavirus Genotypes to Infection and Cervical Disease

Author

Christine Velicer, Heather L. Sings, Alain Luxembourg, Alfred Saah, Gonzalo Perez, Cosette M. Wheeler, Marc Steben, Punnee Pitisuttithum, Jorma Paavonen, Evan Myers, Nubia Munoz, Joseph Monsonego, Dianne Miller, Joaquin Luna, Susanne K. Kjaer, Ole-Erik Iversen, Warner Huh, Mauricio Hernandez-Avila, Anna R. Giuliano, Suzanne M. Garland, Daron Ferris, Jack Cuzick, Darron Brown, F. Xavier Bosch, Kevin A. Ault, and Elmar A. Joura

Abstract

Background: We estimated the prevalence and incidence of 14 human papillomavirus (HPV) types (6/11/16/18/31/33/35/39/45/51/52/56/58/59) in cervicovaginal swabs, and the attribution of these HPV types in cervical intraepithelial neoplasia (CIN), and adenocarcinoma in situ (AIS), using predefined algorithms that adjusted for multiple-type infected lesions.Methods: A total of 10,656 women ages 15 to 26 years and 1,858 women ages 24 to 45 years were enrolled in the placebo arms of one of three clinical trials of a quadrivalent HPV vaccine. We estimated the cumulative incidence of persistent infection and the proportion of CIN/AIS attributable to individual carcinogenic HPV genotypes, as well as the proportion of CIN/AIS lesions potentially preventable by a prophylactic 9-valent HPV6/11/16/18/31/33/45/52/58 vaccine.Results: The cumulative incidence of persistent infection with ≥1 of the seven high-risk types included in the 9-valent vaccine was 29%, 12%, and 6% for women ages 15 to 26, 24 to 34, and 35 to 45 years, respectively. A total of 2,507 lesions were diagnosed as CIN or AIS by an expert pathology panel. After adjusting for multiple-type infected lesions, among women ages 15 to 45 years, these seven high-risk types were attributed to 43% to 55% of CIN1, 70% to 78% of CIN2, 85% to 91% of CIN3, and 95% to 100% of AIS lesions, respectively. The other tested types (HPV35/39/51/56/59) were attributed to 23% to 30% of CIN1, 7% to 14% of CIN2, 3% to 4% of CIN3, and 0% of AIS lesions, respectively.Conclusions: Approximately 85% or more of CIN3/AIS, >70% CIN2, and approximately 50% of CIN1 lesions worldwide are attributed to HPV6/11/16/18/31/33/45/52/58.Impact: If 9-valent HPV vaccination programs are effectively implemented, the majority of CIN2 and CIN3 lesions worldwide could be prevented, in addition to approximately one-half of CIN1. Cancer Epidemiol Biomarkers Prev; 23(10); 1997–2008. ©2014 AACR.

Published
2023

37. Data from A Transcriptome-Wide Association Study Among 97,898 Women to Identify Candidate Susceptibility Genes for Epithelial Ovarian Cancer Risk

Author

Jirong Long, Wei Zheng, Paul D.P. Pharoah, Thomas A. Sellers, Georgia Chenevix-Trench, Ellen L. Goode, Andrew Berchuck, Antonis C. Antoniou, Simon A. Gayther, Kristin K. Zorn, Drakoulis Yannoukakos, Anna H. Wu, Alicja Wolk, Emily White, Nicolas Wentzensen, Jeffrey N. Weitzel, Penelope M. Webb, Digna Velez Edwards, Ana Vega, Adriaan Vanderstichele, Elizabeth J. van Rensburg, Shelley S. Tworoger, Nadine Tung, Antonia Trichopoulou, Amanda E. Toland, Marc Tischkowitz, Mads Thomassen, Soo H. Teo, Manuel R. Teixeira, Anthony J. Swerdlow, Rebecca Sutphen, Amanda B. Spurdle, Melissa C. Southey, Honglin Song, Christian F. Singer, Jacques Simard, Weiva Sieh, Priyanka Sharma, Veronica W. Setiawan, Rita K. Schmutzler, Dale P. Sandler, Iwona K. Rzepecka, Mary Anne Rossing, Matti A. Rookus, Isabelle Romieu, Cristina Rodríguez-Antona, Gustavo C. Rodriguez, Harvey Risch, Gad Rennert, Susan J. Ramus, Miquel Angel Pujana, Catherine M. Phelan, Paolo Peterlongo, Tanja Pejovic, Petra H.M. Peeters, Michael T. Parsons, Sue K. Park, Ana Osorio, Håkan Olsson, Sara H. Olson, Olufunmilayo I. Olopade, Edith Olah, Kenneth Offit, Robert L. Nussbaum, Liene Nikitina-Zake, Finn C. Nielsen, Heli Nevanlinna, Susan L. Neuhausen, Marco Montagna, Francesmary Modugno, Melissa A. Merritt, Iain A. McNeish, Lesley McGuffog, Taymaa May, Amalia Mattiello, Douglas A. Levine, Fabienne Lesueur, Goska Leslie, Nhu D. Le, Ava Kwong, Susanne K. Kjaer, Lambertus A. Kiemeney, Linda E. Kelemen, Beth Y. Karlan, Paul James, Anna Jakubowska, Claudine Isaacs, Evgeny N. Imyanitov, David G. Huntsman, Peter J. Hulick, Antoinette Hollestelle, Claus K. Høgdall, Michelle A.T. Hildebrandt, Florian Heitz, Ute Hamann, Jacek Gronwald, Mark H. Greene, Marc T. Goodman, David E. Goldgar, Andrew K. Godwin, Graham G. Giles, Judy Garber, Patricia A. Ganz, Eitan Friedman, George Fountzilas, Renée T. Fortner, Peter A. Fasching, Diana M. Eccles, Douglas F. Easton, Thilo Dörk, Susan M. Domchek, Orland Diez, Joe Dennis, Anna deFazio, Mary B. Daly, Daniel W. Cramer, Fergus J. Couch, Kathleen B.M. Claes, Jenny Chang-Claude, Ian Campbell, Maria A. Caligo, Trinidad Caldes, Ralf Butzow, James Brenton, Line Bjorge, Javier Benitez, Daniel R. Barnes, Rosa B. Barkardottir, Elisa V. Bandera, Banu K. Arun, Hoda Anton-Culver, Irene L. Andrulis, Kirsten B. Moysich, Jamie K. Teer, Brett M. Reid, Jennifer B. Permuth, Yian A. Chen, Hae Kyung Im, Joellen M. Schildkraut, Bingshan Li, Xingyi Guo, Lang Wu, Alicia Beeghly-Fadiel, and Yingchang Lu

Abstract

Large-scale genome-wide association studies (GWAS) have identified approximately 35 loci associated with epithelial ovarian cancer (EOC) risk. The majority of GWAS-identified disease susceptibility variants are located in noncoding regions, and causal genes underlying these associations remain largely unknown. Here, we performed a transcriptome-wide association study to search for novel genetic loci and plausible causal genes at known GWAS loci. We used RNA sequencing data (68 normal ovarian tissue samples from 68 individuals and 6,124 cross-tissue samples from 369 individuals) and high-density genotyping data from European descendants of the Genotype-Tissue Expression (GTEx V6) project to build ovarian and cross-tissue models of genetically regulated expression using elastic net methods. We evaluated 17,121 genes for their cis-predicted gene expression in relation to EOC risk using summary statistics data from GWAS of 97,898 women, including 29,396 EOC cases. With a Bonferroni-corrected significance level of P < 2.2 × 10−6, we identified 35 genes, including FZD4 at 11q14.2 (Z = 5.08, P = 3.83 × 10−7, the cross-tissue model; 1 Mb away from any GWAS-identified EOC risk variant), a potential novel locus for EOC risk. All other 34 significantly associated genes were located within 1 Mb of known GWAS-identified loci, including 23 genes at 6 loci not previously linked to EOC risk. Upon conditioning on nearby known EOC GWAS-identified variants, the associations for 31 genes disappeared and three genes remained (P < 1.47 × 10−3). These data identify one novel locus (FZD4) and 34 genes at 13 known EOC risk loci associated with EOC risk, providing new insights into EOC carcinogenesis.Significance: Transcriptomic analysis of a large cohort confirms earlier GWAS loci and reveals FZD4 as a novel locus associated with EOC risk. Cancer Res; 78(18); 5419–30. ©2018 AACR.

Published
2023

38. Supplemental Tables from Investigation of Exomic Variants Associated with Overall Survival in Ovarian Cancer

Author

Ellen L. Goode, Thomas A. Sellers, Brooke L. Fridley, Paul D.P. Pharoah, Catherine M. Phelan, Jennifer Permuth-Wey, Joellen M. Schildkraut, Andrew Berchuck, Argyrios Ziogas, Hannah Yang, Anna H. Wu, Lynne R. Wilkens, Christine Walsh, Allison F. Vitonis, Robert A. Vierkant, David J. van den Berg, Jonathan P. Tyrer, Pamela J. Thompson, Kathryn L. Terry, Honglin Song, Susan J. Ramus, Malcolm C. Pike, Irene Orlow, Kirsten B. Moysich, Francesmary Modugno, Janusz Menkiszak, Jan Lubinski, Jolanta Lissowska, Hui-Yi Lin, Jenny Lester, Sharon E. Johnatty, Allan Jensen, Edwin S. Iversen, Martin Gore, Aleksandra Gentry-Maharaj, Simon A. Gayther, Robert P. Edwards, Ed M. Dicks, Anna deFazio, Cezary Cybulski, Julie M. Cunningham, Michael E. Carney, Louise A. Brinton, Maria Bisogna, Yukie T. Bean, Nicolas Wentzensen, Mary Anne Rossing, Tanja Pejovic, Celeste L. Pearce, Roberta B. Ness, Usha Menon, Douglas A. Levine, Susanne K. Kjaer, Beth Y. Karlan, Jacek Gronwald, Marc T. Goodman, Jennifer A. Doherty, Daniel Cramer, Elisa V. Bandera, Hoda Anton-Culver, Madalene A. Earp, Zachary C. Fogarty, Melissa C. Larson, Yian Ann Chen, Ailith Pirie, and Stacey J. Winham

Abstract

Supplemental Table S1: Number of invasive EOC patients by study site. Supplemental Table S2: Results of Set 1 single variant analysis, for variants with P

Published
2023

39. Suplemmentary Tables 1-6, Suppementary References from Germline Mutation in BRCA1 or BRCA2 and Ten-Year Survival for Women Diagnosed with Epithelial Ovarian Cancer

Author

Paul D.P. Pharoah, David Bowtell, Simon A. Gayther, Georgia Chenevix-Trench, Antonis Antoniou, Douglas F. Easton, Marc Tischkowitz, James D. Brenton, Debra Frost, Steve Ellis, Diether Lambrechts, Amanda E. Toland, Kirsten Moysich, Jennifer T. Loud, Phuong L. Mai, Mark H. Greene, Mary Daly, Robert Nussbaum, Susan Neuhausen, Estrid Høgdall, Allan Jensen, Susanne K. Kjaer, Ava Kwong, Angela Chetrit, Siegal Sadetzki, Elisa Alducci, Marco Montagna, Weiva Sieh, Valerie McGuire, Alice S. Whittemore, Conxi Lazaro, Ignacio Blanco, Gord Glendon, Anna Marie Mulligan, Irene Andrulis, Maria J. Garcia, Javier J. Benitez, Martin Gore, Håkan Olsson, Ilana Cass, Christine Walsh, Jenny Lester, Beth Karlan, Caroline Michie, Charlie Gourley, Kelly L. Bolton, Sian Fereday, Gillian Mitchell, Anna de Fazio, Susan J. Ramus, Patricia Harrington, Ed Dicks, Kathryn Alsop, Melissa C. Larson, Brooke L. Fridley, Julie M. Cunningham, Ellen L. Goode, Honglin Song, and Francisco J. Candido-dos-Reis

Abstract

Supplementary Tables S1-S6, Supplementary References. Supplementary Table S1. Characteristics of included studies; S2. Complete-case analysis of ten years estimated hazard ratios (HR) for all cause death in patients with ovarian cancer. S3. Complete-case analysis of ten years estimated subhazard ratios (SHR) for ovarian cancer death in patients with ovarian cancer. S4. Ten years estimated subhazard ratios (SHR) for ovarian cancer death in patients with ovarian cancer (with multiple imputation for missing grade and stage). S5. Complete-case analysis of ten years estimated hazard ratios (HR) for all cause death in patients with high grade serous ovarian cancer. S6. Ten years estimated hazard ratios (HR) for all cause death in patients with high grade serous ovarian cancer (with multiple imputation for missing stage).

Published
2023

40. Supplementary Material from Attribution of 12 High-Risk Human Papillomavirus Genotypes to Infection and Cervical Disease

Author

Christine Velicer, Heather L. Sings, Alain Luxembourg, Alfred Saah, Gonzalo Perez, Cosette M. Wheeler, Marc Steben, Punnee Pitisuttithum, Jorma Paavonen, Evan Myers, Nubia Munoz, Joseph Monsonego, Dianne Miller, Joaquin Luna, Susanne K. Kjaer, Ole-Erik Iversen, Warner Huh, Mauricio Hernandez-Avila, Anna R. Giuliano, Suzanne M. Garland, Daron Ferris, Jack Cuzick, Darron Brown, F. Xavier Bosch, Kevin A. Ault, and Elmar A. Joura

Abstract

HPV DNA Detection

Published
2023

41. Supplementary Tables 1-2 from Attribution of 12 High-Risk Human Papillomavirus Genotypes to Infection and Cervical Disease

Author

Christine Velicer, Heather L. Sings, Alain Luxembourg, Alfred Saah, Gonzalo Perez, Cosette M. Wheeler, Marc Steben, Punnee Pitisuttithum, Jorma Paavonen, Evan Myers, Nubia Munoz, Joseph Monsonego, Dianne Miller, Joaquin Luna, Susanne K. Kjaer, Ole-Erik Iversen, Warner Huh, Mauricio Hernandez-Avila, Anna R. Giuliano, Suzanne M. Garland, Daron Ferris, Jack Cuzick, Darron Brown, F. Xavier Bosch, Kevin A. Ault, and Elmar A. Joura

Abstract

Supplementary Table 1 - Study design and comparison of protocols 013, 015 and 019. Supplementary Table 2 - Selected Characteristics at Baseline by Histologic Diagnosis.

Published
2023

42. Supplemental Figure Legends from Investigation of Exomic Variants Associated with Overall Survival in Ovarian Cancer

Author

Ellen L. Goode, Thomas A. Sellers, Brooke L. Fridley, Paul D.P. Pharoah, Catherine M. Phelan, Jennifer Permuth-Wey, Joellen M. Schildkraut, Andrew Berchuck, Argyrios Ziogas, Hannah Yang, Anna H. Wu, Lynne R. Wilkens, Christine Walsh, Allison F. Vitonis, Robert A. Vierkant, David J. van den Berg, Jonathan P. Tyrer, Pamela J. Thompson, Kathryn L. Terry, Honglin Song, Susan J. Ramus, Malcolm C. Pike, Irene Orlow, Kirsten B. Moysich, Francesmary Modugno, Janusz Menkiszak, Jan Lubinski, Jolanta Lissowska, Hui-Yi Lin, Jenny Lester, Sharon E. Johnatty, Allan Jensen, Edwin S. Iversen, Martin Gore, Aleksandra Gentry-Maharaj, Simon A. Gayther, Robert P. Edwards, Ed M. Dicks, Anna deFazio, Cezary Cybulski, Julie M. Cunningham, Michael E. Carney, Louise A. Brinton, Maria Bisogna, Yukie T. Bean, Nicolas Wentzensen, Mary Anne Rossing, Tanja Pejovic, Celeste L. Pearce, Roberta B. Ness, Usha Menon, Douglas A. Levine, Susanne K. Kjaer, Beth Y. Karlan, Jacek Gronwald, Marc T. Goodman, Jennifer A. Doherty, Daniel Cramer, Elisa V. Bandera, Hoda Anton-Culver, Madalene A. Earp, Zachary C. Fogarty, Melissa C. Larson, Yian Ann Chen, Ailith Pirie, and Stacey J. Winham

Abstract

Supplemental Figure Legends

Published
2023

43. Supplementary Tables 1 through 3 from Variation in NF-κB Signaling Pathways and Survival in Invasive Epithelial Ovarian Cancer

Author

Ellen L. Goode, Julie M. Cunningham, Brooke L. Fridley, Kimberly R. Kalli, Jonathan Tyrer, Honglin Song, Anna deFazio, Sharon E. Johnatty, Jennifer A. Doherty, Catherine M. Phelan, Thomas A. Sellers, Keith L. Knutson, David N. Rider, Starr M. Ramirez, Allison F. Vitonis, Kathryn L. Terry, David Van Den Berg, Malcolm C. Pike, Anna H. Wu, Andrew Berchuck, Aleksandra Gentry-Maharaj, Susan J. Ramus, Simon A. Gayther, Allan Jensen, Janusz Menkiszak, Cezary Cybulski, Jan Lubiński, Argyrios Ziogas, Joseph H. Rothstein, Valerie McGuire, Weiva Sieh, Jenny Lester, Christine S. Walsh, Ignace Vergote, Sandrina Lambrechts, Evelyn Despierre, Montserrat Garcia-Closas, Hannah Yang, Louise A. Brinton, Izabela Ziolkowska-Seta, Iwona K. Rzepecka, Agnieszka Dansonka-Mieszkowska, Ursula Eilber, Anja Rudolph, Lisa E. Paddock, Irene Orlow, Sara H. Olson, Lene Lundvall, Claus K. Hogdall, Ira Schwaab, Andreas du Bois, Philipp Harter, James M. Flanagan, Robert Brown, James Paul, Arif B. Ekici, Matthias W. Beckmann, Alexander Hein, Diana Eccles, Galina Lurie, Laura E. Hays, Yukie T. Bean, Tanja Pejovic, Marc T. Goodman, Ian Campbell, Peter A. Fasching, Stanley B. Kaye, Florian Heitz, Estrid Hogdall, Elisa V. Bandera, Jenny Chang-Claude, Jolanta Kupryjanczyk, Nicolas Wentzensen, Diether Lambrechts, Beth Y. Karlan, Alice S. Whittemore, Hoda Anton Culver, Jacek Gronwald, Douglas A. Levine, Susanne K. Kjaer, Usha Menon, Joellen Schildkraut, Celeste Leigh Pearce, Daniel Cramer, Mary Anne Rossing, Paul D.P. Pharoah, William R. Bamlet, Zachary Fogarty, Robert A. Vierkant, Bridget Charbonneau, and Matthew S. Block

Abstract

PDF - 149K, Supplemental Table 1. Participating invasive epithelial ovarian cancer studies. Supplementary Table 2. NF-κB genes studied. Supplemental Table 3. Association between clinical variables and overall survival.

Published
2023

44. Supplemental Tables S1-S4 from Chronic Recreational Physical Inactivity and Epithelial Ovarian Cancer Risk: Evidence from the Ovarian Cancer Association Consortium

Author

Kirsten B. Moysich, Linda E. Kelemen, Kathryn L. Terry, Joellen M. Schildkraut, Francesmary Modugno, Anna H. Wu, Stacey J. Winham, Kristine G. Wicklund, Nicolas Wentzensen, Penelope M. Webb, Robert A. Vierkant, Chiu-Chen Tseng, Pamela J. Thompson, Elizabeth A. Szamreta, Mary Anne Rossing, Malcolm C. Pike, Celeste Leigh Pearce, Sara H. Olson, Catherine M. Olsen, Roberta B. Ness, Keitaro Matsuo, Susanne K. Kjaer, Susan Jordan, Allan Jensen, Satoyo Hosono, Estrid Hogdall, Marc T. Goodman, Ellen L. Goode, Brooke L. Fridley, Robert P. Edwards, Jennifer A. Doherty, Daniel Cramer, Andrew Berchuck, Elisa V. Bandera, Gary R. Zirpoli, Albina N. Minlikeeva, Emily Gower, Ruediger Klapdor, Barbara Schmalfeldt, Jenny Chang-Claude, J. Brian Szender, Kevin H. Eng, Lara E. Sucheston-Campbell, Chi-Chen Hong, Harvey A. Risch, Michael J. LaMonte, and Rikki Cannioto

Abstract

Supplemental Table S1. Pooled Odds Ratios and 95% Confidence Intervals Representing the Association Between Physical Inactivity and Epithelial Ovarian Cancer by Menopause Status. Supplemental Table S2. Age-Adjusted And Multivariable-Adjusted Pooled Odds Ratios And 95% Confidence Intervals (CI) Representing The Association Between Physical Inactivity And Epithelial Ovarian Cancer By Race. Supplemental Table S3. Pooled odds ratios and 95% confidence intervals representing the association between physical inactivity and epithelial ovarian cancer by standard BMI classification. Supplemental Table S4. Pooled odds ratios and 95% confidence intervals representing the association between physical inactivity and epithelial ovarian cancer by dichotomous BMI classification

Published
2023

45. Supplementary Table 3 from Platinum Sensitivity–Related Germline Polymorphism Discovered via a Cell-Based Approach and Analysis of Its Association with Outcome in Ovarian Cancer Patients

Author

M. Eileen Dolan, Georgia Chenevix-Trench, Anna deFazio, Beth Y. Karlan, Jenny Gross, Ignace Vergote, Evelyn Despierre, Diether Lambrechts, Jim Paul, Robert Brown, Kunle Odunsi, Matthew Grasela, Kirsten B. Moysich, Allan Jensen, Susanne K. Kjaer, Estrid Hogdall, Brooke L. Fridley, Robert A. Vierkant, Ellen L. Goode, Stuart MacGregor, Yi Lu, Nancy J. Cox, Soma Das, Yarden S. Fraiman, Peter H. O'Donnell, Shuangli Mi, Jonathan Beesley, Peixian Chen, Emily O. Kistner, Wei Zhang, Shiwei Duan, Dana Ziliak, Hae Kyung Im, Eric R. Gamazon, Sharon E. Johnatty, and R. Stephanie Huang

Abstract

PDF - 76K

Published
2023

46. Data from Is Pelvic Inflammatory Disease a Risk Factor for Ovarian Cancer?

Author

Susanne K. Kjaer, Klaus K. Andersen, Vanna Albieri, Allan Jensen, and Christina B. Rasmussen

Abstract

Background: Pelvic inflammatory disease (PID) has been proposed as a risk factor for ovarian cancer. However, the existing literature on the association between PID and ovarian cancer risk is inconclusive, and only few cohort studies have been conducted.Methods: Using nationwide Danish registries, we conducted a population-based cohort study including all women from the birth cohorts 1940 to 1970 in Denmark during 1978–2012 (n = 1,318,929) to investigate the association between PID and subsequent risk of epithelial ovarian cancer. Among women in the cohort, 81,281 women were diagnosed with PID and 5,356 women developed ovarian cancer during follow-up through 2012. Cox regression models were used to estimate HRs and 95% confidence intervals (CI) for the association between PID and ovarian cancer, both overall and according to histotype.Results: For ovarian cancer overall, we observed no association with PID (HR, 1.05; 95% CI, 0.92–1.20). However, in histotype-specific analyses, we found a statistically significantly increased risk of serous ovarian cancer among women with PID (HR, 1.19; 1.00–1.41; P = 0.047). Conversely, PID was not convincingly associated with risk of any of the other histotypes of ovarian cancer.Conclusions: PID was associated with a modestly increased risk of serous ovarian cancer, but not other histotypes.Impact: Our results indicate that PID is not a strong risk factor for ovarian cancer. Whether PID is slightly associated with risk of serous ovarian cancer has to be confirmed in other studies. Cancer Epidemiol Biomarkers Prev; 26(1); 104–9. ©2016 AACR.

Published
2023

47. Supplementary Tables S1-6, Figures S1-2 from Network-Based Integration of GWAS and Gene Expression Identifies a HOX-Centric Network Associated with Serous Ovarian Cancer Risk

Author

Paul D.P. Pharoah, Simon A. Gayther, Matthew L. Freedman, Alvaro N.A. Monteiro, Thomas A. Sellers, Argyrios Ziogas, Wei Zheng, Hannah Yang, Anna Wu, Xifeng Wu, Yin-Ling Woo, Lynne R. Wilkens, Kristine G. Wicklund, Alice S. Whittemore, Nicolas Wentzensen, Christine Walsh, Shan Wang-Gohrke, Robert A. Vierkant, Ignace Vergote, Els Van Nieuwenhuysen, Anne M. van Altena, Shelley S. Tworoger, Ya-Yu Tsai, Agnieszka Timorek, Pamela J. Thompson, Kathryn L. Terry, Soo-Hwang Teo, Ingvild L. Tangen, Lara E. Sucheston-Campbell, Melissa C. Southey, Honglin Song, Weiva Sieh, Nadeem Siddiqui, Yurii B. Shvetsov, Xiao-Ou Shu, Ira Schwaab, Joellen M. Schildkraut, Helga B. Salvesen, Iwona K. Rzepecka, Ingo B. Runnebaum, Anja Rudolph, Joseph H. Rothstein, Mary Anne Rossing, Barry Rosen, Harvey A. Risch, Susan J. Ramus, Elizabeth M. Poole, Malcolm C. Pike, Catherine M. Phelan, Jennifer Permuth-Wey, Liisa M. Pelttari, Tanja Pejovic, Celeste Leigh Pearce, Rachel Palmieri Weber, Sandra Orsulic, Irene Orlow, Sara H. Olson, Kunle Odunsi, Heli Nevanlinna, Roberta B. Ness, Lotte Nedergaard, Steven A. Narod, Kirsten B. Moysich, Francesmary Modugno, Usha Menon, Iain A. McNeish, John R. McLaughlin, Valerie McGuire, Keitaro Matsuo, Leon Massuger, Lene Lundvall, Jan Lubinski, Karen Lu, Jolanta Lissowska, Dong Liang, Douglas A. Levine, Jenny Lester, Arto Leminen, Shashi Lele, Alice W. Lee, Nhu D. Le, Sandrina Lambrechts, Diether Lambrechts, Jolanta Kupryjanczyk, Camilla Krakstad, Lambertus A. Kiemeney, Joseph Kelley, Melissa Kellar, Linda E. Kelemen, Susanne K. Kjaer, Beth Y. Karlan, Bu-Tian Ji, Allan Jensen, James Paul, Anna Jakubowska, Edwin S. Iversen, Satoyo Hosono, Claus K. Hogdall, Estrid Hogdall, Peter Hillemanns, Michelle A.T. Hildebrandt, Florian Heitz, Alexander Hein, Philipp Harter, Patricia Harrington, Jacek Grownwald, Marc T. Goodman, Ellen L. Goode, Rosalind Glasspool, Graham G. Giles, Aleksandra Gentry-Maharaj, Yu-Tang Gao, Brooke L. Fridley, Peter A. Fasching, Arif B. Ekici, Robert P. Edwards, Douglas F. Easton, Diana Eccles, Matthias Dürst, Andreas du Bois, Thilo Dörk, Jennifer A. Doherty, Ed Dicks, Joe Dennis, Agnieszka Dansonka-Mieszkowska, Cezary Cybulski, Julie M. Cunningham, Daniel Cramer, Linda S. Cook, Zhihua Chen, Yian Ann Chen, Jenny Chang-Claude, Karen Carty, Ian Campbell, Ralf Butzow, Angela Brooks-Wilson, Louise Brinton, Natalia Bogdanova, Line Bjørge, Maria Bisogna, Andrew Berchuck, Matthias W. Beckmann, Yukie T. Bean, Elisa V. Bandera, Helen Baker, Georgia Chenevix-Trench, Natalia Antonenkova, Hoda Anton-Culver, Katja K.H. Aben, Kate Lawrenson, Qiyuan Li, Jonathan P. Tyrer, and Siddhartha P. Kar

Abstract

Supplementary Tables S1-6, Figures S1-2. Supplementary Table S1: Summary of serous EOC GWAS data sets; Supplementary Table S2: Genes in the six significant co-expression networks; Supplementary Table S3: GSEA results after LD-based clumping of SNPs; Supplementary Table S4: GSEA results for the replication data set (COGS); Supplementary Table S5: GSEA results for all networks with > 10 genes; Supplementary Table S6: Number of intragenic SNPs and genes covered by SNPs in the different analyses; Supplementary Figure S1: Q-Q plots of the minimum P-value among all SNPs in each gene with and without the modified Sidak correction; Supplementary Figure S2: Disease Association Protein-Protein Link Evaluator (DAPPLE) protein-protein interaction network

Published
2023

48. Supplemental Table 1 from History of Comorbidities and Survival of Ovarian Cancer Patients, Results from the Ovarian Cancer Association Consortium

Author

Kirsten B. Moysich, Penelope M. Webb, Allan Jensen, Jolanta Kupryjanczyk, Anna H. Wu, Celeste L. Pearce, Aleksandra Gentry-Maharaj, Susan J. Ramus, Simon A. Gayther, Usha Menon, Argyrios Ziogas, Hoda Anton-Culver, Rebecca Sutphen, Leon F.A.G. Massuger, Lambertus A. Kiemeney, Lisa E. Paddock, Elisa V. Bandera, Daniel W. Cramer, Kathryn L. Terry, Joellen M. Schildkraut, Estrid Høgdall, Susanne K. Kjær, Ellen L. Goode, Beth Y. Karlan, Mika Mizuno, Keitaro Matsuo, Roberta B. Ness, Francesmary Modugno, Robert Edwards, Thilo Dörk, Marc T. Goodman, Jenny Chang-Claude, Jennifer A. Doherty, Mary Anne Rossing, Harvey A. Risch, Matthias W. Beckmann, Peter A. Fasching, Susan J. Jordan, Anna deFazio, Helen Steed, Martin Köbel, Linda E. Kelemen, Emese Zsiros, Brenda Diergaarde, Paul Mayor, Kunle Odunsi, Brahm Segal, J. Brian Szender, Grace Friel, Rikki A. Cannioto, Kevin H. Eng, Jo L. Freudenheim, and Albina N. Minlikeeva

Abstract

Description of the studies included in the pooled analysis and methods of data collection

Published
2023

49. Supplementary Methods and References from The BRCA1-Δ11q Alternative Splice Isoform Bypasses Germline Mutations and Promotes Therapeutic Resistance to PARP Inhibition and Cisplatin

Author

Neil Johnson, Violeta Serra, Judith Balmaña, Jos Jonkers, Peter Bouwman, Elizabeth M. Swisher, Mary B. Daly, Denise C. Connolly, David L. Wiest, Geoffrey I. Shapiro, Alan D. D'Andrea, Susanne K. Kjaer, Simon A. Gayther, Siegal Sadetzki, Robert Nussbaum, Martin Gore, Mark H. Greene, Javier J. Benitez, Håkan Olsson, Georgia Chenevix-Trench, Diether Lambrechts, Charlie Gourley, Beth Karlan, Paul D. P. Pharoah, Francisco J. Candido Dos Reis, Shawn F. Johnson, Maribel I. Harrell, Yong Zhang, Shane W. O'Brien, Ingrid van der Heijden, Hanneke van der Gulden, Suraj Peri, Emmanuelle Nicolas, Joseph Nacson, John J. Krais, Cristina Cruz, Andrea J. Bernhardy, and Yifan Wang

Abstract

Description of additional methods and procedures used in the study. Also includes Supplementary References.

Published
2023

50. Endometriosis and menopausal hormone therapy impact the hysterectomy-ovarian cancer association

Author

Marc T. Goodman, Argyrios Ziogas, Jenny Chang-Claude, Anna H. Wu, Susan J. Jordan, Joellen M. Schildkraut, Minh Tung Phung, Francesmary Modugno, Penelope M. Webb, Daniel W. Cramer, Rachel Palmieri Weber, Andrew Berchuck, Bhramar Mukherjee, Holly R. Harris, Kathleen R. Cho, Hoda Anton-Culver, Harvey A. Risch, Kirsten B. Moysich, Renée T. Fortner, Celeste Leigh Pearce, Gillian E. Hanley, Kathryn L. Terry, Susanne K. Kjaer, Lilah Khoja, Alice W. Lee, Malcolm C. Pike, Allan Jensen, Karen McLean, Aruna Muthukumar, and Jennifer A. Doherty

Subjects
medicine.medical_specialty, Inverse Association, medicine.drug_class, medicine.medical_treatment, Endometriosis, Hysterectomy, Article, medicine, Humans, Ovarian Neoplasms, Gynecology, business.industry, Estrogen Replacement Therapy, Obstetrics and Gynecology, Cancer, Odds ratio, medicine.disease, Oncology, Estrogen, Case-Control Studies, Female, Hormone therapy, Menopause, business, Ovarian cancer
Abstract

Objective To evaluate the association between hysterectomy and ovarian cancer, and to understand how hormone therapy (HT) use and endometriosis affect this association. Methods We conducted a pooled analysis of self-reported data from 11 case-control studies in the Ovarian Cancer Association Consortium (OCAC). Women with (n = 5350) and without ovarian cancer (n = 7544) who never used HT or exclusively used either estrogen-only therapy (ET) or estrogen+progestin therapy (EPT) were included. Risk of invasive epithelial ovarian cancer adjusted for duration of ET and EPT use and stratified on history of endometriosis was determined using odds ratios (ORs) with 95% confidence intervals (CIs). Results Overall and among women without endometriosis, there was a positive association between ovarian cancer risk and hysterectomy (OR = 1.19, 95% CI 1.09-1.31 and OR = 1.20, 95% CI 1.09-1.32, respectively), but no association upon adjusting for duration of ET and EPT use (OR = 1.04, 95% CI 0.94-1.16 and OR = 1.06, 95% CI 0.95-1.18, respectively). Among women with a history of endometriosis, there was a slight inverse association between hysterectomy and ovarian cancer risk (OR = 0.93, 95% CI 0.69-1.26), but this association became stronger and statistically significant after adjusting for duration of ET and EPT use (OR = 0.69, 95% CI 0.48-0.99). Conclusions The hysterectomy-ovarian cancer association is complex and cannot be understood without considering duration of ET and EPT use and history of endometriosis. Failure to take these exposures into account in prior studies casts doubt on their conclusions. Overall, hysterectomy is not risk-reducing for ovarian cancer, however the inverse association among women with endometriosis warrants further investigation.

Published
2022

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