Antitumor activity of rucaparib plus PLX038A in serous endometrial carcinoma

Abstract Background Serous endometrial cancer (SEC) is a genomically and morphologically distinct endometrial cancer (EC) subtype with a poor progression-free and overall survival. The development of novel therapies is needed to improve outcomes. Methods We used serous and serous-like EC patient-der...

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Main Authors: Xiaonan Hou, Valentina Zanfagnin, Conway Xu, Erik Jessen, Yuanhang Liu, Chen Wang, Yajue Huang, Shaun D. Fontaine, Daniel V. Santi, Gerardo Colon-Otero, Sarah E. Gill, Gretchen E. Glaser, Kristina A. Butler, Jamie N. Bakkum-Gamez, Sean C. Dowdy, Ann L. Oberg, Melissa C. Larson, Hunter J. Atkinson, Laura N. Duffield, Kevin L. Peterson, Scott H. Kaufmann, S. John Weroha
Format: Article
Language:English
Published: BMC 2025-05-01
Series:Journal of Experimental & Clinical Cancer Research
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Online Access:https://doi.org/10.1186/s13046-025-03406-7
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author Xiaonan Hou
Valentina Zanfagnin
Conway Xu
Erik Jessen
Yuanhang Liu
Chen Wang
Yajue Huang
Shaun D. Fontaine
Daniel V. Santi
Gerardo Colon-Otero
Sarah E. Gill
Gretchen E. Glaser
Kristina A. Butler
Jamie N. Bakkum-Gamez
Sean C. Dowdy
Ann L. Oberg
Melissa C. Larson
Hunter J. Atkinson
Laura N. Duffield
Kevin L. Peterson
Scott H. Kaufmann
S. John Weroha
author_facet Xiaonan Hou
Valentina Zanfagnin
Conway Xu
Erik Jessen
Yuanhang Liu
Chen Wang
Yajue Huang
Shaun D. Fontaine
Daniel V. Santi
Gerardo Colon-Otero
Sarah E. Gill
Gretchen E. Glaser
Kristina A. Butler
Jamie N. Bakkum-Gamez
Sean C. Dowdy
Ann L. Oberg
Melissa C. Larson
Hunter J. Atkinson
Laura N. Duffield
Kevin L. Peterson
Scott H. Kaufmann
S. John Weroha
author_sort Xiaonan Hou
collection DOAJ
description Abstract Background Serous endometrial cancer (SEC) is a genomically and morphologically distinct endometrial cancer (EC) subtype with a poor progression-free and overall survival. The development of novel therapies is needed to improve outcomes. Methods We used serous and serous-like EC patient-derived xenografts (PDXs) to test a novel drug combination in vitro and in vivo: rucaparib and pegylated SN-38 (PLX038A). Sensitivity to treatment was correlated with indicators of homologous recombination (HR) deficiency. Efficacy in fresh primary patient tumors was also tested ex vivo. Results Five of eight PDXs had genomic instability scores ≥ 42, but only one of these five had evidence of HR deficiency in assays of irradiation-induced RAD51 foci formation. Moreover, PARP inhibitor (PARPi) monotherapy failed to induce regressions in any of the five SEC models treated with rucaparib in vivo, suggesting limited clinical activity of PARPi in SEC. In further studies, we assessed the response of these models to the sustained release topoisomerase 1 inhibitor, PLX038A, as monotherapy and in combination with rucaparib ex vivo and in vivo. Results of these studies showed that PLX038A had limited monotherapy activity, but combination therapy induced significant regressions in two of five SEC PDXs and markedly slowed tumor growth in the other three regardless of underlying homologous recombination repair deficiency. In addition, 11 of 20 (55%) primary tumors showed synergy with rucaparib + SN-38. Conclusions Collectively, these studies identify a set of genomically characterized PDX models for preclinical testing of potential SEC therapies and a therapeutic combination that warrants further preclinical investigation.
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spelling doaj-art-75c2bc90f8a74285aca0fad21b6005ac2025-08-20T01:53:15ZengBMCJournal of Experimental & Clinical Cancer Research1756-99662025-05-0144111510.1186/s13046-025-03406-7Antitumor activity of rucaparib plus PLX038A in serous endometrial carcinomaXiaonan Hou0Valentina Zanfagnin1Conway Xu2Erik Jessen3Yuanhang Liu4Chen Wang5Yajue Huang6Shaun D. Fontaine7Daniel V. Santi8Gerardo Colon-Otero9Sarah E. Gill10Gretchen E. Glaser11Kristina A. Butler12Jamie N. Bakkum-Gamez13Sean C. Dowdy14Ann L. Oberg15Melissa C. Larson16Hunter J. Atkinson17Laura N. Duffield18Kevin L. Peterson19Scott H. Kaufmann20S. John Weroha21Division of Medical Oncology, Mayo ClinicDivision of Medical Oncology, Mayo ClinicDivision of Medical Oncology, Mayo ClinicDepartment of Health Sciences Research, Mayo ClinicDepartment of Health Sciences Research, Mayo ClinicDepartment of Health Sciences Research, Mayo ClinicDivision of Anatomic Pathology, Mayo ClinicProLynx LLCProLynx LLCHematology/Oncology, Mayo Clinic FloridaDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, Mayo ClinicDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, Mayo ClinicMedical & Surgical Gynecology Department, Mayo ClinicDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, Mayo ClinicDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, Mayo ClinicDepartment of Quantitative Health Sciences, Division of Computational Biology, Mayo ClinicDepartment of Quantitative Health Sciences, Division of Clinical Trials and Biostatistics, Mayo ClinicDepartment of Quantitative Health Sciences, Division of Clinical Trials and Biostatistics, Mayo ClinicDivision of Oncology Research, Mayo ClinicDivision of Oncology Research, Mayo ClinicDivision of Oncology Research, Mayo ClinicDivision of Medical Oncology, Mayo ClinicAbstract Background Serous endometrial cancer (SEC) is a genomically and morphologically distinct endometrial cancer (EC) subtype with a poor progression-free and overall survival. The development of novel therapies is needed to improve outcomes. Methods We used serous and serous-like EC patient-derived xenografts (PDXs) to test a novel drug combination in vitro and in vivo: rucaparib and pegylated SN-38 (PLX038A). Sensitivity to treatment was correlated with indicators of homologous recombination (HR) deficiency. Efficacy in fresh primary patient tumors was also tested ex vivo. Results Five of eight PDXs had genomic instability scores ≥ 42, but only one of these five had evidence of HR deficiency in assays of irradiation-induced RAD51 foci formation. Moreover, PARP inhibitor (PARPi) monotherapy failed to induce regressions in any of the five SEC models treated with rucaparib in vivo, suggesting limited clinical activity of PARPi in SEC. In further studies, we assessed the response of these models to the sustained release topoisomerase 1 inhibitor, PLX038A, as monotherapy and in combination with rucaparib ex vivo and in vivo. Results of these studies showed that PLX038A had limited monotherapy activity, but combination therapy induced significant regressions in two of five SEC PDXs and markedly slowed tumor growth in the other three regardless of underlying homologous recombination repair deficiency. In addition, 11 of 20 (55%) primary tumors showed synergy with rucaparib + SN-38. Conclusions Collectively, these studies identify a set of genomically characterized PDX models for preclinical testing of potential SEC therapies and a therapeutic combination that warrants further preclinical investigation.https://doi.org/10.1186/s13046-025-03406-7Endometrial cancerXenograftsPARP inhibitorRucaparibHomologous recombinationDNA repair
spellingShingle Xiaonan Hou
Valentina Zanfagnin
Conway Xu
Erik Jessen
Yuanhang Liu
Chen Wang
Yajue Huang
Shaun D. Fontaine
Daniel V. Santi
Gerardo Colon-Otero
Sarah E. Gill
Gretchen E. Glaser
Kristina A. Butler
Jamie N. Bakkum-Gamez
Sean C. Dowdy
Ann L. Oberg
Melissa C. Larson
Hunter J. Atkinson
Laura N. Duffield
Kevin L. Peterson
Scott H. Kaufmann
S. John Weroha
Antitumor activity of rucaparib plus PLX038A in serous endometrial carcinoma
Journal of Experimental & Clinical Cancer Research
Endometrial cancer
Xenografts
PARP inhibitor
Rucaparib
Homologous recombination
DNA repair
title Antitumor activity of rucaparib plus PLX038A in serous endometrial carcinoma
title_full Antitumor activity of rucaparib plus PLX038A in serous endometrial carcinoma
title_fullStr Antitumor activity of rucaparib plus PLX038A in serous endometrial carcinoma
title_full_unstemmed Antitumor activity of rucaparib plus PLX038A in serous endometrial carcinoma
title_short Antitumor activity of rucaparib plus PLX038A in serous endometrial carcinoma
title_sort antitumor activity of rucaparib plus plx038a in serous endometrial carcinoma
topic Endometrial cancer
Xenografts
PARP inhibitor
Rucaparib
Homologous recombination
DNA repair
url https://doi.org/10.1186/s13046-025-03406-7
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