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Stromal Reactivity Differentially Drives Tumor Cell Evolution and Prostate Cancer Progression

Ziv Frankenstein, View ORCID ProfileDavid Basanta, Omar E. Franco, Yan Gao, Rodrigo A. Javier, Douglas W. Strand, MinJae Lee, View ORCID ProfileSimon W. Hayward, Gustavo Ayala, View ORCID ProfileAlexander R.A. Anderson
doi: https://doi.org/10.1101/159616
Ziv Frankenstein
1Department of Integrated Mathematical Oncology, H. Lee Moffitt Cancer Center and Research Institute, 12902 USF Magnolia Drive Tampa, FL 33612
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David Basanta
1Department of Integrated Mathematical Oncology, H. Lee Moffitt Cancer Center and Research Institute, 12902 USF Magnolia Drive Tampa, FL 33612
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Omar E. Franco
2Department of Surgery, NorthShore University HealthSystem Research Institute, 1001 University Place, Evanston, IL 60201
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Yan Gao
3Department of Pathology and Laboratory Medicine, University of Texas Health Science Center, 6431 Fannin Street, Houston, Texas 77030
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Rodrigo A. Javier
2Department of Surgery, NorthShore University HealthSystem Research Institute, 1001 University Place, Evanston, IL 60201
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Douglas W. Strand
4Department of Urology, UT Southwestern, 5323 Harry Hines Blvd, JA5.150D Dallas TX 75390
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MinJae Lee
5Biostatistics/Epidemiology/Research Design (BERD) Core, Department of Internal Medicine, University of Texas Health Science Center, 6431 Fannin Street, Houston, Texas 77030
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Simon W. Hayward
2Department of Surgery, NorthShore University HealthSystem Research Institute, 1001 University Place, Evanston, IL 60201
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Gustavo Ayala
3Department of Pathology and Laboratory Medicine, University of Texas Health Science Center, 6431 Fannin Street, Houston, Texas 77030
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Alexander R.A. Anderson
1Department of Integrated Mathematical Oncology, H. Lee Moffitt Cancer Center and Research Institute, 12902 USF Magnolia Drive Tampa, FL 33612
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  • ORCID record for Alexander R.A. Anderson
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Abstract

We implemented a hybrid multiscale model of carcinogenesis that merges data from biology and pathology on the microenvironmental regulation of prostate cancer (PCa) cell behavior. It recapitulates the biology of stromal influence in prostate cancer progression. Our data indicate that the interactions between the tumor cells and reactive stroma shape the evolutionary dynamics of PCa cells and explain overall tumor aggressiveness. We show that the degree of stromal reactivity, when coupled with the current clinical biomarkers, significantly improves PCa prognostication, both for death and recurrence, that may alter treatment decisions. We also show that stromal reactivity correlates directly with tumor growth but inversely modulates tumor evolution. This suggests that the aggressive stromal independent PCa may be an inevitable evolutionary result of poor stromal reactivity. It also suggests that purely tumor centric metrics of aggressiveness may be misleading in terms on clinical outcome.

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  • ↵* Joint 1st author

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted August 21, 2017.
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Stromal Reactivity Differentially Drives Tumor Cell Evolution and Prostate Cancer Progression
Ziv Frankenstein, David Basanta, Omar E. Franco, Yan Gao, Rodrigo A. Javier, Douglas W. Strand, MinJae Lee, Simon W. Hayward, Gustavo Ayala, Alexander R.A. Anderson
bioRxiv 159616; doi: https://doi.org/10.1101/159616
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Stromal Reactivity Differentially Drives Tumor Cell Evolution and Prostate Cancer Progression
Ziv Frankenstein, David Basanta, Omar E. Franco, Yan Gao, Rodrigo A. Javier, Douglas W. Strand, MinJae Lee, Simon W. Hayward, Gustavo Ayala, Alexander R.A. Anderson
bioRxiv 159616; doi: https://doi.org/10.1101/159616

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