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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. Menopausal hormone therapy prior to the diagnosis of ovarian cancer is associated with improved survival

Author

Brieger, Katharine K, Peterson, Siri, Lee, Alice W, Mukherjee, Bhramar, Bakulski, Kelly M, Alimujiang, Aliya, Anton-Culver, Hoda, Anglesio, Michael S, Bandera, Elisa V, Berchuck, Andrew, Bowtell, David DL, Chenevix-Trench, Georgia, Cho, Kathleen R, Cramer, Daniel W, DeFazio, Anna, Doherty, Jennifer A, Fortner, Renée T, Garsed, Dale W, Gayther, Simon A, Gentry-Maharaj, Aleksandra, Goode, Ellen L, Goodman, Marc T, Harris, Holly R, Høgdall, Estrid, Huntsman, David G, Shen, Hui, Jensen, Allan, Johnatty, Sharon E, Jordan, Susan J, Kjaer, Susanne K, Kupryjanczyk, Jolanta, Lambrechts, Diether, McLean, Karen, Menon, Usha, Modugno, Francesmary, Moysich, Kirsten, Ness, Roberta, Ramus, Susan J, Richardson, Jean, Risch, Harvey, Rossing, Mary Anne, Trabert, Britton, Wentzensen, Nicolas, Ziogas, Argyrios, Terry, Kathryn L, Wu, Anna H, Hanley, Gillian E, Pharoah, Paul, Webb, Penelope M, Pike, Malcolm C, Pearce, Celeste Leigh, and Consortium, for the Ovarian Cancer Association

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Estrogen, Rare Diseases, Cancer, Ovarian Cancer, Aging, Aged, Estrogen Replacement Therapy, Female, Hormone Replacement Therapy, Humans, Middle Aged, Neoplasm Staging, Neoplasm, Residual, Ovarian Neoplasms, Postmenopause, Progestins, Progression-Free Survival, Proportional Hazards Models, Survival Rate, Ovarian Cancer Association Consortium, Paediatrics and Reproductive Medicine, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis, Reproductive medicine
Abstract

PurposePrior studies of menopausal hormone therapy (MHT) and ovarian cancer survival have been limited by lack of hormone regimen detail and insufficient sample sizes. To address these limitations, a comprehensive analysis of 6419 post-menopausal women with pathologically confirmed ovarian carcinoma was conducted to examine the association between MHT use prior to diagnosis and survival.MethodsData from 15 studies in the Ovarian Cancer Association Consortium were included. MHT use was examined by type (estrogen-only (ET) or estrogen+progestin (EPT)), duration, and recency of use relative to diagnosis. Cox proportional hazards models were used to estimate the association between hormone therapy use and survival. Logistic regression and mediation analysis was used to explore the relationship between MHT use and residual disease following debulking surgery.ResultsUse of ET or EPT for at least five years prior to diagnosis was associated with better ovarian cancer survival (hazard ratio, 0.80; 95% CI, 0.74 to 0.87). Among women with advanced stage, high-grade serous carcinoma, those who used MHT were less likely to have any macroscopic residual disease at the time of primary debulking surgery (p for trend

Published
2020

6. 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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7. Preclinical Models of Ovarian Cancer

Author

Karnezis, Anthony N and Cho, Kathleen R

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Ovarian Cancer, Prevention, Rare Diseases, Animals, Carcinoma, Chemoprevention, Chickens, Disease Models, Animal, Female, Humans, Mice, Ovarian Neoplasms, Ovariectomy, Prophylactic Surgical Procedures, Salpingectomy, ovarian cancer, ovary, fallopian tube, mouse model, laying hen, prevention, Paediatrics and Reproductive Medicine, Obstetrics & Reproductive Medicine, Reproductive medicine
Abstract

Preclinical models are relatively underutilized and underfunded resources for modeling the pathogenesis and prevention of ovarian cancers. Several reviews have detailed the numerous published models of ovarian cancer. In this review, we will provide an overview of experimental model systems, their strengths and limitations, and use selected models to illustrate how they can be used to address specific issues about ovarian cancer pathogenesis. We will then highlight some of the preclinical prevention studies performed to date and discuss experiments needed to address important unanswered questions about ovarian cancer prevention strategies.

Published
2017

8. Impact of oviductal versus ovarian epithelial cell of origin on ovarian endometrioid carcinoma phenotype in the mouse

Author

Wu, Rong, Zhai, Yali, Kuick, Rork, Karnezis, Anthony N, Garcia, Paloma, Naseem, Anum, Hu, Tom C, Fearon, Eric R, and Cho, Kathleen R

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Rare Diseases, Genetics, Cancer, Ovarian Cancer, Aetiology, 2.1 Biological and endogenous factors, Adenomatous Polyposis Coli Protein, Animals, Animals, Genetically Modified, Carcinoma, Endometrioid, Carcinoma, Ovarian Epithelial, Cell Differentiation, Disease Models, Animal, Epithelial Cells, Epithelium, Fallopian Tubes, Female, Glycoproteins, Humans, Integrases, Male, Mice, Neoplasms, Glandular and Epithelial, Ovarian Neoplasms, Ovary, PTEN Phosphohydrolase, Phenotype, Promoter Regions, Genetic, Tamoxifen, mouse ovarian cancer model, cell of origin, Fallopian tube, oviduct, endometrioid carcinoma, Clinical Sciences, Pathology, Clinical sciences, Oncology and carcinogenesis
Abstract

Endometrioid carcinoma (EC) is a relatively indolent ovarian carcinoma subtype that is nonetheless deadly if detected late. Existing genetically engineered mouse models (GEMMs) of the disease, based on transformation of the ovarian surface epithelium (OSE), take advantage of known ovarian EC driver gene lesions, but do not fully recapitulate the disease features seen in patients. An EC model in which the Apc and Pten tumour suppressor genes are conditionally deleted in murine OSE yields tumours that are biologically more aggressive and significantly less differentiated than human ECs. Importantly, OSE is not currently thought to be the tissue of origin of most ovarian cancers, including ECs, suggesting that tumour initiation in Müllerian epithelium may produce tumours that more closely resemble their human tumour counterparts. We have developed Ovgp1-iCreERT2 mice in which the Ovgp1 promoter controls expression of tamoxifen (TAM)-regulated Cre recombinase in oviductal epithelium - the murine equivalent of human Fallopian tube epithelium. Ovgp1-iCreERT2 ;Apcfl/fl ;Ptenfl/fl mice treated with TAM or injected with adenovirus expressing Cre into the ovarian bursa uniformly develop oviductal or ovarian ECs, respectively. On the basis of their morphology and global gene expression profiles, the oviduct-derived tumours more closely resemble human ovarian ECs than do OSE-derived tumours. Furthermore, mice with oviductal tumours survive much longer than their counterparts with ovarian tumours. The slow progression and late metastasis of oviductal tumours resembles the relatively indolent behaviour characteristic of so-called Type I ovarian carcinomas in humans, for which EC is a prototype. Our studies demonstrate the utility of Ovgp1-iCreERT2 mice for manipulating genes of interest specifically in the oviductal epithelium, and establish that the cell of origin is an important consideration in mouse ovarian cancer GEMMs. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Published
2016

9. Epithelial Tumors of the Ovary

Author

Seidman, Jeffrey D., Ronnett, Brigitte M., Shih, Ie-Ming, Cho, Kathleen R., Kurman, Robert J., Kurman, Robert J., editor, Hedrick Ellenson, Lora, editor, and Ronnett, Brigitte M., editor

Published
2019
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10. 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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11. 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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13. Epigenetic driver mutations in ARID1A shape cancer immune phenotype and immunotherapy

Author

Li, Jing, Wang, Weichao, Zhang, Yajia, Cieslik, Marcin, Guo, Jipeng, Tan, Mengyao, Green, Michael D., Wang, Weimin, Lin, Heng, Li, Wei, Wei, Shuang, Zhou, Jiajia, Li, Gaopeng, Jing, Xiaojun, Vatan, Linda, Zhao, Lili, Bitler, Benjamin, Zhang, Rugang, Cho, Kathleen R., Dou, Yali, Kryczek, Ilona, Chan, Timothy A., Huntsman, David, Chinnaiyan, Arul M., and Zou, Weiping

Subjects
Cancer treatment -- Analysis, Epigenetic inheritance -- Genetic aspects -- Analysis, Cancer genetics -- Genetic aspects -- Development and progression, Cancer -- Genetic aspects -- Development and progression, Genes -- Analysis -- Genetic aspects, Chromatin -- Genetic aspects -- Analysis, Immunotherapy -- Analysis, Gene expression -- Analysis -- Genetic aspects, T cells -- Genetic aspects -- Analysis, Biochemistry, Cancer research, Tumors, Health care industry, University of Michigan. Medical School
Abstract

Whether mutations in cancer driver genes directly affect cancer immune phenotype and T cell immunity remains a standing question. ARID1A is a core member of the polymorphic BRG/BRM-associated factor chromatin remodeling complex. ARID1A mutations occur in human cancers and drive cancer development. Here, we studied the molecular, cellular, and clinical impact of ARID1A aberrations on cancer immunity. We demonstrated that ARID1A aberrations resulted in limited chromatin accessibility to IFN-responsive genes, impaired IFN gene expression, anemic T cell tumor infiltration, poor tumor immunity, and shortened host survival in many human cancer histologies and in murine cancer models. Impaired IFN signaling was associated with poor immunotherapy response. Mechanistically, ARID1A interacted with EZH2 via its carboxyl terminal and antagonized EZH2-mediated IFN responsiveness. Thus, the interaction between ARID1A and EZH2 defines cancer IFN responsiveness and immune evasion. Our work indicates that cancer epigenetic driver mutations can shape cancer immune phenotype and immunotherapy., Introduction Tumor-infiltrating T cells are positively associated with patient survival in many types of human cancer (1-3). Type I and type II IFN gene signatures correlate with clinical responses to [...]

Published
2020
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15. 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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24. 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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27. 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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33. 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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34. 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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35. 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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43. 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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48. 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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49. 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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50. 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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