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Start Over Author "Pienta A" Publisher american association for cancer research (aacr)
534 results on '"Pienta A"'

1. Data from Drug-resilient Cancer Cell Phenotype Is Acquired via Polyploidization Associated with Early Stress Response Coupled to HIF2α Transcriptional Regulation

Author

Carroll, Christopher, primary, Manaprasertsak, Auraya, primary, Boffelli Castro, Arthur, primary, van den Bos, Hilda, primary, Spierings, Diana C.J., primary, Wardenaar, René, primary, Bukkuri, Anuraag, primary, Engström, Niklas, primary, Baratchart, Etienne, primary, Yang, Minjun, primary, Biloglav, Andrea, primary, Cornwallis, Charlie K., primary, Johansson, Bertil, primary, Hagerling, Catharina, primary, Arsenian-Henriksson, Marie, primary, Paulsson, Kajsa, primary, Amend, Sarah R., primary, Mohlin, Sofie, primary, Foijer, Floris, primary, McIntyre, Alan, primary, Pienta, Kenneth J., primary, and Hammarlund, Emma U., primary

Published
2024
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2. Drug-resilient Cancer Cell Phenotype Is Acquired via Polyploidization Associated with Early Stress Response Coupled to HIF2α Transcriptional Regulation

Author

Carroll, Christopher, primary, Manaprasertsak, Auraya, additional, Boffelli Castro, Arthur, additional, van den Bos, Hilda, additional, Spierings, Diana C.J., additional, Wardenaar, René, additional, Bukkuri, Anuraag, additional, Engström, Niklas, additional, Baratchart, Etienne, additional, Yang, Minjun, additional, Biloglav, Andrea, additional, Cornwallis, Charlie K., additional, Johansson, Bertil, additional, Hagerling, Catharina, additional, Arsenian-Henriksson, Marie, additional, Paulsson, Kajsa, additional, Amend, Sarah R., additional, Mohlin, Sofie, additional, Foijer, Floris, additional, McIntyre, Alan, additional, Pienta, Kenneth J., additional, and Hammarlund, Emma U., additional

Published
2024
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3. Updating the Definition of Cancer

Author

Brown, Joel S., primary, Amend, Sarah R., additional, Austin, Robert H., additional, Gatenby, Robert A., additional, Hammarlund, Emma U., additional, and Pienta, Kenneth J., additional

Published
2023
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4. Abstract 4631: Multiplex IHC assay to explore regional heterogeneity of FAP and inflammatory cell density in localized prostatic adenocarcinoma

Author

Pereira, Fernanda Caramella, primary, Meeker, Alan K., additional, Pienta, Kenneth, additional, Zheng, Qizhi, additional, Jones, Tracy, additional, Yegnasubramanian, Srinivasan, additional, Hicks, Jessica L., additional, Roy, Sujayita, additional, De Marzo, Angelo M., additional, and Brennen, W. Nathaniel, additional

Published
2023
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6. Abstract 1686: Leiomyosarcoma poly-aneuploid cancer cells form in response to chemotherapy and contribute to chemoresistance

Author

Abegglen, Lisa M., primary, Bhachech, Niraja, additional, Mitchell, Gareth, additional, Kennington, Ryan, additional, Nelson, Brad, additional, Sharp, Miranda, additional, Buccilli, Matthew, additional, Iovino, Anthony, additional, Rohaj, Aarushi, additional, Fletcher, Jonathan A., additional, Liu, Ting, additional, Rijn, Matt van de, additional, Amend, Sarah R., additional, Pienta, Kenneth J., additional, and Schiffman, Joshua D., additional

Published
2023
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10. Supplementary Table 3 from Molecular Characterization of Neuroendocrine Prostate Cancer and Identification of New Drug Targets

Author

Beltran, Himisha, primary, Rickman, David S., primary, Park, Kyung, primary, Chae, Sung Suk, primary, Sboner, Andrea, primary, MacDonald, Theresa Y., primary, Wang, Yuwei, primary, Sheikh, Karen L., primary, Terry, Stéphane, primary, Tagawa, Scott T., primary, Dhir, Rajiv, primary, Nelson, Joel B., primary, de la Taille, Alexandre, primary, Allory, Yves, primary, Gerstein, Mark B., primary, Perner, Sven, primary, Pienta, Kenneth J., primary, Chinnaiyan, Arul M., primary, Wang, Yuzhuo, primary, Collins, Colin C., primary, Gleave, Martin E., primary, Demichelis, Francesca, primary, Nanus, David M., primary, and Rubin, Mark A., primary

Published
2023
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11. Data from Identification of Targetable FGFR Gene Fusions in Diverse Cancers

Author

Wu, Yi-Mi, primary, Su, Fengyun, primary, Kalyana-Sundaram, Shanker, primary, Khazanov, Nickolay, primary, Ateeq, Bushra, primary, Cao, Xuhong, primary, Lonigro, Robert J., primary, Vats, Pankaj, primary, Wang, Rui, primary, Lin, Su-Fang, primary, Cheng, Ann-Joy, primary, Kunju, Lakshmi P., primary, Siddiqui, Javed, primary, Tomlins, Scott A., primary, Wyngaard, Peter, primary, Sadis, Seth, primary, Roychowdhury, Sameek, primary, Hussain, Maha H., primary, Feng, Felix Y., primary, Zalupski, Mark M., primary, Talpaz, Moshe, primary, Pienta, Kenneth J., primary, Rhodes, Daniel R., primary, Robinson, Dan R., primary, and Chinnaiyan, Arul M., primary

Published
2023
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16. Data from Molecular Characterization of Neuroendocrine Prostate Cancer and Identification of New Drug Targets

Author

Beltran, Himisha, primary, Rickman, David S., primary, Park, Kyung, primary, Chae, Sung Suk, primary, Sboner, Andrea, primary, MacDonald, Theresa Y., primary, Wang, Yuwei, primary, Sheikh, Karen L., primary, Terry, Stéphane, primary, Tagawa, Scott T., primary, Dhir, Rajiv, primary, Nelson, Joel B., primary, de la Taille, Alexandre, primary, Allory, Yves, primary, Gerstein, Mark B., primary, Perner, Sven, primary, Pienta, Kenneth J., primary, Chinnaiyan, Arul M., primary, Wang, Yuzhuo, primary, Collins, Colin C., primary, Gleave, Martin E., primary, Demichelis, Francesca, primary, Nanus, David M., primary, and Rubin, Mark A., primary

Published
2023
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18. Supplementary Figures 1-15, Supplementary Tables 1-2, Supplementary Methods from Molecular Characterization of Neuroendocrine Prostate Cancer and Identification of New Drug Targets

Author

Beltran, Himisha, primary, Rickman, David S., primary, Park, Kyung, primary, Chae, Sung Suk, primary, Sboner, Andrea, primary, MacDonald, Theresa Y., primary, Wang, Yuwei, primary, Sheikh, Karen L., primary, Terry, Stéphane, primary, Tagawa, Scott T., primary, Dhir, Rajiv, primary, Nelson, Joel B., primary, de la Taille, Alexandre, primary, Allory, Yves, primary, Gerstein, Mark B., primary, Perner, Sven, primary, Pienta, Kenneth J., primary, Chinnaiyan, Arul M., primary, Wang, Yuzhuo, primary, Collins, Colin C., primary, Gleave, Martin E., primary, Demichelis, Francesca, primary, Nanus, David M., primary, and Rubin, Mark A., primary

Published
2023
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19. Supplementary Figures from Identification of Targetable FGFR Gene Fusions in Diverse Cancers

Author

Wu, Yi-Mi, primary, Su, Fengyun, primary, Kalyana-Sundaram, Shanker, primary, Khazanov, Nickolay, primary, Ateeq, Bushra, primary, Cao, Xuhong, primary, Lonigro, Robert J., primary, Vats, Pankaj, primary, Wang, Rui, primary, Lin, Su-Fang, primary, Cheng, Ann-Joy, primary, Kunju, Lakshmi P., primary, Siddiqui, Javed, primary, Tomlins, Scott A., primary, Wyngaard, Peter, primary, Sadis, Seth, primary, Roychowdhury, Sameek, primary, Hussain, Maha H., primary, Feng, Felix Y., primary, Zalupski, Mark M., primary, Talpaz, Moshe, primary, Pienta, Kenneth J., primary, Rhodes, Daniel R., primary, Robinson, Dan R., primary, and Chinnaiyan, Arul M., primary

Published
2023
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21. Supplementary Tables from Identification of Targetable FGFR Gene Fusions in Diverse Cancers

Author

Wu, Yi-Mi, primary, Su, Fengyun, primary, Kalyana-Sundaram, Shanker, primary, Khazanov, Nickolay, primary, Ateeq, Bushra, primary, Cao, Xuhong, primary, Lonigro, Robert J., primary, Vats, Pankaj, primary, Wang, Rui, primary, Lin, Su-Fang, primary, Cheng, Ann-Joy, primary, Kunju, Lakshmi P., primary, Siddiqui, Javed, primary, Tomlins, Scott A., primary, Wyngaard, Peter, primary, Sadis, Seth, primary, Roychowdhury, Sameek, primary, Hussain, Maha H., primary, Feng, Felix Y., primary, Zalupski, Mark M., primary, Talpaz, Moshe, primary, Pienta, Kenneth J., primary, Rhodes, Daniel R., primary, Robinson, Dan R., primary, and Chinnaiyan, Arul M., primary

Published
2023
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23. Supplementary Table 3 from Molecular Characterization of Neuroendocrine Prostate Cancer and Identification of New Drug Targets

Author

Mark A. Rubin, David M. Nanus, Francesca Demichelis, Martin E. Gleave, Colin C. Collins, Yuzhuo Wang, Arul M. Chinnaiyan, Kenneth J. Pienta, Sven Perner, Mark B. Gerstein, Yves Allory, Alexandre de la Taille, Joel B. Nelson, Rajiv Dhir, Scott T. Tagawa, Stéphane Terry, Karen L. Sheikh, Yuwei Wang, Theresa Y. MacDonald, Andrea Sboner, Sung Suk Chae, Kyung Park, David S. Rickman, and Himisha Beltran

Abstract

PDF file - 635K

Published
2023
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24. Supplementary Figures 1-15, Supplementary Tables 1-2, Supplementary Methods from Molecular Characterization of Neuroendocrine Prostate Cancer and Identification of New Drug Targets

Author

Mark A. Rubin, David M. Nanus, Francesca Demichelis, Martin E. Gleave, Colin C. Collins, Yuzhuo Wang, Arul M. Chinnaiyan, Kenneth J. Pienta, Sven Perner, Mark B. Gerstein, Yves Allory, Alexandre de la Taille, Joel B. Nelson, Rajiv Dhir, Scott T. Tagawa, Stéphane Terry, Karen L. Sheikh, Yuwei Wang, Theresa Y. MacDonald, Andrea Sboner, Sung Suk Chae, Kyung Park, David S. Rickman, and Himisha Beltran

Abstract

PDF file - 4.12MB

Published
2023
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25. Data from Disseminated Prostate Cancer Cells Can Instruct Hematopoietic Stem and Progenitor Cells to Regulate Bone Phenotype

Author

Russell S. Taichman, Kenneth J. Pienta, Evan T. Keller, Jingcheng Wang, Janet Linn Zalucha, Anjali Mishra, Elisabeth Pedersen, Jin Koo Kim, Younghun Jung, Yusuke Shiozawa, and Jeena Joseph

Abstract

Prostate cancer metastases and hematopoietic stem cells (HSC) frequently home to the bone marrow, where they compete to occupy the same HSC niche. We have also shown that under conditions of hematopoietic stress, HSCs secrete the bone morphogenetic proteins (BMP)-2 and BMP-6 that drives osteoblastic differentiation from mesenchymal precursors. As it is not known, we examined whether metastatic prostate cancer cells can alter regulation of normal bone formation by HSCs and hematopoietic progenitor cells (HPC). HSC/HPCs isolated from mice bearing nonmetastatic and metastatic tumor cells were isolated and their ability to influence osteoblastic and osteoclastic differentiation was evaluated. When the animals were inoculated with the LNCaP C4-2B cell line, which produces mixed osteoblastic and osteolytic lesions in bone, HPCs, but not HSCs, were able to induced stromal cells to differentiate down an osteoblastic phenotype. Part of the mechanism responsible for this activity was the production of BMP-2. On the other hand, when the animals were implanted with PC3 cells that exhibits predominantly osteolytic lesions in bone, HSCs derived from these animals were capable of directly differentiating into tartrate-resistant acid phosphatase–positive osteoclasts through an interleukin-6–mediated pathway. These studies for the first time identify HSC/HPCs as novel targets for future therapy involved in the bone abnormalities of prostate cancer. Mol Cancer Res; 10(3); 282–92. ©2012 AACR.

Published
2023
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26. Supplementary Tables from Identification of Targetable FGFR Gene Fusions in Diverse Cancers

Author

Arul M. Chinnaiyan, Dan R. Robinson, Daniel R. Rhodes, Kenneth J. Pienta, Moshe Talpaz, Mark M. Zalupski, Felix Y. Feng, Maha H. Hussain, Sameek Roychowdhury, Seth Sadis, Peter Wyngaard, Scott A. Tomlins, Javed Siddiqui, Lakshmi P. Kunju, Ann-Joy Cheng, Su-Fang Lin, Rui Wang, Pankaj Vats, Robert J. Lonigro, Xuhong Cao, Bushra Ateeq, Nickolay Khazanov, Shanker Kalyana-Sundaram, Fengyun Su, and Yi-Mi Wu

Abstract

Supplementary Tables - PDF file 753K, Supplementary Tables S1-S15 include transcriptome and exome sequencing results for the FGFR fusion positive index cases, and summaries of sequencing cohorts

Published
2023
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27. Supplementary File 2 - Supplementary figures and table from AXL Is a Putative Tumor Suppressor and Dormancy Regulator in Prostate Cancer

Author

Kenneth J. Pienta, Angelo M. DeMarzo, Gonzalo Torga, Princy Parsana, Jessica L. Hicks, Sarah R. Amend, Kenneth C. Valkenburg, and Haley D. Axelrod

Abstract

S1. Generation and characterization of AXL knockout cells. S2. Generation and characterization of AXL overexpression cells. S3. Aggregate characterization. S4. Characterization of bone signal in AXL-on mice at time of death. Supplementary Table 1: Differentially regulated genes in doxycycline-treated Tet-Axl 2 cells compared to Tet-Axl 1.

Published
2023
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28. Supplementary Figures from Identification of Targetable FGFR Gene Fusions in Diverse Cancers

Author

Arul M. Chinnaiyan, Dan R. Robinson, Daniel R. Rhodes, Kenneth J. Pienta, Moshe Talpaz, Mark M. Zalupski, Felix Y. Feng, Maha H. Hussain, Sameek Roychowdhury, Seth Sadis, Peter Wyngaard, Scott A. Tomlins, Javed Siddiqui, Lakshmi P. Kunju, Ann-Joy Cheng, Su-Fang Lin, Rui Wang, Pankaj Vats, Robert J. Lonigro, Xuhong Cao, Bushra Ateeq, Nickolay Khazanov, Shanker Kalyana-Sundaram, Fengyun Su, and Yi-Mi Wu

Abstract

Supplementary Figures - PDF file 639K, Supplementary Figures S1-S9 show the phenotypic effects and signaling pathways of FGFR fusions in vitro and in vivo

Published
2023
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30. Data from RB Loss Promotes Prostate Cancer Metastasis

Author

Robert B. Den, Karen E. Knudsen, Adam P. Dicker, Felix Y. Feng, Kenneth J. Pienta, Eva A. Turley, James B. McCarthy, Ruth Birbe, Shuang G. Zhao, James R. Hernandez, Matt Price, Chris McNair, Adam Snook, Jeffry L. Dean, Paolo Cotzia, Stephen J. Ciment, Noelle Williams, Sankar Addya, Anshul Bhardwaj, Adam Ertel, Alex Haber, Yi Liu, Ettickan Boopathi, and Chellappagounder Thangavel

Abstract

RB loss occurs commonly in neoplasia but its contributions to advanced cancer have not been assessed directly. Here we show that RB loss in multiple murine models of cancer produces a prometastatic phenotype. Gene expression analyses showed that regulation of the cell motility receptor RHAMM by the RB/E2F pathway was critical for epithelial–mesenchymal transition, motility, and invasion by cancer cells. Genetic modulation or pharmacologic inhibition of RHAMM activity was sufficient and necessary for metastatic phenotypes induced by RB loss in prostate cancer. Mechanistic studies in this setting established that RHAMM stabilized F-actin polymerization by controlling ROCK signaling. Collectively, our findings show how RB loss drives metastatic capacity and highlight RHAMM as a candidate therapeutic target for treating advanced prostate cancer. Cancer Res; 77(4); 982–95. ©2016 AACR.

Published
2023
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33. Data from Supraphysiologic Testosterone Induces Ferroptosis and Activates Immune Pathways through Nucleophagy in Prostate Cancer

Author

Sushant K. Kachhap, Samuel R. Denmeade, Michael A. Carducci, Drew M. Pardoll, Kenneth J. Pienta, David Z. Qian, Emmanuel S. Antonarakis, Mark C. Markowski, Angelo M. De Marzo, John T. Isaacs, W. Nathaniel Brennen, Sadie Wiens, Liang Dong, Marc Rosen, Tracy Jones, Busra Ozbek, Carolina Gomes, Deven Topiwala, Max Coffey, Suthicha Kanacharoen, Naiju Thomas, Kavya Boyapati, Olutosin Owoyemi, Janet Mendonca, and Rajendra Kumar

Abstract

The discovery that androgens play an important role in the progression of prostate cancer led to the development of androgen deprivation therapy (ADT) as a first line of treatment. However, paradoxical growth inhibition has been observed in a subset of prostate cancer upon administration of supraphysiologic levels of testosterone (SupraT), both experimentally and clinically. Here we report that SupraT activates cytoplasmic nucleic acid sensors and induces growth inhibition of SupraT-sensitive prostate cancer cells. This was initiated by the induction of two parallel autophagy-mediated processes, namely, ferritinophagy and nucleophagy. Consequently, autophagosomal DNA activated nucleic acid sensors converge on NFκB to drive immune signaling pathways. Chemokines and cytokines secreted by the tumor cells in response to SupraT resulted in increased migration of cytotoxic immune cells to tumor beds in xenograft models and patient tumors. Collectively, these findings indicate that SupraT may inhibit a subset of prostate cancer by activating nucleic acid sensors and downstream immune signaling.Significance:This study demonstrates that supraphysiologic testosterone induces two parallel autophagy-mediated processes, ferritinophagy and nucleophagy, which then activate nucleic acid sensors to drive immune signaling pathways in prostate cancer.

Published
2023
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35. Supplemental Table 1 from RB Loss Promotes Prostate Cancer Metastasis

Author

Robert B. Den, Karen E. Knudsen, Adam P. Dicker, Felix Y. Feng, Kenneth J. Pienta, Eva A. Turley, James B. McCarthy, Ruth Birbe, Shuang G. Zhao, James R. Hernandez, Matt Price, Chris McNair, Adam Snook, Jeffry L. Dean, Paolo Cotzia, Stephen J. Ciment, Noelle Williams, Sankar Addya, Anshul Bhardwaj, Adam Ertel, Alex Haber, Yi Liu, Ettickan Boopathi, and Chellappagounder Thangavel

Abstract

nucleotide sequence

Published
2023
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36. Data from Molecularly Targeted Radiosensitization of Human Prostate Cancer by Modulating Inhibitor of Apoptosis

Author

Liang Xu, Theodore Lawrence, Kenneth Pienta, Mary Davis, Ezra Burstein, Jeffrey DeSano, Wenhua Tang, Meilan Liu, and Yao Dai

Abstract

Purpose: The inhibitor of apoptosis proteins (IAP) are overexpressed in hormone-refractory prostate cancer, rendering the cancer cells resistant to radiation. This study aims to investigate the radiosensitizing effect of small-molecule IAP inhibitor both in vitro and in vivo in androgen-independent prostate cancer and the possible mechanism of radiosensitization.Experimental Design: Radiosensitization of SH-130 in human prostate cancer DU-145 cells was determined by clonogenic survival assay. Combination effect of SH-130 and ionizing radiation was evaluated by apoptosis assays. Pull-down and immunoprecipitation assays were employed to investigate the interaction between SH-130 and IAPs. DU-145 xenografts in nude mice were treated with SH-130, radiation, or combination, and tumor suppression effect was determined by caliper measurement or bioluminescence imaging. Nuclear factor-κB activation was detected by luciferase reporter assay and quantitative real-time PCR.Results: SH-130 potently enhanced radiation-induced caspase activation and apoptosis in DU-145 cells. Both X-linked IAP and cIAP-1 can be pulled down by SH-130 but not by inactive SH-123. Moreover, SH-130 interrupted interaction between X-linked IAP/cIAP-1 and Smac. In a nude mouse xenograft model, SH-130 potently sensitized the DU-145 tumors to X-ray radiation without increasing systemic toxicity. The combination therapy suppressed tumor growth more significantly than either treatment alone, with over 80% of complete tumor regression. Furthermore, SH-130 partially blocked tumor necrosis factor-α- and radiation-induced nuclear factor-κB activation in DU-145 cells.Conclusions: Our results show that small-molecule inhibitors of IAPs can overcome apoptosis resistance and radiosensitize human prostate cancer with high levels of IAPs. Molecular modulation of IAPs may improve the outcome of prostate cancer radiotherapy.

Published
2023
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37. Data from CXCL12γ Promotes Metastatic Castration-Resistant Prostate Cancer by Inducing Cancer Stem Cell and Neuroendocrine Phenotypes

Author

Russell S. Taichman, Todd M. Morgan, Kenneth J. Pienta, Paul H. Krebsbach, Amy M. Gursky, Jae-Seung Chung, Yugang Wang, Eunsohl Lee, Jin Koo Kim, Jingcheng Wang, Ann M. Decker, Kenji Yumoto, Frank C. Cackowski, and Younghun Jung

Abstract

There is evidence that cancer stem-like cells (CSC) and neuroendocrine behavior play critical roles in the pathogenesis and clinical course of metastatic castration-resistant prostate cancer (m-CRPC). However, there is limited mechanistic understanding of how CSC and neuroendocrine phenotypes impact the development of m-CRPC. In this study, we explored the role of the intracellular chemokine CXCL12γ in CSC induction and neuroendocrine differentiation and its impact on m-CRPC. CXCL12γ expression was detected in small-cell carcinoma of metastatic tissues and circulating tumor cells from m-CRPC patients and in prostate cancer cells displaying an neuroendocrine phenotype. Mechanistic investigations demonstrated that overexpression of CXCL12γ induced CSC and neuroendocrine phenotypes in prostate cancer cells through CXCR4-mediated PKCα/NFκB signaling, which promoted prostate tumor outgrowth, metastasis, and chemoresistance in vivo. Together, our results establish a significant function for CXCL12γ in m-CRPC development and suggest it as a candidate therapeutic target to control aggressive disease.Significance: Expression of CXCL12γ induces the expression of a cancer stem cell and neuroendocrine phenotypes, resulting in the development of aggressive m-CRPC. Cancer Res; 78(8); 2026–39. ©2018 AACR.

Published
2023
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38. Supplemental figures 3-6 from Tenascin-C and Integrin α9 Mediate Interactions of Prostate Cancer with the Bone Microenvironment

Author

David R. Rowley, Kenneth J. Pienta, Andrew G. Sikora, María C. Piña-Barba, Susan G. Hilsenbeck, Sung Yun Jung, Antrix Jain, Ravi Pathak, and Rebeca San Martin

Abstract

Characterization of the osteogenic organoids: Smooth alpha actin expression, viability, co-culture with prostate-derived cell lines. Adhesion of prostate cancer cell lines to tenascin-C

Published
2023
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39. Supplemental Figure 3 from CUE-101, a Novel E7-pHLA-IL2-Fc Fusion Protein, Enhances Tumor Antigen-Specific T-Cell Activation for the Treatment of HPV16-Driven Malignancies

Author

Mary Ellen Simcox, Kenneth J. Pienta, Saso Cemerski, Anish Suri, Ronald Seidel, Rodolfo Chaparro, Steven Almo, Peter A. Kiener, John F. Ross, Emily Spaulding, Mark Haydock, Jonathan Soriano, Jessica Ryabin, Luke Witt, Dominic R. Beal, Lauren D. Kraemer, Alyssa Nelson, Sandrine Hulot, Paige Ruthardt, Miguel Moreta, Fan Zhao, Alex Histed, Melissa M. Kemp, Zohra Merazga, Dharma R. Thapa, Natasha Girgis, and Steven N. Quayle

Abstract

Supplementary Figure 3. Representative gating strategy for the analysis of blood and spleen samples from HLA-A2 transgenic mice.

Published
2023
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42. Supplemental Figures from TWIST1-WDR5-Hottip Regulates Hoxa9 Chromatin to Facilitate Prostate Cancer Metastasis

Author

Phuoc T. Tran, Colm Morrissey, Paula J. Hurley, Kenneth J. Pienta, Edward M. Schaeffer, Ashley E. Ross, Theodore L. DeWeese, Steven S. An, Lawrence True, Arum R. Yoon, Ghali Lemtiri-Chlieh, Kekoa Taparra, Hailun Wang, Katriana Nugent, Brian W. Simons, Belinda Nghiem, Russell D. Williams, Rajendra P. Gajula, and Reem Malek

Abstract

This document contains supplemental details such as antibodies and primers, list of genes overrepresented in TWIST1 and TWIST1 mutants, IHC staining for TWIST1 in mouse prostate development, IHC staining for TWIST1 and HOXA9 in various mouse models of prostate cancer, correlation of TWIST1 and HOXA9 alteration with poor survival in human prostate cancer patients, IHC for TWIST1 and HOXA9 on primary tumors and bone metastasis from prostate cancer patients, IHC for HOXA9 on cell pellets expressing HOXA9 or control and on adult mouse prostate, data showing sufficiency of HOXA9 for some pro-metastatic behaviour in prostate cancer cells, data showing requirement of WDR5 and HOTTIP for TWIST1-dependent pro-metastatic behavior, ChIP data showing binding of TWIST1 and HOXA9 at the HOXA9 promoter, data showing effect of drugs that can inhibit HOXA9 on prostate cancer cell viability and pro metastatic behaviour.

Published
2023
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43. Supplementary Figures from Supraphysiologic Testosterone Induces Ferroptosis and Activates Immune Pathways through Nucleophagy in Prostate Cancer

Author

Sushant K. Kachhap, Samuel R. Denmeade, Michael A. Carducci, Drew M. Pardoll, Kenneth J. Pienta, David Z. Qian, Emmanuel S. Antonarakis, Mark C. Markowski, Angelo M. De Marzo, John T. Isaacs, W. Nathaniel Brennen, Sadie Wiens, Liang Dong, Marc Rosen, Tracy Jones, Busra Ozbek, Carolina Gomes, Deven Topiwala, Max Coffey, Suthicha Kanacharoen, Naiju Thomas, Kavya Boyapati, Olutosin Owoyemi, Janet Mendonca, and Rajendra Kumar

Abstract

Supplementary Figures S1-S9

Published
2023
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44. Supplementary Table S1 from Supraphysiologic Testosterone Induces Ferroptosis and Activates Immune Pathways through Nucleophagy in Prostate Cancer

Author

Sushant K. Kachhap, Samuel R. Denmeade, Michael A. Carducci, Drew M. Pardoll, Kenneth J. Pienta, David Z. Qian, Emmanuel S. Antonarakis, Mark C. Markowski, Angelo M. De Marzo, John T. Isaacs, W. Nathaniel Brennen, Sadie Wiens, Liang Dong, Marc Rosen, Tracy Jones, Busra Ozbek, Carolina Gomes, Deven Topiwala, Max Coffey, Suthicha Kanacharoen, Naiju Thomas, Kavya Boyapati, Olutosin Owoyemi, Janet Mendonca, and Rajendra Kumar

Abstract

Oligo sequences

Published
2023
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45. Supplementary Figure and Table Legends from Characterization of Bone Metastases from Rapid Autopsies of Prostate Cancer Patients

Author

Kenneth J. Pienta, Arul M. Chinnaiyan, Rajal B. Shah, David C. Smith, Xuhong Cao, Bo Han, Javed Siddiqui, Neena E. Philips, Xiaojun Jing, Robert J. Lonigro, Sunita Shankar, Chandan Kumar-Sinha, and Rohit Mehra

Abstract

Supplementary Figure and Table Legends from Characterization of Bone Metastases from Rapid Autopsies of Prostate Cancer Patients

Published
2023
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48. Supplemental Figure 5 from CUE-101, a Novel E7-pHLA-IL2-Fc Fusion Protein, Enhances Tumor Antigen-Specific T-Cell Activation for the Treatment of HPV16-Driven Malignancies

Author

Mary Ellen Simcox, Kenneth J. Pienta, Saso Cemerski, Anish Suri, Ronald Seidel, Rodolfo Chaparro, Steven Almo, Peter A. Kiener, John F. Ross, Emily Spaulding, Mark Haydock, Jonathan Soriano, Jessica Ryabin, Luke Witt, Dominic R. Beal, Lauren D. Kraemer, Alyssa Nelson, Sandrine Hulot, Paige Ruthardt, Miguel Moreta, Fan Zhao, Alex Histed, Melissa M. Kemp, Zohra Merazga, Dharma R. Thapa, Natasha Girgis, and Steven N. Quayle

Abstract

Supplementary Figure 5. Antitumor activity of mCUE-101 in TC-1 tumors.

Published
2023
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49. Supplemental Figures from CXCL12γ Promotes Metastatic Castration-Resistant Prostate Cancer by Inducing Cancer Stem Cell and Neuroendocrine Phenotypes

Author

Russell S. Taichman, Todd M. Morgan, Kenneth J. Pienta, Paul H. Krebsbach, Amy M. Gursky, Jae-Seung Chung, Yugang Wang, Eunsohl Lee, Jin Koo Kim, Jingcheng Wang, Ann M. Decker, Kenji Yumoto, Frank C. Cackowski, and Younghun Jung

Abstract

Supplemental Figure 1: Small cell carcinoma in PCa patient tissues. Supplemental Figure 2: Metastatic potential of CXCL12 γ expression in PCa cells and CXCL12 γ expression in normal human and mouse tissues. Supplemental Figure 3: CXCL12 γ induces CSCs, which promotes BCa tumor growth. Supplemental Figure 4: CXCL12 γ induces a NE phenotype in BCa cells. Supplemental Figure 5: Regression analyses of ENO2 mRNA expression and serum Enolase 2/NSE, Chromogranin A, and PSA in m-CRPC patients. Supplemental Figure 6: CSCs in NE PCa cells and The role of CXCL12 γ in AR-dependent PCa cells. Supplemental Figure 7: CXCL12 γ contributes activation of CXCR4-mediated PKC α /NF κ B signaling in CSC and NE inductions in BCa cells.

Published
2023
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50. Data from CUE-101, a Novel E7-pHLA-IL2-Fc Fusion Protein, Enhances Tumor Antigen-Specific T-Cell Activation for the Treatment of HPV16-Driven Malignancies

Author

Mary Ellen Simcox, Kenneth J. Pienta, Saso Cemerski, Anish Suri, Ronald Seidel, Rodolfo Chaparro, Steven Almo, Peter A. Kiener, John F. Ross, Emily Spaulding, Mark Haydock, Jonathan Soriano, Jessica Ryabin, Luke Witt, Dominic R. Beal, Lauren D. Kraemer, Alyssa Nelson, Sandrine Hulot, Paige Ruthardt, Miguel Moreta, Fan Zhao, Alex Histed, Melissa M. Kemp, Zohra Merazga, Dharma R. Thapa, Natasha Girgis, and Steven N. Quayle

Abstract

Purpose:To assess the potential for CUE-101, a novel therapeutic fusion protein, to selectively activate and expand HPV16 E711-20-specific CD8+ T cells as an off-the shelf therapy for the treatment of HPV16-driven tumors, including head and neck squamous cell carcinoma (HNSCC), cervical, and anal cancers.Experimental Design:CUE-101 is an Fc fusion protein composed of a human leukocyte antigen (HLA) complex, an HPV16 E7 peptide epitope, reduced affinity human IL2 molecules, and an effector attenuated human IgG1 Fc domain. Human E7-specific T cells and human peripheral blood mononuclear cells (PBMC) were tested to demonstrate cellular activity and specificity of CUE-101, whereas in vivo activity of CUE-101 was assessed in HLA-A2 transgenic mice. Antitumor efficacy with a murine surrogate (mCUE-101) was tested in the TC-1 syngeneic tumor model.Results:CUE-101 demonstrates selective binding, activation, and expansion of HPV16 E711-20-specific CD8+ T cells from PBMCs relative to nontarget cells. Intravenous administration of CUE-101 induced selective expansion of HPV16 E711-20-specific CD8+ T cells in HLA-A2 (AAD) transgenic mice, and anticancer efficacy and immunologic memory was demonstrated in TC-1 tumor-bearing mice treated with mCUE-101. Combination therapy with anti-PD-1 checkpoint blockade further enhanced the observed efficacy.Conclusions:Consistent with its design, CUE-101 demonstrates selective expansion of an HPV16 E711-20-specific population of cytotoxic CD8+ T cells, a favorable safety profile, and in vitro and in vivo evidence supporting its potential for clinical efficacy in an ongoing phase I trial (NCT03978689).

Published
2023
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