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5. Mass Transport Model of Radiation Response: Calibration and Application to Chemoradiation for Pancreatic Cancer

Author

Wang, Charles X., Elganainy, Dalia, Zaid, Mohamed M., Butner, Joseph D., Agrawal, Anshuman, Nizzero, Sara, Minsky, Bruce D., Holliday, Emma B., Taniguchi, Cullen M., Smith, Grace L., Koong, Albert C., Herman, Joseph M., Das, Prajnan, Maitra, Anirban, Wang, Huamin, Wolff, Robert A., Katz, Matthew H.G., Crane, Christopher H., Cristini, Vittorio, and Koay, Eugene J.

Published
2022
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8. Translational modeling-based evidence for enhanced efficacy of standard-of-care drugs in combination with anti-microRNA-155 in non-small-cell lung cancer

Author

Dogra, Prashant, primary, Shinglot, Vrushaly, additional, Ruiz-Ramírez, Javier, additional, Cave, Joseph, additional, Butner, Joseph D., additional, Schiavone, Carmine, additional, Duda, Dan G., additional, Kaseb, Ahmed O., additional, Chung, Caroline, additional, Koay, Eugene J., additional, Cristini, Vittorio, additional, Ozpolat, Bulent, additional, Calin, George A., additional, and Wang, Zhihui, additional

Published
2024
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13. Supplementary Table from A Phase 2 Trial of Enhancing Immune Checkpoint Blockade by Stereotactic Radiation and In Situ Virus Gene Therapy in Metastatic Triple-Negative Breast Cancer

Author

Sun, Kai, primary, Xu, Yitian, primary, Zhang, Licheng, primary, Niravath, Polly, primary, Darcourt, Jorge, primary, Patel, Tejal, primary, Teh, Bin S., primary, Farach, Andrew M., primary, Guerrero, Carlo, primary, Mathur, Sunil, primary, Sultenfuss, Mark A., primary, Gupta, Nakul, primary, Schwartz, Mary R., primary, Haley, Susan L., primary, Nair, Sindhu, primary, Li, Xiaoxian, primary, Nguyen, Thi Truc Anh, primary, Butner, Joseph D., primary, Ensor, Joe, primary, Mejia, Jaime A., primary, Mei, Zhuyong, primary, Butler, E. Brian, primary, Chen, Shu-hsia, primary, Bernicker, Eric H., primary, and Chang, Jenny C., primary

Published
2023
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14. Supplementary Figure from A Phase 2 Trial of Enhancing Immune Checkpoint Blockade by Stereotactic Radiation and In Situ Virus Gene Therapy in Metastatic Triple-Negative Breast Cancer

Author

Sun, Kai, primary, Xu, Yitian, primary, Zhang, Licheng, primary, Niravath, Polly, primary, Darcourt, Jorge, primary, Patel, Tejal, primary, Teh, Bin S., primary, Farach, Andrew M., primary, Guerrero, Carlo, primary, Mathur, Sunil, primary, Sultenfuss, Mark A., primary, Gupta, Nakul, primary, Schwartz, Mary R., primary, Haley, Susan L., primary, Nair, Sindhu, primary, Li, Xiaoxian, primary, Nguyen, Thi Truc Anh, primary, Butner, Joseph D., primary, Ensor, Joe, primary, Mejia, Jaime A., primary, Mei, Zhuyong, primary, Butler, E. Brian, primary, Chen, Shu-hsia, primary, Bernicker, Eric H., primary, and Chang, Jenny C., primary

Published
2023
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20. A Phase 2 Trial of Enhancing Immune Checkpoint Blockade by Stereotactic Radiation and In Situ Virus Gene Therapy in Metastatic Triple-Negative Breast Cancer

Author

Sun, Kai, primary, Xu, Yitian, additional, Zhang, Licheng, additional, Niravath, Polly, additional, Darcourt, Jorge, additional, Patel, Tejal, additional, Teh, Bin S., additional, Farach, Andrew M., additional, Guerrero, Carlo, additional, Mathur, Sunil, additional, Sultenfuss, Mark A., additional, Gupta, Nakul, additional, Schwartz, Mary R., additional, Haley, Susan L., additional, Nair, Sindhu, additional, Li, Xiaoxian, additional, Nguyen, Thi Truc Anh, additional, Butner, Joseph D., additional, Ensor, Joe, additional, Mejia, Jaime A., additional, Mei, Zhuyong, additional, Butler, E. Brian, additional, Chen, Shu-hsia, additional, Bernicker, Eric H., additional, and Chang, Jenny C., additional

Published
2022
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21. Immune‐checkpoint inhibitor therapy response evaluation using oncophysics‐based mathematical models.

Author

Syed, Mustafa, Cagely, Matthew, Dogra, Prashant, Hollmer, Lauren, Butner, Joseph D., Cristini, Vittorio, and Koay, Eugene J.

Abstract

The field of oncology has transformed with the advent of immunotherapies. The standard of care for multiple cancers now includes novel drugs that target key checkpoints that function to modulate immune responses, enabling the patient's immune system to elicit an effective anti‐tumor response. While these immune‐based approaches can have dramatic effects in terms of significantly reducing tumor burden and prolonging survival for patients, the therapeutic approach remains active only in a minority of patients and is often not durable. Multiple biological investigations have identified key markers that predict response to the most common form of immunotherapy—immune checkpoint inhibitors (ICI). These biomarkers help enrich patients for ICI but are not 100% predictive. Understanding the complex interactions of these biomarkers with other pathways and factors that lead to ICI resistance remains a major goal. Principles of oncophysics—the idea that cancer can be described as a multiscale physical aberration—have shown promise in recent years in terms of capturing the essence of the complexities of ICI interactions. Here, we review the biological knowledge of mechanisms of ICI action and how these are incorporated into modern oncophysics‐based mathematical models. Building on the success of oncophysics‐based mathematical models may help to discover new, rational methods to engineer immunotherapy for patients in the future. This article is categorized under:Therapeutic Approaches and Drug Discovery > Nanomedicine for Oncologic Disease [ABSTRACT FROM AUTHOR]

Published
2023
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23. Early prediction of clinical response to checkpoint inhibitor therapy in human solid tumors through mathematical modeling

Author

Butner, Joseph D, primary, Martin, Geoffrey V, primary, Wang, Zhihui, primary, Corradetti, Bruna, additional, Ferrari, Mauro, additional, Esnaola, Nestor, additional, Chung, Caroline, additional, Hong, David S, additional, Welsh, James W, additional, Hasegawa, Naomi, additional, Mittendorf, Elizabeth A, additional, Curley, Steven A, additional, Chen, Shu-Hsia, additional, Pan, Ping-Ying, additional, Libutti, Steven K, additional, Ganesan, Shridar, additional, Sidman, Richard L, additional, Pasqualini, Renata, additional, Arap, Wadih, additional, Koay, Eugene J, additional, and Cristini, Vittorio, additional

Published
2021
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25. Translational Modeling Identifies Synergy between Nanoparticle-Delivered miRNA-22 and Standard-of-Care Drugs in Triple Negative Breast Cancer

Author

Dogra, Prashant, primary, Ruiz Ramirez, Javier, additional, Butner, Joseph D., additional, Pelaez, Maria J., additional, Chung, Caroline, additional, Hooda-Nehra, Anupama, additional, Pasqualini, Renata, additional, Arap, Wadih, additional, Cristini, Vittorio, additional, Calin, George A., additional, Ozpolat, Bulent, additional, and Wang, Zhihui, additional

Published
2021
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26. Author response: Early prediction of clinical response to checkpoint inhibitor therapy in human solid tumors through mathematical modeling

Author

Butner, Joseph D, primary, Martin, Geoffrey V, primary, Wang, Zhihui, primary, Corradetti, Bruna, additional, Ferrari, Mauro, additional, Esnaola, Nestor, additional, Chung, Caroline, additional, Hong, David S, additional, Welsh, James W, additional, Hasegawa, Naomi, additional, Mittendorf, Elizabeth A, additional, Curley, Steven A, additional, Chen, Shu-Hsia, additional, Pan, Ping-Ying, additional, Libutti, Steven K, additional, Ganesan, Shridar, additional, Sidman, Richard L, additional, Pasqualini, Renata, additional, Arap, Wadih, additional, Koay, Eugene J, additional, and Cristini, Vittorio, additional

Published
2021
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28. Early prediction of clinical response to checkpoint inhibitor therapy in human solid tumors through mathematical modeling

Author

Butner, Joseph D., primary, Martin, Geoffrey V., additional, Wang, Zhihui, additional, Corradetti, Bruna, additional, Ferrari, Mauro, additional, Esnaola, Nestor, additional, Chung, Caroline, additional, Hong, David S., additional, Welsh, James, additional, Hasegawa, Naomi, additional, Mittendorf, Elizabeth A., additional, Curley, Steven A., additional, Chen, Shu-Hsia, additional, Pan, Ping-Ying, additional, Libutti, Steven K., additional, Ganesan, Shridar, additional, Sidman, Richard L., additional, Pasqualini, Renata, additional, Arap, Wadih, additional, Koay, Eugene J., additional, and Cristini, Vittorio, additional

Published
2021
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30. A Mathematical Model to Estimate Chemotherapy Concentration at the Tumor-Site and Predict Therapy Response in Colorectal Cancer Patients with Liver Metastases

Author

Anaya, Daniel A., primary, Dogra, Prashant, additional, Wang, Zhihui, additional, Haider, Mintallah, additional, Ehab, Jasmina, additional, Jeong, Daniel K., additional, Ghayouri, Masoumeh, additional, Lauwers, Gregory Y., additional, Thomas, Kerry, additional, Kim, Richard, additional, Butner, Joseph D., additional, Nizzero, Sara, additional, Ramírez, Javier Ruiz, additional, Plodinec, Marija, additional, Sidman, Richard L., additional, Cavenee, Webster K., additional, Pasqualini, Renata, additional, Arap, Wadih, additional, Fleming, Jason B., additional, and Cristini, Vittorio, additional

Published
2021
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31. Innate Immunity Plays a Key Role in Controlling Viral Load in COVID-19: Mechanistic Insights from a Whole-Body Infection Dynamics Model

Author

Dogra, Prashant, primary, Ruiz-Ramírez, Javier, additional, Sinha, Kavya, additional, Butner, Joseph D., additional, Peláez, Maria J., additional, Rawat, Manmeet, additional, Yellepeddi, Venkata K., additional, Pasqualini, Renata, additional, Arap, Wadih, additional, Sostman, H. Dirk, additional, Cristini, Vittorio, additional, and Wang, Zhihui, additional

Published
2020
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33. Mathematical prediction of clinical outcomes in advanced cancer patients treated with checkpoint inhibitor immunotherapy

Author

Butner, Joseph D., primary, Elganainy, Dalia, additional, Wang, Charles X., additional, Wang, Zhihui, additional, Chen, Shu-Hsia, additional, Esnaola, Nestor F., additional, Pasqualini, Renata, additional, Arap, Wadih, additional, Hong, David S., additional, Welsh, James, additional, Koay, Eugene J., additional, and Cristini, Vittorio, additional

Published
2020
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35. Image‐guided mathematical modeling for pharmacological evaluation of nanomaterials and monoclonal antibodies

Author

Dogra, Prashant, primary, Butner, Joseph D., additional, Nizzero, Sara, additional, Ruiz Ramírez, Javier, additional, Noureddine, Achraf, additional, Peláez, María J., additional, Elganainy, Dalia, additional, Yang, Zhen, additional, Le, Anh‐Dung, additional, Goel, Shreya, additional, Leong, Hon S., additional, Koay, Eugene J., additional, Brinker, C. Jeffrey, additional, Cristini, Vittorio, additional, and Wang, Zhihui, additional

Published
2020
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36. A Mathematical Model to Estimate Chemotherapy Concentration at the Tumor-Site and Predict Therapy Response in Colorectal Cancer Patients with Liver Metastases

Author

Anaya, Daniel A., primary, Dogra, Prashant, additional, Wang, Zhihui, additional, Haider, Mintallah, additional, Ehab, Jasmina, additional, Jeong, Daniel, additional, Ghayouri, Masoumeh, additional, Lauwers, Gregory Y., additional, Thomas, Kerry, additional, Kim, Richard, additional, Butner, Joseph D., additional, Nizzero, Sara, additional, Ramírez, Javier Ruiz, additional, Plodinec, Marija, additional, Sidman, Richard L., additional, Pasqualini, Renata, additional, Arap, Wadih, additional, Fleming, Jason B., additional, and Cristini, Vittorio, additional

Published
2020
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40. A Multiscale Agent-Based Model of Ductal Carcinoma In Situ.

Author

Butner, Joseph D., Fuentes, David, Ozpolat, Bulent, Calin, George A., Zhou, Xiaobo, Lowengrub, John, Cristini, Vittorio, and Wang, Zhihui

Subjects
*MULTISCALE modeling, *DUCTAL carcinoma, *POPULATION dynamics, *MODELS & modelmaking, *MOLECULAR models, *MULLERIAN ducts, *SIALOLITHIASIS
Abstract

Objective: we present a multiscale agent-based model of Ductal Carcinoma in Situ (DCIS) in order to gain a detailed understanding of the cell-scale population dynamics, phenotypic distributions, and the associated interplay of important molecular signaling pathways that are involved in DCIS ductal invasion into the duct cavity (a process we refer to as duct advance rate here). Methods: DCIS is modeled mathematically through a hybridized discrete cell-scale model and a continuum molecular scale model, which are explicitly linked through a bidirectional feedback mechanism. Results: we find that duct advance rates occur in two distinct phases, characterized by an early exponential population expansion, followed by a long-term steady linear phase of population expansion, a result that is consistent with other modeling work. We further found that the rates were influenced most strongly by endocrine and paracrine signaling intensity, as well as by the effects of cell density induced quiescence within the DCIS population. Conclusion: our model analysis identified a complex interplay between phenotypic diversity that may provide a tumor adaptation mechanism to overcome proliferation limiting conditions, allowing for dynamic shifts in phenotypic populations in response to variation in molecular signaling intensity. Further, sensitivity analysis determined DCIS axial advance rates and calcification rates were most sensitive to cell cycle time variation. Significance: this model may serve as a useful tool to study the cell-scale dynamics involved in DCIS initiation and intraductal invasion, and may provide insights into promising areas of future experimental research. [ABSTRACT FROM AUTHOR]

Published
2020
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42. A MULTISCALE MODELING STUDY OF THE MAMMARY GLAND

Author

Andrew P. Shreve, Vittorio Cristini, Jeffrey Brinker, Zhihui Wang, Butner, Joseph D., Andrew P. Shreve, Vittorio Cristini, Jeffrey Brinker, Zhihui Wang, and Butner, Joseph D.

Subjects
Mathematical Modeling
Abstract

Multiscale, hybrid computer modeling has emerged as a valuable tool in the fields of computational systems biology and mathematical oncology. In this work, we present an overview of the motivations for, and development and implementation of, three hybrid multiscale models of the mammary gland system and early stage ductal carcinoma in situ (DCIS) in the gland. Pubertal mammary gland development was described first using a two-dimensional, lattice-based hybrid agent-based model description of the mammary terminal end bud (TEB), and then with a three-dimensional lattice-free TEB model. Both models implement a discrete, agent-based description of the cell scale, and a continuum, finite element method description of tissue scale spatiotemporal molecular profiles, which are explicitly linked into a hybrid model. This lattice-free pubertal development TEB model was then transitioned into a post-menopausal early stage DCIS model, used for study of the phenotypic dynamics and molecular signaling disruptions involved in development of the DCIS tumor mass. Both TEB and DCIS models implemented simplified, literature-based cellular phenotypic developmental hierarchies and endocrine and paracrine signaling pathways. All models provided valuable insights into the effects of these aspects on the development of both the healthy gland and the pre-invasive DCIS cancer state, and results from model outputs were found to be within literature supported ranges. Cells of both healthy and cancerous phenotypes were found to be sensitive to changes in molecular signaling intensities and phenotypic hierarchies, which played an important part in overall development in both cases, with all cases demonstrating a greater effect of upstream estrogen paracrine signaling relative to the downstream AREG-FGF epithelial to stromal pathway also tested. Here, we provide detailed descriptions of these studies and results, as well as other useful discoveries, and also an overview of the modeling approac

Published
2017

46. Theory and Experimental Validation of a Spatio-temporal Model of Chemotherapy Transport to Enhance Tumor Cell Kill

Author

Wang, Zhihui, primary, Kerketta, Romica, additional, Chuang, Yao-Li, additional, Dogra, Prashant, additional, Butner, Joseph D., additional, Brocato, Terisse A., additional, Day, Armin, additional, Xu, Rong, additional, Shen, Haifa, additional, Simbawa, Eman, additional, AL-Fhaid, A. S., additional, Mahmoud, S. R., additional, Curley, Steven A., additional, Ferrari, Mauro, additional, Koay, Eugene J., additional, and Cristini, Vittorio, additional

Published
2016
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50. A MULTISCALE MODELING STUDY OF THE MAMMARY GLAND

Author

Butner, Joseph D.

Subjects
Mathematical Modeling, Hybrid Modeling, Agent-based Modeling, Mammary Gland, Cancer Biology, Developmental Biology, Disease Modeling, Other Biomedical Engineering and Bioengineering
Abstract

Multiscale, hybrid computer modeling has emerged as a valuable tool in the fields of computational systems biology and mathematical oncology. In this work, we present an overview of the motivations for, and development and implementation of, three hybrid multiscale models of the mammary gland system and early stage ductal carcinoma in situ (DCIS) in the gland. Pubertal mammary gland development was described first using a two-dimensional, lattice-based hybrid agent-based model description of the mammary terminal end bud (TEB), and then with a three-dimensional lattice-free TEB model. Both models implement a discrete, agent-based description of the cell scale, and a continuum, finite element method description of tissue scale spatiotemporal molecular profiles, which are explicitly linked into a hybrid model. This lattice-free pubertal development TEB model was then transitioned into a post-menopausal early stage DCIS model, used for study of the phenotypic dynamics and molecular signaling disruptions involved in development of the DCIS tumor mass. Both TEB and DCIS models implemented simplified, literature-based cellular phenotypic developmental hierarchies and endocrine and paracrine signaling pathways. All models provided valuable insights into the effects of these aspects on the development of both the healthy gland and the pre-invasive DCIS cancer state, and results from model outputs were found to be within literature supported ranges. Cells of both healthy and cancerous phenotypes were found to be sensitive to changes in molecular signaling intensities and phenotypic hierarchies, which played an important part in overall development in both cases, with all cases demonstrating a greater effect of upstream estrogen paracrine signaling relative to the downstream AREG-FGF epithelial to stromal pathway also tested. Here, we provide detailed descriptions of these studies and results, as well as other useful discoveries, and also an overview of the modeling approaches, techniques, and rationale for their specific designs and implementations.

Published
2017

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