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3. Validation of biomarkers of aging

Author

Moqri, Mahdi, Herzog, Chiara, Poganik, Jesse R., Ying, Kejun, Justice, Jamie N., Belsky, Daniel W., Higgins-Chen, Albert T., Chen, Brian H., Cohen, Alan A., Fuellen, Georg, Hägg, Sara, Marioni, Riccardo E., Widschwendter, Martin, Fortney, Kristen, Fedichev, Peter O., Zhavoronkov, Alex, Barzilai, Nir, Lasky-Su, Jessica, Kiel, Douglas P., Kennedy, Brian K., Cummings, Steven, Slagboom, P. Eline, Verdin, Eric, Maier, Andrea B., Sebastiano, Vittorio, Snyder, Michael P., Gladyshev, Vadim N., Horvath, Steve, and Ferrucci, Luigi

Published
2024
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6. Biomarkers of aging for the identification and evaluation of longevity interventions

Author

Moqri, Mahdi, Herzog, Chiara, Poganik, Jesse R., Justice, Jamie, Belsky, Daniel W., Higgins-Chen, Albert, Moskalev, Alexey, Fuellen, Georg, Cohen, Alan A., Bautmans, Ivan, Widschwendter, Martin, Ding, Jingzhong, Fleming, Alexander, Mannick, Joan, Han, Jing-Dong Jackie, Zhavoronkov, Alex, Barzilai, Nir, Kaeberlein, Matt, Cummings, Steven, Kennedy, Brian K., Ferrucci, Luigi, Horvath, Steve, Verdin, Eric, Maier, Andrea B., Snyder, Michael P., Sebastiano, Vittorio, and Gladyshev, Vadim N.

Published
2023
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7. Molecular and cellular mechanisms of microglia-mediated neuroprotection

Author

Herzog, Chiara Maria Stella, Herrgen, Leah, and Becker, Catherina

Subjects
617.4, traumatic brain injury, zebrafish, microglia, excitotoxicity, secondary cell death, calcium waves
Abstract

Traumatic brain injury (TBI) is a major cause of death and long-term disability worldwide. It is elicited by an external force injuring the brain, and leads to two phases of neuronal cell death: primary cell death, resulting from direct mechanical disruption of the tissue, and secondary cell death, caused by delayed cytotoxic cascades. While primary cell death can only be prevented by avoiding physical injury, secondary cell death occurs within hours to weeks following the initial injury and therefore lies within a therapeutic window during which pharmacological agents targeting the pathomechanisms of TBI could be applied. Pre-clinical models of brain injury in rodents have identified several neuroprotective compounds, but not a single drug has shown improved patient outcome over placebo in multi-centre phase III clinical trials. Intriguingly, the largest randomised controlled trial for TBI to date reported a higher mortality in patients treated with an immunosuppressive drug compared to patients treated with placebo, suggesting that the immune system may play a neuroprotective role following brain injuries. To investigate the role of the immune system in more detail, I developed a model of brain injury in larval zebrafish. Larval zebrafish are amenable to genetic and pharmacological manipulation, and their optical transparency in combination with the availability of a multitude of transgenic reporter lines allows for efficient in vivo (timelapse) microscopy. This allowed me to visualise the cellular and molecular reactions to brain injury in real-time in a living vertebrate organism, which provided an advantage compared to the majority of studies so far, which had been done either in rodents with static end points, or in vitro. Characterisation of cell death dynamics revealed that larval zebrafish reproducibly exhibit primary and secondary cell death following brain injury. In line with mammalian TBI models, I demonstrated that excitotoxicity contributes to secondary cell death. Furthermore, I described early calcium waves in reponse to injury that may instruct repair mechanisms; using pharmacological agents, I identified the release of glutamate, acting on neurons surrounding the injury site, and ATP, acting predominantly on glial cells, as the upstream mechanisms of calcium waves. In contrast to observations in rodent models and human TBI patients, I observed little infiltration of peripheral macrophages or neutrophils. Microglia, the resident immune cells of the brain, were rapidly recruited to the injury site and significantly increased their phagocytic activity upon injury. Inhibition of microglial phagocytosis by targeting phosphatidyl serine receptors either pharmacologically or genetically via CRISPR/Cas9-mediated gene editing resulted in a significant increase in the rate of secondary cell death. This result demonstrated a role for rapid phagocytosis of debris in limiting the extent of secondary cell death, and suggested an overall neuroprotective role for microglial phagocytosis. Probing into the transcriptome of microglia/macrophages following injury using RNA sequencing of sorted cells revealed profound transcriptomic changes within two hours of injury, and will aid the future investigation of the role of microglia in neuroprotection. To summarise, this body of work provides evidence for a neuroprotective role of microglia in a new larval zebrafish model of brain injury, and the transcriptomic analysis will form the basis of a more in-depth study of microglia-derived neuroprotective molecules. Using CRISPR/Cas9-guided mutation of genes of interest in larval zebrafish, we will be able to investigate the role of these genes following injury in microglia-mediated neuroprotection. Following further validation, these findings could potentially be exploited for prevention of secondary cell death after human TBI.

Published
2019

19. High performance of the DNA methylation‐based WID‐qEC test for detecting uterine cancers independent of sampling modalities

Author

Illah, Ojone, primary, Scott, Malcolm, additional, Redl, Elisa, additional, Barrett, James E., additional, Schreiberhuber, Lena, additional, Herzog, Chiara, additional, Vavourakis, Charlotte D., additional, Jones, Allison, additional, Evans, Iona, additional, Reisel, Dan, additional, Chandrasekaran, Dhivya, additional, Doufekas, Kostas, additional, Graham, Radha, additional, Kotsopoulos, Ioannis C., additional, MacDonald, Nicola, additional, Arora, Rupali, additional, Olaitan, Adeola, additional, Rosenthal, Adam, additional, and Widschwendter, Martin, additional

Published
2024
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23. Correction: Antiprogestins reduce epigenetic field cancerization in breast tissue of young healthy women

Author

Bartlett, Thomas E., Evans, Iona, Jones, Allison, Barrett, James E., Haran, Shaun, Reisel, Daniel, Papaikonomou, Kiriaki, Jones, Louise, Herzog, Chiara, Pashayan, Nora, Simões, Bruno M., Clarke, Robert B., Evans, D. Gareth, Ghezelayagh, Talayeh S., Ponandai-Srinivasan, Sakthivignesh, Boggavarapu, Nageswara R., Lalitkumar, Parameswaran G., Howell, Sacha J., Risques, Rosa Ana, Rådestad, Angelique Flöter, Dubeau, Louis, Gemzell-Danielsson, Kristina, and Widschwendter, Martin

Published
2022
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24. Antiprogestins reduce epigenetic field cancerization in breast tissue of young healthy women

Author

Bartlett, Thomas E., Evans, Iona, Jones, Allison, Barrett, James E., Haran, Shaun, Reisel, Daniel, Papaikonomou, Kiriaki, Jones, Louise, Herzog, Chiara, Pashayan, Nora, Simões, Bruno M., Clarke, Robert B., Evans, D. Gareth, Ghezelayagh, Talayeh S., Ponandai-Srinivasan, Sakthivignesh, Boggavarapu, Nageswara R., Lalitkumar, Parameswaran G., Howell, Sacha J., Risques, Rosa Ana, Rådestad, Angelique Flöter, Dubeau, Louis, Gemzell-Danielsson, Kristina, and Widschwendter, Martin

Published
2022
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27. The WID-BC-index identifies women with primary poor prognostic breast cancer based on DNA methylation in cervical samples

Author

Barrett, James E., Herzog, Chiara, Jones, Allison, Leavy, Olivia C., Evans, Iona, Knapp, Susanne, Reisel, Daniel, Nazarenko, Tatiana, Kim, Yoo-Na, Franchi, Dorella, Ryan, Andy, Franks, Joanna, Bjørge, Line, Zikan, Michal, Cibula, David, Harbeck, Nadia, Colombo, Nicoletta, Dudbridge, Frank, Jones, Louise, Sundström, Karin, Dillner, Joakim, Rådestad, Angelique Flöter, Gemzell-Danielsson, Kristina, Pashayan, Nora, and Widschwendter, Martin

Published
2022
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30. Natural Killer Cell Dysfunction in Premenopausal BRCA1 Mutation Carriers: A Potential Mechanism for Ovarian Carcinogenesis

Author

Haran, Shaun, primary, Chindera, Kantaraja, additional, Sabry, May, additional, Wilkinson, Nafisa, additional, Arora, Rupali, additional, Zubiak, Agnieszka, additional, Bartlett, Thomas E., additional, Evans, Iona, additional, Jones, Allison, additional, Reisel, Daniel, additional, Herzog, Chiara, additional, Alkasalias, Twana, additional, Newman, Mark, additional, Kim, Jaeyeon, additional, Rådestad, Angelique Flöter, additional, Gemzell-Danielsson, Kristina, additional, Rosenthal, Adam N., additional, Dubeau, Louis, additional, Lowdell, Mark W., additional, and Widschwendter, Martin, additional

Published
2024
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31. Abstract IA007: The WID-qEC test for simple and accurate endometrial cancer detection

Author

Widschwendter, Martin, primary, Evans, Iona, additional, Reisel, Daniel, additional, Jones, Allison, additional, Bajrami, Alba, additional, Nijjar, Simrit, additional, Solangon, Sarah A, additional, Arora, Rupali, additional, Redl, Elisa, additional, Schreiberhuber, Lena, additional, Ishaq-Parveen, Isma, additional, Rothärmel, Julia, additional, Herzog, Chiara, additional, and Jurkovic, Davor, additional

Published
2024
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32. Dietary restriction in senolysis and prevention and treatment of disease.

Author

Aminzadeh-Gohari, Sepideh, Kofler, Barbara, and Herzog, Chiara

Subjects
LOW-calorie diet, PREVENTIVE medicine, THERAPEUTICS, METABOLIC reprogramming, DISEASE risk factors, AGE factors in disease
Abstract

Aging represents a key risk factor for a plethora of diseases. Targeting detrimental processes which occur during aging, especially before onset of age-related disease, could provide drastic improvements in healthspan. There is increasing evidence that dietary restriction (DR), including caloric restriction, fasting, or fasting-mimicking diets, extend both lifespan and healthspan. This has sparked interest in the use of dietary regimens as a non-pharmacological means to slow aging and prevent disease. Here, we review the current evidence on the molecular mechanisms underlying DR-induced health improvements, including removal of senescent cells, metabolic reprogramming, and epigenetic rejuvenation. [ABSTRACT FROM AUTHOR]

Published
2024
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33. Plasma cell‐free DNA methylation analysis for ovarian cancer detection: Analysis of samples from a case‐control study and an ovarian cancer screening trial.

Author

Herzog, Chiara, Jones, Allison, Evans, Iona, Reisel, Daniel, Olaitan, Adeola, Doufekas, Konstantinos, MacDonald, Nicola, Rådestad, Angelique Flöter, Gemzell‐Danielsson, Kristina, Zikan, Michal, Cibula, David, Dostálek, Lukáš, Paprotka, Tobias, Leimbach, Andreas, Schmitt, Markus, Ryan, Andy, Gentry‐Maharaj, Aleksandra, Apostolidou, Sophia, Rosenthal, Adam N, and Menon, Usha

Subjects
CELL-free DNA, OVARIAN cancer, DNA methylation, DNA analysis, EARLY detection of cancer, CIRCULATING tumor DNA, CASE-control method
Abstract

Analysis of cell‐free DNA methylation (cfDNAme), alone or combined with CA125, could help to detect ovarian cancers earlier and may reduce mortality. We assessed cfDNAme in regions of ZNF154, C2CD4D and WNT6 via targeted bisulfite sequencing in diagnostic and early detection (preceding diagnosis) settings. Diagnostic samples were obtained via prospective blood collection in cell‐free DNA tubes in a convenience series of patients with a pelvic mass. Early detection samples were matched case‐control samples derived from the UK Familial Ovarian Cancer Screening Study (UKFOCSS). In the diagnostic set (ncases = 27, ncontrols = 41), the specificity of cfDNAme was 97.6% (95% CI: 87.1%‐99.9%). High‐risk cancers were detected with a sensitivity of 80% (56.3%‐94.3%). Combination of cfDNAme and CA125 resulted in a sensitivity of 94.4% (72.7%‐99.9%) for high‐risk cancers. Despite technical issues in the early detection set (ncases = 29, ncontrols = 29), the specificity of cfDNAme was 100% (88.1%‐100.0%). We detected 27.3% (6.0%‐61.0%) of high‐risk cases with relatively lower genomic DNA (gDNA) contamination. The sensitivity rose to 33.3% (7.5%‐70.1%) in samples taken <1 year before diagnosis. We detected ovarian cancer in several patients up to 1 year before diagnosis despite technical limitations associated with archival samples (UKFOCSS). Combined cfDNAme and CA125 assessment may improve ovarian cancer screening in high‐risk populations, but future large‐scale prospective studies will be required to validate current findings. [ABSTRACT FROM AUTHOR]

Published
2024
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39. The WID‐EC test for the detection and risk prediction of endometrial cancer

Author

Barrett, James E., primary, Jones, Allison, additional, Evans, Iona, additional, Herzog, Chiara, additional, Reisel, Daniel, additional, Olaitan, Adeola, additional, Mould, Tim, additional, MacDonald, Nicola, additional, Doufekas, Konstantinos, additional, Newton, Claire, additional, Crosbie, Emma J., additional, Bjørge, Line, additional, Colombo, Nicoletta, additional, Dostalek, Lukas, additional, Costas, Laura, additional, Peremiquel‐Trillas, Paula, additional, Ponce, Jordi, additional, Matias‐Guiu, Xavier, additional, Zikan, Michal, additional, Cibula, David, additional, Wang, Jiangrong, additional, Sundström, Karin, additional, Dillner, Joakim, additional, and Widschwendter, Martin, additional

Published
2023
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42. A Simple Cervicovaginal Epigenetic Test for Screening and Rapid Triage of Women With Suspected Endometrial Cancer: Validation in Several Cohort and Case/Control Sets

Author

Herzog, Chiara, primary, Marín, Fátima, additional, Jones, Allison, additional, Evans, Iona, additional, Reisel, Daniel, additional, Redl, Elisa, additional, Schreiberhuber, Lena, additional, Paytubi, Sonia, additional, Pelegrina, Beatriz, additional, Carmona, Álvaro, additional, Peremiquel-Trillas, Paula, additional, Frias-Gomez, Jon, additional, Pineda, Marta, additional, Brunet, Joan, additional, Ponce, Jordi, additional, Matias-Guiu, Xavier, additional, de Sanjosé, Silvia, additional, Alemany, Laia, additional, Olaitan, Adeola, additional, Wong, Michael, additional, Jurkovic, Davor, additional, Crosbie, Emma J., additional, Rosenthal, Adam N., additional, Bjørge, Line, additional, Zikan, Michal, additional, Dostalek, Lukas, additional, Cibula, David, additional, Sundström, Karin, additional, Dillner, Joakim, additional, Costas, Laura, additional, and Widschwendter, Martin, additional

Published
2022
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43. HEAP Knowledge Engine. Public deliverable 6.2

Author

Ormenisan, Alex, Mukhedkar, Dhananjay, Arroyo, Sara, Pimenoff, Ville, Zhang, Allison, Trier Møller, Frederik, Herzog, Chiara, and Bala, Piotr

Subjects
exposome, exposome research, research, data analysis, informatics, knowledge engine, SaaS
Abstract

This document provides a full view of the capabilities of the Knowledge Engine within the Human Exposome Assessment Platform (HEAP). The HEAP software platform is built on top of the open-source Hopsworks platform. This document describes the improvements to the Knowledge Engine in Hopsworks (scalable and secure data storage, querying, and annotation) as well as the steps done and planned to implement all the partner pipelines into the HEAP platform. The goal is for the pipelines to fully utilise the benefits of horizontal scaling and sharing of data and code as some of the base qualities of the platform. The implementation presented in this document is coordinated with work package 3 - Large sample cohorts from population-based interventions, work package 4 - Consumer exposure monitoring system, work package 8 - Epigenomics Analysis, and work package 9 - Metagenomic analysis.

Published
2022
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44. The WID‐qEC test: Performance in a hospital‐based cohort and feasibility to detect endometrial and cervical cancers

Author

Schreiberhuber, Lena, primary, Herzog, Chiara, additional, Vavourakis, Charlotte D., additional, Redl, Elisa, additional, Kastner, Christine, additional, Jones, Allison, additional, Evans, Iona, additional, Zikan, Michal, additional, Cibula, David, additional, Widschwendter, Peter, additional, Pfau, Karin, additional, Math, Barbara, additional, Seewald, Martin, additional, Amory, Sylvain, additional, Obrist, Peter, additional, and Widschwendter, Martin, additional

Published
2022
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45. Ageing DNAme signatures. Public deliverable 8.2

Author

Herzog, Chiara and Widschwendter, Martin

Subjects
exposome, exposome research, research, data analysis, informatics, epigenome, epigenomics, DNA, DNA methylation
Abstract

The epigenome is at the interface between intrinsic (genetic) and external (environmental) factors influencing cellular behaviour. DNA methylation, defined as the addition of methyl groups on the C5 position of cytosines on the DNA in the context of CpGs, is a key part of the epigenome which integrates these intrinsic and external factors and records them as a signature on the DNA. DNA methylation is also influenced by cellular ageing and forms the basis of several existing “epigenetic clocks” which utilise a combination of age-associated differentially methylated positions to predict chronological age. Many age-related DNA methylation changes are common across most tissue types. Whether discordant tick rates between cell type-specific and general epigenetic clocks play a role in health or disease has remained largely unexplored. Recently we reported that cervical samples, consisting of a mixture of hormone-sensitive epithelial and immune cells, are a suitable surrogate tissue for prediction of breast cancer and may reflect systemic epigenetic programming defects. We therefore aimed to investigate if cell type-specific ageing signatures in cervical samples are associated with breast cancer risk. Using DNA methylation analysis of cervical samples, we developed the WID (Women’s cancer risk IDentification) general clock, shared by both epithelial and immune cells and optimised for cervical samples. Surprisingly, the WID general clock outperforms two commonly used epigenetic clocks for age prediction in several tissues. Via computational inference of sample composition, we also identified epithelial- and immune-specific epigenetic clocks. A discordance between WID-general and epithelial age (WID-relative-epithelial-age, WID-REA) in cervical samples is associated with breast cancer. The same effect is observed in breast tissue from individuals at increased risk of breast cancer (BRCA1/2 mutation carriers) but could be rescued via risk-reducing pharmacological intervention in a clinical study. Interestingly, the WID-REA also differs between women who received hormone replacement therapy (HRT) and did or did not develop breast cancer, indicating a potential to monitor individual breast cancer risk on HRT using the WID-REA. We therefore provide novel general and tissue-specific epigenetic clocks which are accurate at predicting chronological age and may further be an informatic measure of disease risk.

Published
2022
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46. Author Correction: Susceptibility to hormone-mediated cancer is reflected by different tick rates of the epithelial and general epigenetic clock

Author

Barrett, J James E, Barrett, J, Herzog, C, Kim, Y, Bartlett, T, Jones, A, Evans, I, Cibula, D, Zikan, M, Bjørge, L, Harbeck, N, Colombo, N, Howell, S, Rådestad, A, Gemzell-Danielsson, K, Widschwendter, M, Barrett, J James E, Herzog, Chiara, Kim, Yoo-Na, Bartlett, Thomas E, Jones, Allison, Evans, Iona, Cibula, David, Zikan, Michal, Bjørge, Line, Harbeck, Nadia, Colombo, Nicoletta, Howell, Sacha J, Rådestad, Angelique Flöter, Gemzell-Danielsson, Kristina, Widschwendter, Martin, Barrett, J James E, Barrett, J, Herzog, C, Kim, Y, Bartlett, T, Jones, A, Evans, I, Cibula, D, Zikan, M, Bjørge, L, Harbeck, N, Colombo, N, Howell, S, Rådestad, A, Gemzell-Danielsson, K, Widschwendter, M, Barrett, J James E, Herzog, Chiara, Kim, Yoo-Na, Bartlett, Thomas E, Jones, Allison, Evans, Iona, Cibula, David, Zikan, Michal, Bjørge, Line, Harbeck, Nadia, Colombo, Nicoletta, Howell, Sacha J, Rådestad, Angelique Flöter, Gemzell-Danielsson, Kristina, and Widschwendter, Martin

Abstract

Following publication of the original article [1], it was brought to our attention that one of the references was incorrect. The text of the article reads: The general, epithelial and immune clocks are significantly, albeit weakly, correlated with two mitotic clocks, the pcgtAge score based on promoter CpGs at polycomb group target genes [24] and an alternative mitotic clock model recently developed using “solo-WCGWs” [25] The correct reference for citation 24 should be as follows: 24. Yang Z, Wong A, Kuh D, Paul DS, Rakyan VK, Leslie RD et al. Correlation of an epigenetic mitotic clock with cancer risk. Genome Biology 2016; 17: 205 Also, we wish to add an additional reference to that cited as citation 25. It has been brought to our attention that it would also be relevant to cite the following: 25. Teschendorff AE. A comparison of epigenetic mitotic-like clocks for cancer risk prediction. Genome Medicine 2020; 12: 56 We apologize for the previous errors in the reference list.

Published
2022

47. The WID-BC-index identifies women with primary poor prognostic breast cancer based on DNA methylation in cervical samples

Author

Barrett, J, Herzog, C, Jones, A, Leavy, O, Evans, I, Knapp, S, Reisel, D, Nazarenko, T, Kim, Y, Franchi, D, Ryan, A, Franks, J, Bjørge, L, Zikan, M, Cibula, D, Harbeck, N, Colombo, N, Dudbridge, F, Jones, L, Sundström, K, Dillner, J, Rådestad, A, Gemzell-Danielsson, K, Pashayan, N, Widschwendter, M, Barrett, James E, Herzog, Chiara, Jones, Allison, Leavy, Olivia C, Evans, Iona, Knapp, Susanne, Reisel, Daniel, Nazarenko, Tatiana, Kim, Yoo-Na, Franchi, Dorella, Ryan, Andy, Franks, Joanna, Bjørge, Line, Zikan, Michal, Cibula, David, Harbeck, Nadia, Colombo, Nicoletta, Dudbridge, Frank, Jones, Louise, Sundström, Karin, Dillner, Joakim, Rådestad, Angelique Flöter, Gemzell-Danielsson, Kristina, Pashayan, Nora, Widschwendter, Martin, Barrett, J, Herzog, C, Jones, A, Leavy, O, Evans, I, Knapp, S, Reisel, D, Nazarenko, T, Kim, Y, Franchi, D, Ryan, A, Franks, J, Bjørge, L, Zikan, M, Cibula, D, Harbeck, N, Colombo, N, Dudbridge, F, Jones, L, Sundström, K, Dillner, J, Rådestad, A, Gemzell-Danielsson, K, Pashayan, N, Widschwendter, M, Barrett, James E, Herzog, Chiara, Jones, Allison, Leavy, Olivia C, Evans, Iona, Knapp, Susanne, Reisel, Daniel, Nazarenko, Tatiana, Kim, Yoo-Na, Franchi, Dorella, Ryan, Andy, Franks, Joanna, Bjørge, Line, Zikan, Michal, Cibula, David, Harbeck, Nadia, Colombo, Nicoletta, Dudbridge, Frank, Jones, Louise, Sundström, Karin, Dillner, Joakim, Rådestad, Angelique Flöter, Gemzell-Danielsson, Kristina, Pashayan, Nora, and Widschwendter, Martin

Abstract

Genetic and non-genetic factors contribute to breast cancer development. An epigenome-based signature capturing these components in easily accessible samples could identify women at risk. Here, we analyse the DNA methylome in 2,818 cervical, 357 and 227 matched buccal and blood samples respectively, and 42 breast tissue samples from women with and without breast cancer. Utilising cervical liquid-based cytology samples, we develop the DNA methylation-based Women's risk IDentification for Breast Cancer index (WID-BC-index) that identifies women with breast cancer with an AUROC (Area Under the Receiver Operator Characteristic) of 0.84 (95% CI: 0.80-0.88) and 0.81 (95% CI: 0.76-0.86) in internal and external validation sets, respectively. CpGs at progesterone receptor binding sites hypomethylated in normal breast tissue of women with breast cancer or in BRCA mutation carriers are also hypomethylated in cervical samples of women with poor prognostic breast cancer. Our data indicate that a systemic epigenetic programming defect is highly prevalent in women who develop breast cancer. Further studies validating the WID-BC-index may enable clinical implementation for monitoring breast cancer risk.

Published
2022

48. The WID‐qEC test: Performance in a hospital‐based cohort and feasibility to detect endometrial and cervical cancers.

Author

Schreiberhuber, Lena, Herzog, Chiara, Vavourakis, Charlotte D., Redl, Elisa, Kastner, Christine, Jones, Allison, Evans, Iona, Zikan, Michal, Cibula, David, Widschwendter, Peter, Pfau, Karin, Math, Barbara, Seewald, Martin, Amory, Sylvain, Obrist, Peter, and Widschwendter, Martin

Subjects
CERVICAL cancer, ENDOMETRIAL cancer, UTERINE hemorrhage, RECEIVER operating characteristic curves, CANCER patients, DNA methylation
Abstract

The majority of endometrial and cervical cancers present with abnormal vaginal bleeding but only a small proportion of women suffering from vaginal bleeding actually have such a cancer. A simple, operator‐independent and accurate test to correctly identify women presenting with abnormal bleeding as a consequence of endometrial or cervical cancer is urgently required. We have recently developed and validated the WID‐qEC test, which assesses DNA methylation of ZSCAN12 and GYPC via real‐time PCR, to triage women with symptoms suggestive of endometrial cancer using ThinPrep‐based liquid cytology samples. Here, we investigated whether the WID‐qEC test can additionally identify women with cervical cancer. Moreover, we evaluate the test's applicability in a SurePath‐based hospital‐cohort by comparing its ability to detect endometrial and cervical cancer to cytology. In a set of 23 cervical cancer cases and 28 matched controls the receiver operating characteristic (ROC) area under the curve (AUC) is 0.99 (95% confidence interval [CI]: 0.97‐1.00) with a sensitivity and specificity of 100% and 92.9%, respectively. Amongst the hospital‐cohort (n = 330), the ROC AUC is 0.99 (95% CI: 0.98‐1) with a sensitivity and specificity of 100% and 82.5% for the WID‐qEC test, respectively, and 33.3% and 96.9% for cytology (considering PAP IV/V as positive). Our data suggest that the WID‐qEC test detects both endometrial and cervical cancer with high accuracy. [ABSTRACT FROM AUTHOR]

Published
2023
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49. Additional file 1 of DNA methylation-based detection and prediction of cervical intraepithelial neoplasia grade 3 and invasive cervical cancer with the WID™-qCIN test

Author

Herzog, Chiara, Sundström, Karin, Jones, Allison, Evans, Iona, Barrett, James E., Wang, Jiangrong, Redl, Elisa, Schreiberhuber, Lena, Costas, Laura, Paytubi, Sonia, Dostalek, Lukas, Zikan, Michal, Cibula, David, Sroczynski, Gaby, Siebert, Uwe, Dillner, Joakim, and Widschwendter, Martin

Abstract

Additional file 1: Additional figures and tables.

Published
2022
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50. Additional file 1 of Susceptibility to hormone-mediated cancer is reflected by different tick rates of the epithelial and general epigenetic clock

Author

Barrett, James E., Herzog, Chiara, Kim, Yoo-Na, Bartlett, Thomas E., Jones, Allison, Evans, Iona, Cibula, David, Zikan, Michal, Bj��rge, Line, Harbeck, Nadia, Colombo, Nicoletta, Howell, Sacha J., R��destad, Angelique Fl��ter, Gemzell-Danielsson, Kristina, and Widschwendter, Martin

Abstract

Additional file 1: Fig. S1. Datasets and experimental design. Fig. S2. Detailed comparison of the WID general clock and other epigenetic clocks, and assessments of cell composition in response to menopause, hormone replacement and cancer. Fig. S3. Detailed epidemiological assessment of the WID general clock age acceleration. Fig. S4. Association of the WID general, epithelial and immune clocks with menopause, replicative age, and solo-WCGW methylation. Fig. S5. Association of WID-relative-epithelial- and -immune-age with chronological age and immune cell proportion and breast cancer subtype. Fig. S6. Epidemiological associations of the WID-relative-epithelial-age. Fig. S7. Epidemiological associations of the WID-relative-immune-age. Table S1. Epidemiological and clinical characteristics of the training set. Table S2. Epidemiological and clinical characteristics of the validation set 1. Table S3. WID-REA quantiles and pre-menopausal breast cancer risk. Table S4. Ages of individuals in the breast tissue sets. Table S5. Epidemiological and clinical characteristics of Validation set 2. Table S6. List of samples used to assess the performance of age prediction.

Published
2022
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