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1. A framework for assessing interactions for risk stratification models: the example of ovarian cancer

Author

Phung, Minh Tung, Lee, Alice W, McLean, Karen, Anton-Culver, Hoda, Bandera, Elisa V, Carney, Michael E, Chang-Claude, Jenny, Cramer, Daniel W, Doherty, Jennifer Anne, Fortner, Renee T, Goodman, Marc T, Harris, Holly R, Jensen, Allan, Modugno, Francesmary, Moysich, Kirsten B, Pharoah, Paul DP, Qin, Bo, Terry, Kathryn L, Titus, Linda J, Webb, Penelope M, Wu, Anna H, Zeinomar, Nur, Ziogas, Argyrios, Berchuck, Andrew, Cho, Kathleen R, Hanley, Gillian E, Meza, Rafael, Mukherjee, Bhramar, Pike, Malcolm C, Pearce, Celeste Leigh, and Trabert, Britton

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Rare Diseases, Women's Health, Ovarian Cancer, Cancer, Prevention, Aetiology, 2.1 Biological and endogenous factors, 2.5 Research design and methodologies (aetiology), Good Health and Well Being, Humans, Female, Ovarian Neoplasms, Risk Factors, Risk Assessment, Case-Control Studies, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

Generally, risk stratification models for cancer use effect estimates from risk/protective factor analyses that have not assessed potential interactions between these exposures. We have developed a 4-criterion framework for assessing interactions that includes statistical, qualitative, biological, and practical approaches. We present the application of this framework in an ovarian cancer setting because this is an important step in developing more accurate risk stratification models. Using data from 9 case-control studies in the Ovarian Cancer Association Consortium, we conducted a comprehensive analysis of interactions among 15 unequivocal risk and protective factors for ovarian cancer (including 14 non-genetic factors and a 36-variant polygenic score) with age and menopausal status. Pairwise interactions between the risk/protective factors were also assessed. We found that menopausal status modifies the association among endometriosis, first-degree family history of ovarian cancer, breastfeeding, and depot-medroxyprogesterone acetate use and disease risk, highlighting the importance of understanding multiplicative interactions when developing risk prediction models.

Published
2023

2. Progestogen-driven B7-H4 contributes to onco-fetal immune tolerance

Author

Yu, Jiali, Yan, Yijian, Li, Shasha, Xu, Ying, Parolia, Abhijit, Rizvi, Syed, Wang, Weichao, Zhai, Yiwen, Xiao, Rongxin, Li, Xiong, Liao, Peng, Zhou, Jiajia, Okla, Karolina, Lin, Heng, Lin, Xun, Grove, Sara, Wei, Shuang, Vatan, Linda, Hu, Jiantao, Szumilo, Justyna, Kotarski, Jan, Freeman, Zachary T., Skala, Stephanie, Wicha, Max, Cho, Kathleen R., Chinnaiyan, Arul M., Schon, Samantha, Wen, Fei, Kryczek, Ilona, Wang, Shaomeng, Chen, Lieping, and Zou, Weiping

Published
2024
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3. High pre-diagnosis inflammation-related risk score associated with decreased ovarian cancer survival

Author

Brieger, Katharine K, Phung, Minh Tung, Mukherjee, Bhramar, Bakulski, Kelly M, Anton-Culver, Hoda, Bandera, Elisa V, Bowtell, David DL, Cramer, Daniel W, DeFazio, Anna, Doherty, Jennifer A, Fereday, Sian, Fortner, Renée Turzanski, Gentry-Maharaj, Aleksandra, Goode, Ellen L, Goodman, Marc T, Harris, Holly R, Matsuo, Keitaro, Menon, Usha, Modugno, Francesmary, Moysich, Kirsten B, Qin, Bo, Ramus, Susan J, Risch, Harvey A, Rossing, Mary Anne, Schildkraut, Joellen M, Trabert, Britton, Vierkant, Robert A, Winham, Stacey J, Wentzensen, Nicolas, Wu, Anna H, Ziogas, Argyrios, Khoja, Lilah, Cho, Kathleen R, McLean, Karen, Richardson, Jean, Grout, Bronwyn, Chase, Anne, Deurloo, Cindy McKinnon, Odunsi, Kunle, Nelson, Brad H, Brenton, James D, Terry, Kathryn L, Pharoah, Paul DP, Berchuck, Andrew, Hanley, Gillian E, Webb, Penelope M, Pike, Malcolm C, and Pearce, Celeste Leigh

Subjects
Epidemiology, Biomedical and Clinical Sciences, Health Sciences, Tobacco Smoke and Health, Prevention, Ovarian Cancer, Tobacco, Cancer, Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Aged, Carcinoma, Ovarian Epithelial, Female, Health Behavior, Humans, Inflammation, Middle Aged, Ovarian Neoplasms, Proportional Hazards Models, Risk Assessment, Ovarian Cancer Association Consortium, Medical and Health Sciences, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundThere is suggestive evidence that inflammation is related to ovarian cancer survival. However, more research is needed to identify inflammation-related factors that are associated with ovarian cancer survival and to determine their combined effects.MethodsThis analysis used pooled data on 8,147 women with invasive epithelial ovarian cancer from the Ovarian Cancer Association Consortium. The prediagnosis inflammation-related exposures of interest included alcohol use; aspirin use; other nonsteroidal anti-inflammatory drug use; body mass index; environmental tobacco smoke exposure; history of pelvic inflammatory disease, polycystic ovarian syndrome, and endometriosis; menopausal hormone therapy use; physical inactivity; smoking status; and talc use. Using Cox proportional hazards models, the relationship between each exposure and survival was assessed in 50% of the data. A weighted inflammation-related risk score (IRRS) was developed, and its association with survival was assessed using Cox proportional hazards models in the remaining 50% of the data.ResultsThere was a statistically significant trend of increasing risk of death per quartile of the IRRS [HR = 1.09; 95% confidence interval (CI), 1.03-1.14]. Women in the upper quartile of the IRRS had a 31% higher death rate compared with the lowest quartile (95% CI, 1.11-1.54).ConclusionsA higher prediagnosis IRRS was associated with an increased mortality risk after an ovarian cancer diagnosis. Further investigation is warranted to evaluate whether postdiagnosis exposures are also associated with survival.ImpactGiven that pre- and postdiagnosis exposures are often correlated and many are modifiable, our study results can ultimately motivate the development of behavioral recommendations to enhance survival among patients with ovarian cancer.

Published
2022

5. Metabolic collateral lethal target identification reveals MTHFD2 paralogue dependency in ovarian cancer

Author

Achreja, Abhinav, Yu, Tao, Mittal, Anjali, Choppara, Srinadh, Animasahun, Olamide, Nenwani, Minal, Wuchu, Fulei, Meurs, Noah, Mohan, Aradhana, Jeon, Jin Heon, Sarangi, Itisam, Jayaraman, Anusha, Owen, Sarah, Kulkarni, Reva, Cusato, Michele, Weinberg, Frank, Kweon, Hye Kyong, Subramanian, Chitra, Wicha, Max S., Merajver, Sofia D., Nagrath, Sunitha, Cho, Kathleen R., DiFeo, Analisa, Lu, Xiongbin, and Nagrath, Deepak

Published
2022
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6. Supplementary Tables S1-10 from Cell State of Origin Impacts Development of Distinct Endometriosis-Related Ovarian Carcinoma Histotypes

Author

Beddows, Ian, primary, Fan, Huihui, primary, Heinze, Karolin, primary, Johnson, Benjamin K., primary, Leonova, Anna, primary, Senz, Janine, primary, Djirackor, Svetlana, primary, Cho, Kathleen R., primary, Pearce, Celeste Leigh, primary, Huntsman, David G., primary, Anglesio, Michael S., primary, and Shen, Hui, primary

Published
2024
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7. Supplementary Data from Cell State of Origin Impacts Development of Distinct Endometriosis-Related Ovarian Carcinoma Histotypes

Author

Beddows, Ian, primary, Fan, Huihui, primary, Heinze, Karolin, primary, Johnson, Benjamin K., primary, Leonova, Anna, primary, Senz, Janine, primary, Djirackor, Svetlana, primary, Cho, Kathleen R., primary, Pearce, Celeste Leigh, primary, Huntsman, David G., primary, Anglesio, Michael S., primary, and Shen, Hui, primary

Published
2024
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9. Cell state of origin impacts development of distinct endometriosis-related ovarian carcinoma histotypes

Author

Beddows, Ian, primary, Fan, Huihui, additional, Heinze, Karolin, additional, Johnson, Benjamin K., additional, Leonova, Anna, additional, Senz, Janine, additional, Djirackor, Svetlana, additional, Cho, Kathleen R., additional, Pearce, Celeste Leigh., additional, Huntsman, David G., additional, Anglesio, Michael S., additional, and Shen, Hui, additional

Published
2023
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17. Supplementary Methods, Figure Legends, Figures 1 - 9, Tables 1 - 8 from Multiclonality and Marked Branched Evolution of Low-Grade Endometrioid Endometrial Carcinoma

Author

Lazo de la Vega, Lorena, primary, Samaha, Mia C., primary, Hu, Kevin, primary, Bick, Nolan R., primary, Siddiqui, Javed, primary, Hovelson, Daniel H., primary, Liu, Chia-Jen, primary, Carter, Cody S., primary, Cho, Kathleen R., primary, Sciallis, Andrew P., primary, and Tomlins, Scott A., primary

Published
2023
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20. Supplementary Figure S8 from Murine Oviductal High-Grade Serous Carcinomas Mirror the Genomic Alterations, Gene Expression Profiles, and Immune Microenvironment of Their Human Counterparts

Author

McCool, Kevin W., primary, Freeman, Zachary T., primary, Zhai, Yali, primary, Wu, Rong, primary, Hu, Kevin, primary, Liu, Chia-Jen, primary, Tomlins, Scott A., primary, Fearon, Eric R., primary, Magnuson, Brian, primary, Kuick, Rork, primary, and Cho, Kathleen R., primary

Published
2023
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26. Table S1 from Murine Oviductal High-Grade Serous Carcinomas Mirror the Genomic Alterations, Gene Expression Profiles, and Immune Microenvironment of Their Human Counterparts

Author

McCool, Kevin W., primary, Freeman, Zachary T., primary, Zhai, Yali, primary, Wu, Rong, primary, Hu, Kevin, primary, Liu, Chia-Jen, primary, Tomlins, Scott A., primary, Fearon, Eric R., primary, Magnuson, Brian, primary, Kuick, Rork, primary, and Cho, Kathleen R., primary

Published
2023
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27. Supplementary Methods from Murine Oviductal High-Grade Serous Carcinomas Mirror the Genomic Alterations, Gene Expression Profiles, and Immune Microenvironment of Their Human Counterparts

Author

McCool, Kevin W., primary, Freeman, Zachary T., primary, Zhai, Yali, primary, Wu, Rong, primary, Hu, Kevin, primary, Liu, Chia-Jen, primary, Tomlins, Scott A., primary, Fearon, Eric R., primary, Magnuson, Brian, primary, Kuick, Rork, primary, and Cho, Kathleen R., primary

Published
2023
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28. Supplementary Methods and References from Genomic Profiling of Penile Squamous Cell Carcinoma Reveals New Opportunities for Targeted Therapy

Author

McDaniel, Andrew S., primary, Hovelson, Daniel H., primary, Cani, Andi K., primary, Liu, Chia-Jen, primary, Zhai, Yali, primary, Zhang, Yajia, primary, Weizer, Alon Z., primary, Mehra, Rohit, primary, Feng, Felix Y., primary, Alva, Ajjai S., primary, Morgan, Todd M., primary, Montgomery, Jeffrey S., primary, Siddiqui, Javed, primary, Sadis, Seth, primary, Bandla, Santhoshi, primary, Williams, Paul D., primary, Cho, Kathleen R., primary, Rhodes, Daniel R., primary, and Tomlins, Scott A., primary

Published
2023
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36. Data from Genomic Profiling of Penile Squamous Cell Carcinoma Reveals New Opportunities for Targeted Therapy

Author

McDaniel, Andrew S., primary, Hovelson, Daniel H., primary, Cani, Andi K., primary, Liu, Chia-Jen, primary, Zhai, Yali, primary, Zhang, Yajia, primary, Weizer, Alon Z., primary, Mehra, Rohit, primary, Feng, Felix Y., primary, Alva, Ajjai S., primary, Morgan, Todd M., primary, Montgomery, Jeffrey S., primary, Siddiqui, Javed, primary, Sadis, Seth, primary, Bandla, Santhoshi, primary, Williams, Paul D., primary, Cho, Kathleen R., primary, Rhodes, Daniel R., primary, and Tomlins, Scott A., primary

Published
2023
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41. Supplementary Figures S1-S5 from Genomic Profiling of Penile Squamous Cell Carcinoma Reveals New Opportunities for Targeted Therapy

Author

McDaniel, Andrew S., primary, Hovelson, Daniel H., primary, Cani, Andi K., primary, Liu, Chia-Jen, primary, Zhai, Yali, primary, Zhang, Yajia, primary, Weizer, Alon Z., primary, Mehra, Rohit, primary, Feng, Felix Y., primary, Alva, Ajjai S., primary, Morgan, Todd M., primary, Montgomery, Jeffrey S., primary, Siddiqui, Javed, primary, Sadis, Seth, primary, Bandla, Santhoshi, primary, Williams, Paul D., primary, Cho, Kathleen R., primary, Rhodes, Daniel R., primary, and Tomlins, Scott A., primary

Published
2023
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42. Supplementary Figure Legends from Genomic Profiling of Penile Squamous Cell Carcinoma Reveals New Opportunities for Targeted Therapy

Author

McDaniel, Andrew S., primary, Hovelson, Daniel H., primary, Cani, Andi K., primary, Liu, Chia-Jen, primary, Zhai, Yali, primary, Zhang, Yajia, primary, Weizer, Alon Z., primary, Mehra, Rohit, primary, Feng, Felix Y., primary, Alva, Ajjai S., primary, Morgan, Todd M., primary, Montgomery, Jeffrey S., primary, Siddiqui, Javed, primary, Sadis, Seth, primary, Bandla, Santhoshi, primary, Williams, Paul D., primary, Cho, Kathleen R., primary, Rhodes, Daniel R., primary, and Tomlins, Scott A., primary

Published
2023
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43. Supplementary Tables S1-S4 from Genomic Profiling of Penile Squamous Cell Carcinoma Reveals New Opportunities for Targeted Therapy

Author

McDaniel, Andrew S., primary, Hovelson, Daniel H., primary, Cani, Andi K., primary, Liu, Chia-Jen, primary, Zhai, Yali, primary, Zhang, Yajia, primary, Weizer, Alon Z., primary, Mehra, Rohit, primary, Feng, Felix Y., primary, Alva, Ajjai S., primary, Morgan, Todd M., primary, Montgomery, Jeffrey S., primary, Siddiqui, Javed, primary, Sadis, Seth, primary, Bandla, Santhoshi, primary, Williams, Paul D., primary, Cho, Kathleen R., primary, Rhodes, Daniel R., primary, and Tomlins, Scott A., primary

Published
2023
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46. High Prediagnosis Inflammation-Related Risk Score Associated with Decreased Ovarian Cancer Survival.

Author

Brieger, Katharine K, Brieger, Katharine K, Phung, Minh Tung, Mukherjee, Bhramar, Bakulski, Kelly M, Anton-Culver, Hoda, Bandera, Elisa V, Bowtell, David DL, Cramer, Daniel W, DeFazio, Anna, Doherty, Jennifer A, Fereday, Sian, Fortner, Renée Turzanski, Gentry-Maharaj, Aleksandra, Goode, Ellen L, Goodman, Marc T, Harris, Holly R, Matsuo, Keitaro, Menon, Usha, Modugno, Francesmary, Moysich, Kirsten B, Qin, Bo, Ramus, Susan J, Risch, Harvey A, Rossing, Mary Anne, Schildkraut, Joellen M, Trabert, Britton, Vierkant, Robert A, Winham, Stacey J, Wentzensen, Nicolas, Wu, Anna H, Ziogas, Argyrios, Khoja, Lilah, Cho, Kathleen R, McLean, Karen, Richardson, Jean, Grout, Bronwyn, Chase, Anne, Deurloo, Cindy McKinnon, Odunsi, Kunle, Nelson, Brad H, Brenton, James D, Terry, Kathryn L, Pharoah, Paul DP, Berchuck, Andrew, Hanley, Gillian E, Webb, Penelope M, Pike, Malcolm C, Pearce, Celeste Leigh, Ovarian Cancer Association Consortium, Brieger, Katharine K, Brieger, Katharine K, Phung, Minh Tung, Mukherjee, Bhramar, Bakulski, Kelly M, Anton-Culver, Hoda, Bandera, Elisa V, Bowtell, David DL, Cramer, Daniel W, DeFazio, Anna, Doherty, Jennifer A, Fereday, Sian, Fortner, Renée Turzanski, Gentry-Maharaj, Aleksandra, Goode, Ellen L, Goodman, Marc T, Harris, Holly R, Matsuo, Keitaro, Menon, Usha, Modugno, Francesmary, Moysich, Kirsten B, Qin, Bo, Ramus, Susan J, Risch, Harvey A, Rossing, Mary Anne, Schildkraut, Joellen M, Trabert, Britton, Vierkant, Robert A, Winham, Stacey J, Wentzensen, Nicolas, Wu, Anna H, Ziogas, Argyrios, Khoja, Lilah, Cho, Kathleen R, McLean, Karen, Richardson, Jean, Grout, Bronwyn, Chase, Anne, Deurloo, Cindy McKinnon, Odunsi, Kunle, Nelson, Brad H, Brenton, James D, Terry, Kathryn L, Pharoah, Paul DP, Berchuck, Andrew, Hanley, Gillian E, Webb, Penelope M, Pike, Malcolm C, Pearce, Celeste Leigh, and Ovarian Cancer Association Consortium

Abstract

BackgroundThere is suggestive evidence that inflammation is related to ovarian cancer survival. However, more research is needed to identify inflammation-related factors that are associated with ovarian cancer survival and to determine their combined effects.MethodsThis analysis used pooled data on 8,147 women with invasive epithelial ovarian cancer from the Ovarian Cancer Association Consortium. The prediagnosis inflammation-related exposures of interest included alcohol use; aspirin use; other nonsteroidal anti-inflammatory drug use; body mass index; environmental tobacco smoke exposure; history of pelvic inflammatory disease, polycystic ovarian syndrome, and endometriosis; menopausal hormone therapy use; physical inactivity; smoking status; and talc use. Using Cox proportional hazards models, the relationship between each exposure and survival was assessed in 50% of the data. A weighted inflammation-related risk score (IRRS) was developed, and its association with survival was assessed using Cox proportional hazards models in the remaining 50% of the data.ResultsThere was a statistically significant trend of increasing risk of death per quartile of the IRRS [HR = 1.09; 95% confidence interval (CI), 1.03-1.14]. Women in the upper quartile of the IRRS had a 31% higher death rate compared with the lowest quartile (95% CI, 1.11-1.54).ConclusionsA higher prediagnosis IRRS was associated with an increased mortality risk after an ovarian cancer diagnosis. Further investigation is warranted to evaluate whether postdiagnosis exposures are also associated with survival.ImpactGiven that pre- and postdiagnosis exposures are often correlated and many are modifiable, our study results can ultimately motivate the development of behavioral recommendations to enhance survival among patients with ovarian cancer.

Published
2022

47. High Prediagnosis Inflammation-Related Risk Score Associated with Decreased Ovarian Cancer Survival

Author

Brieger, Katharine K., primary, Phung, Minh Tung, additional, Mukherjee, Bhramar, additional, Bakulski, Kelly M., additional, Anton-Culver, Hoda, additional, Bandera, Elisa V., additional, Bowtell, David D.L., additional, Cramer, Daniel W., additional, DeFazio, Anna, additional, Doherty, Jennifer A., additional, Fereday, Sian, additional, Fortner, Renée Turzanski, additional, Gentry-Maharaj, Aleksandra, additional, Goode, Ellen L., additional, Goodman, Marc T., additional, Harris, Holly R., additional, Matsuo, Keitaro, additional, Menon, Usha, additional, Modugno, Francesmary, additional, Moysich, Kirsten B., additional, Qin, Bo, additional, Ramus, Susan J., additional, Risch, Harvey A., additional, Rossing, Mary Anne, additional, Schildkraut, Joellen M., additional, Trabert, Britton, additional, Vierkant, Robert A., additional, Winham, Stacey J., additional, Wentzensen, Nicolas, additional, Wu, Anna H., additional, Ziogas, Argyrios, additional, Khoja, Lilah, additional, Cho, Kathleen R., additional, McLean, Karen, additional, Richardson, Jean, additional, Grout, Bronwyn, additional, Chase, Anne, additional, Deurloo, Cindy McKinnon, additional, Odunsi, Kunle, additional, Nelson, Brad H., additional, Brenton, James D., additional, Terry, Kathryn L., additional, Pharoah, Paul D.P., additional, Berchuck, Andrew, additional, Hanley, Gillian E., additional, Webb, Penelope M., additional, Pike, Malcolm C., additional, and Pearce, Celeste Leigh, additional

Published
2022
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48. Cell State of Origin Impacts Development of Distinct Endometriosis-Related Ovarian Carcinoma Histotypes.

Author

Beddows I, Fan H, Heinze K, Johnson BK, Leonova A, Senz J, Djirackor S, Cho KR, Pearce CL, Huntsman DG, Anglesio MS, and Shen H

Subjects
Female, Humans, Carcinoma, Ovarian Epithelial, Iron, Endometriosis genetics, Endometriosis metabolism, Ovarian Neoplasms pathology, Carcinoma, Endometrioid genetics, Carcinoma, Endometrioid pathology, Adenocarcinoma, Clear Cell genetics, Adenocarcinoma, Clear Cell metabolism
Abstract

Clear cell ovarian carcinoma (CCOC) and endometrioid ovarian carcinoma (ENOC) are ovarian carcinoma histotypes, which are both thought to arise from ectopic endometrial (or endometrial-like) cells through an endometriosis intermediate. How the same cell type of origin gives rise to two morphologically and biologically different histotypes has been perplexing, particularly given that recurrent genetic mutations are common to both and present in nonmalignant precursors. We used RNA transcription analysis to show that the expression profiles of CCOC and ENOC resemble those of normal endometrium at secretory and proliferative phases of the menstrual cycle, respectively. DNA methylation at the promoter of the estrogen receptor (ER) gene (ESR1) was enriched in CCOC, which could potentially lock the cells in the secretory state. Compared with normal secretory-type endometrium, CCOC was further defined by increased expression of cysteine and glutathione synthesis pathway genes and downregulation of the iron antiporter, suggesting iron addiction and highlighting ferroptosis as a potential therapeutic target. Overall, these findings suggest that while CCOC and ENOC arise from the same cell type, these histotypes likely originate from different cell states. This "cell state of origin" model may help to explain the presence of histologic and molecular cancer subtypes arising in other organs., Significance: Two cancer histotypes diverge from a common cell of origin epigenetically locked in different cell states, highlighting the importance of considering cell state to better understand the cell of origin of cancer., (©2023 The Authors; Published by the American Association for Cancer Research.)

Published
2024
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