Co‐targeting BET and MEK as salvage therapy for MAPK and checkpoint inhibitor‐resistant melanoma

Abstract Despite novel therapies for melanoma, drug resistance remains a significant hurdle to achieving optimal responses. NRAS‐mutant melanoma is an archetype of therapeutic challenges in the field, which we used to test drug combinations to avert drug resistance. We show that BET proteins are ove...

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Main Authors: Ileabett M Echevarría‐Vargas, Patricia I Reyes‐Uribe, Adam N Guterres, Xiangfan Yin, Andrew V Kossenkov, Qin Liu, Gao Zhang, Clemens Krepler, Chaoran Cheng, Zhi Wei, Rajasekharan Somasundaram, Giorgos Karakousis, Wei Xu, Jennifer JD Morrissette, Yiling Lu, Gordon B Mills, Ryan J Sullivan, Miao Benchun, Dennie T Frederick, Genevieve Boland, Keith T Flaherty, Ashani T Weeraratna, Meenhard Herlyn, Ravi Amaravadi, Lynn M Schuchter, Christin E Burd, Andrew E Aplin, Xiaowei Xu, Jessie Villanueva
Format: Article
Language:English
Published: Springer Nature 2018-04-01
Series:EMBO Molecular Medicine
Subjects:
Online Access:https://doi.org/10.15252/emmm.201708446
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author Ileabett M Echevarría‐Vargas
Patricia I Reyes‐Uribe
Adam N Guterres
Xiangfan Yin
Andrew V Kossenkov
Qin Liu
Gao Zhang
Clemens Krepler
Chaoran Cheng
Zhi Wei
Rajasekharan Somasundaram
Giorgos Karakousis
Wei Xu
Jennifer JD Morrissette
Yiling Lu
Gordon B Mills
Ryan J Sullivan
Miao Benchun
Dennie T Frederick
Genevieve Boland
Keith T Flaherty
Ashani T Weeraratna
Meenhard Herlyn
Ravi Amaravadi
Lynn M Schuchter
Christin E Burd
Andrew E Aplin
Xiaowei Xu
Jessie Villanueva
author_facet Ileabett M Echevarría‐Vargas
Patricia I Reyes‐Uribe
Adam N Guterres
Xiangfan Yin
Andrew V Kossenkov
Qin Liu
Gao Zhang
Clemens Krepler
Chaoran Cheng
Zhi Wei
Rajasekharan Somasundaram
Giorgos Karakousis
Wei Xu
Jennifer JD Morrissette
Yiling Lu
Gordon B Mills
Ryan J Sullivan
Miao Benchun
Dennie T Frederick
Genevieve Boland
Keith T Flaherty
Ashani T Weeraratna
Meenhard Herlyn
Ravi Amaravadi
Lynn M Schuchter
Christin E Burd
Andrew E Aplin
Xiaowei Xu
Jessie Villanueva
author_sort Ileabett M Echevarría‐Vargas
collection DOAJ
description Abstract Despite novel therapies for melanoma, drug resistance remains a significant hurdle to achieving optimal responses. NRAS‐mutant melanoma is an archetype of therapeutic challenges in the field, which we used to test drug combinations to avert drug resistance. We show that BET proteins are overexpressed in NRAS‐mutant melanoma and that high levels of the BET family member BRD4 are associated with poor patient survival. Combining BET and MEK inhibitors synergistically curbed the growth of NRAS‐mutant melanoma and prolonged the survival of mice bearing tumors refractory to MAPK inhibitors and immunotherapy. Transcriptomic and proteomic analysis revealed that combining BET and MEK inhibitors mitigates a MAPK and checkpoint inhibitor resistance transcriptional signature, downregulates the transcription factor TCF19, and induces apoptosis. Our studies demonstrate that co‐targeting MEK and BET can offset therapy resistance, offering a salvage strategy for melanomas with no other therapeutic options, and possibly other treatment‐resistant tumor types.
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issn 1757-4676
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publishDate 2018-04-01
publisher Springer Nature
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series EMBO Molecular Medicine
spelling doaj-art-427671eabd2f438dbb2812ca02f929e32025-08-20T03:05:55ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842018-04-0110511510.15252/emmm.201708446Co‐targeting BET and MEK as salvage therapy for MAPK and checkpoint inhibitor‐resistant melanomaIleabett M Echevarría‐Vargas0Patricia I Reyes‐Uribe1Adam N Guterres2Xiangfan Yin3Andrew V Kossenkov4Qin Liu5Gao Zhang6Clemens Krepler7Chaoran Cheng8Zhi Wei9Rajasekharan Somasundaram10Giorgos Karakousis11Wei Xu12Jennifer JD Morrissette13Yiling Lu14Gordon B Mills15Ryan J Sullivan16Miao Benchun17Dennie T Frederick18Genevieve Boland19Keith T Flaherty20Ashani T Weeraratna21Meenhard Herlyn22Ravi Amaravadi23Lynn M Schuchter24Christin E Burd25Andrew E Aplin26Xiaowei Xu27Jessie Villanueva28Molecular & Cellular Oncogenesis Program, The Wistar InstituteMolecular & Cellular Oncogenesis Program, The Wistar InstituteMolecular & Cellular Oncogenesis Program, The Wistar InstituteMolecular & Cellular Oncogenesis Program, The Wistar InstituteMolecular & Cellular Oncogenesis Program, The Wistar InstituteMolecular & Cellular Oncogenesis Program, The Wistar InstituteMolecular & Cellular Oncogenesis Program, The Wistar InstituteMolecular & Cellular Oncogenesis Program, The Wistar InstituteCollege of Computing Sciences, New Jersey Institute of TechnologyCollege of Computing Sciences, New Jersey Institute of TechnologyMolecular & Cellular Oncogenesis Program, The Wistar InstituteAbramson Cancer Center, University of PennsylvaniaAbramson Cancer Center, University of PennsylvaniaCenter for Personalized Diagnostics, Hospital of the University of Pennsylvania, University of PennsylvaniaDepartment of Systems Biology, The University of Texas MD Anderson Cancer CenterDepartment of Systems Biology, The University of Texas MD Anderson Cancer CenterMassachusetts General Hospital Cancer Center, Harvard Medical SchoolMassachusetts General Hospital Cancer Center, Harvard Medical SchoolMassachusetts General Hospital Cancer Center, Harvard Medical SchoolDepartment of Surgery, Massachusetts General Hospital, Harvard Medical SchoolMassachusetts General Hospital Cancer Center, Harvard Medical SchoolMelanoma Research Center, The Wistar InstituteMolecular & Cellular Oncogenesis Program, The Wistar InstituteDepartment of Surgery, Hospital of the University of PennsylvaniaDepartment of Surgery, Hospital of the University of PennsylvaniaDepartments of Molecular Genetics and Cancer Biology and Genetics, Ohio State UniversityDepartment of Cancer Biology and Sidney Kimmel Cancer Center, Thomas Jefferson UniversityDepartment of Surgery, Hospital of the University of PennsylvaniaMolecular & Cellular Oncogenesis Program, The Wistar InstituteAbstract Despite novel therapies for melanoma, drug resistance remains a significant hurdle to achieving optimal responses. NRAS‐mutant melanoma is an archetype of therapeutic challenges in the field, which we used to test drug combinations to avert drug resistance. We show that BET proteins are overexpressed in NRAS‐mutant melanoma and that high levels of the BET family member BRD4 are associated with poor patient survival. Combining BET and MEK inhibitors synergistically curbed the growth of NRAS‐mutant melanoma and prolonged the survival of mice bearing tumors refractory to MAPK inhibitors and immunotherapy. Transcriptomic and proteomic analysis revealed that combining BET and MEK inhibitors mitigates a MAPK and checkpoint inhibitor resistance transcriptional signature, downregulates the transcription factor TCF19, and induces apoptosis. Our studies demonstrate that co‐targeting MEK and BET can offset therapy resistance, offering a salvage strategy for melanomas with no other therapeutic options, and possibly other treatment‐resistant tumor types.https://doi.org/10.15252/emmm.201708446BETcombination therapydrug resistancemelanomamutant NRAS
spellingShingle Ileabett M Echevarría‐Vargas
Patricia I Reyes‐Uribe
Adam N Guterres
Xiangfan Yin
Andrew V Kossenkov
Qin Liu
Gao Zhang
Clemens Krepler
Chaoran Cheng
Zhi Wei
Rajasekharan Somasundaram
Giorgos Karakousis
Wei Xu
Jennifer JD Morrissette
Yiling Lu
Gordon B Mills
Ryan J Sullivan
Miao Benchun
Dennie T Frederick
Genevieve Boland
Keith T Flaherty
Ashani T Weeraratna
Meenhard Herlyn
Ravi Amaravadi
Lynn M Schuchter
Christin E Burd
Andrew E Aplin
Xiaowei Xu
Jessie Villanueva
Co‐targeting BET and MEK as salvage therapy for MAPK and checkpoint inhibitor‐resistant melanoma
EMBO Molecular Medicine
BET
combination therapy
drug resistance
melanoma
mutant NRAS
title Co‐targeting BET and MEK as salvage therapy for MAPK and checkpoint inhibitor‐resistant melanoma
title_full Co‐targeting BET and MEK as salvage therapy for MAPK and checkpoint inhibitor‐resistant melanoma
title_fullStr Co‐targeting BET and MEK as salvage therapy for MAPK and checkpoint inhibitor‐resistant melanoma
title_full_unstemmed Co‐targeting BET and MEK as salvage therapy for MAPK and checkpoint inhibitor‐resistant melanoma
title_short Co‐targeting BET and MEK as salvage therapy for MAPK and checkpoint inhibitor‐resistant melanoma
title_sort co targeting bet and mek as salvage therapy for mapk and checkpoint inhibitor resistant melanoma
topic BET
combination therapy
drug resistance
melanoma
mutant NRAS
url https://doi.org/10.15252/emmm.201708446
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