Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis

Summary: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC...
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Autor*in:	Hyunho Han [verfasserIn] Yan Wang [verfasserIn] Josue Curto [verfasserIn] Sreeharsha Gurrapu [verfasserIn] Sara Laudato [verfasserIn] Alekya Rumandla [verfasserIn] Goutam Chakraborty [verfasserIn] Xiaobo Wang [verfasserIn] Hong Chen [verfasserIn] Yan Jiang [verfasserIn] Dhiraj Kumar [verfasserIn] Emily G. Caggiano [verfasserIn] Monica Capogiri [verfasserIn] Boyu Zhang [verfasserIn] Yan Ji [verfasserIn] Sankar N. Maity [verfasserIn] Min Hu [verfasserIn] Shanshan Bai [verfasserIn] Ana M. Aparicio [verfasserIn] Eleni Efstathiou [verfasserIn] Christopher J. Logothetis [verfasserIn] Nicholas Navin [verfasserIn] Nora M. Navone [verfasserIn] Yu Chen [verfasserIn] Filippo G. Giancotti [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	CP: Cancer

Übergeordnetes Werk:	In: Cell Reports - Elsevier, 2015, 39(2022), 1, Seite 110595-
Übergeordnetes Werk:	volume:39 ; year:2022 ; number:1 ; pages:110595-

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.celrep.2022.110595

Katalog-ID:	DOAJ050941992

Internformat


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520			\|a Summary: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC (MSPC), and neuroendocrine PC (NEPC). A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. These results define MSPC, trace its origin to therapy-induced lineage plasticity, and reveal its sensitivity to HER2/3 inhibition.
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700	0		\|a Yu Chen \|e verfasserin \|4 aut
700	0		\|a Filippo G. Giancotti \|e verfasserin \|4 aut
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allfields	10.1016/j.celrep.2022.110595 doi (DE-627)DOAJ050941992 (DE-599)DOAJ577c4a7ae5774bfabb0ebff830f751f6 DE-627 ger DE-627 rakwb eng QH301-705.5 Hyunho Han verfasserin aut Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC (MSPC), and neuroendocrine PC (NEPC). A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. These results define MSPC, trace its origin to therapy-induced lineage plasticity, and reveal its sensitivity to HER2/3 inhibition. CP: Cancer Biology (General) Yan Wang verfasserin aut Josue Curto verfasserin aut Sreeharsha Gurrapu verfasserin aut Sara Laudato verfasserin aut Alekya Rumandla verfasserin aut Goutam Chakraborty verfasserin aut Xiaobo Wang verfasserin aut Hong Chen verfasserin aut Yan Jiang verfasserin aut Dhiraj Kumar verfasserin aut Emily G. Caggiano verfasserin aut Monica Capogiri verfasserin aut Boyu Zhang verfasserin aut Yan Ji verfasserin aut Sankar N. Maity verfasserin aut Min Hu verfasserin aut Shanshan Bai verfasserin aut Ana M. Aparicio verfasserin aut Eleni Efstathiou verfasserin aut Christopher J. Logothetis verfasserin aut Nicholas Navin verfasserin aut Nora M. Navone verfasserin aut Yu Chen verfasserin aut Filippo G. Giancotti verfasserin aut In Cell Reports Elsevier, 2015 39(2022), 1, Seite 110595- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:39 year:2022 number:1 pages:110595- https://doi.org/10.1016/j.celrep.2022.110595 kostenfrei https://doaj.org/article/577c4a7ae5774bfabb0ebff830f751f6 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124722003436 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 39 2022 1 110595-
spelling	10.1016/j.celrep.2022.110595 doi (DE-627)DOAJ050941992 (DE-599)DOAJ577c4a7ae5774bfabb0ebff830f751f6 DE-627 ger DE-627 rakwb eng QH301-705.5 Hyunho Han verfasserin aut Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC (MSPC), and neuroendocrine PC (NEPC). A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. These results define MSPC, trace its origin to therapy-induced lineage plasticity, and reveal its sensitivity to HER2/3 inhibition. CP: Cancer Biology (General) Yan Wang verfasserin aut Josue Curto verfasserin aut Sreeharsha Gurrapu verfasserin aut Sara Laudato verfasserin aut Alekya Rumandla verfasserin aut Goutam Chakraborty verfasserin aut Xiaobo Wang verfasserin aut Hong Chen verfasserin aut Yan Jiang verfasserin aut Dhiraj Kumar verfasserin aut Emily G. Caggiano verfasserin aut Monica Capogiri verfasserin aut Boyu Zhang verfasserin aut Yan Ji verfasserin aut Sankar N. Maity verfasserin aut Min Hu verfasserin aut Shanshan Bai verfasserin aut Ana M. Aparicio verfasserin aut Eleni Efstathiou verfasserin aut Christopher J. Logothetis verfasserin aut Nicholas Navin verfasserin aut Nora M. Navone verfasserin aut Yu Chen verfasserin aut Filippo G. Giancotti verfasserin aut In Cell Reports Elsevier, 2015 39(2022), 1, Seite 110595- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:39 year:2022 number:1 pages:110595- https://doi.org/10.1016/j.celrep.2022.110595 kostenfrei https://doaj.org/article/577c4a7ae5774bfabb0ebff830f751f6 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124722003436 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 39 2022 1 110595-
allfields_unstemmed	10.1016/j.celrep.2022.110595 doi (DE-627)DOAJ050941992 (DE-599)DOAJ577c4a7ae5774bfabb0ebff830f751f6 DE-627 ger DE-627 rakwb eng QH301-705.5 Hyunho Han verfasserin aut Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC (MSPC), and neuroendocrine PC (NEPC). A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. These results define MSPC, trace its origin to therapy-induced lineage plasticity, and reveal its sensitivity to HER2/3 inhibition. CP: Cancer Biology (General) Yan Wang verfasserin aut Josue Curto verfasserin aut Sreeharsha Gurrapu verfasserin aut Sara Laudato verfasserin aut Alekya Rumandla verfasserin aut Goutam Chakraborty verfasserin aut Xiaobo Wang verfasserin aut Hong Chen verfasserin aut Yan Jiang verfasserin aut Dhiraj Kumar verfasserin aut Emily G. Caggiano verfasserin aut Monica Capogiri verfasserin aut Boyu Zhang verfasserin aut Yan Ji verfasserin aut Sankar N. Maity verfasserin aut Min Hu verfasserin aut Shanshan Bai verfasserin aut Ana M. Aparicio verfasserin aut Eleni Efstathiou verfasserin aut Christopher J. Logothetis verfasserin aut Nicholas Navin verfasserin aut Nora M. Navone verfasserin aut Yu Chen verfasserin aut Filippo G. Giancotti verfasserin aut In Cell Reports Elsevier, 2015 39(2022), 1, Seite 110595- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:39 year:2022 number:1 pages:110595- https://doi.org/10.1016/j.celrep.2022.110595 kostenfrei https://doaj.org/article/577c4a7ae5774bfabb0ebff830f751f6 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124722003436 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 39 2022 1 110595-
allfieldsGer	10.1016/j.celrep.2022.110595 doi (DE-627)DOAJ050941992 (DE-599)DOAJ577c4a7ae5774bfabb0ebff830f751f6 DE-627 ger DE-627 rakwb eng QH301-705.5 Hyunho Han verfasserin aut Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC (MSPC), and neuroendocrine PC (NEPC). A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. These results define MSPC, trace its origin to therapy-induced lineage plasticity, and reveal its sensitivity to HER2/3 inhibition. CP: Cancer Biology (General) Yan Wang verfasserin aut Josue Curto verfasserin aut Sreeharsha Gurrapu verfasserin aut Sara Laudato verfasserin aut Alekya Rumandla verfasserin aut Goutam Chakraborty verfasserin aut Xiaobo Wang verfasserin aut Hong Chen verfasserin aut Yan Jiang verfasserin aut Dhiraj Kumar verfasserin aut Emily G. Caggiano verfasserin aut Monica Capogiri verfasserin aut Boyu Zhang verfasserin aut Yan Ji verfasserin aut Sankar N. Maity verfasserin aut Min Hu verfasserin aut Shanshan Bai verfasserin aut Ana M. Aparicio verfasserin aut Eleni Efstathiou verfasserin aut Christopher J. Logothetis verfasserin aut Nicholas Navin verfasserin aut Nora M. Navone verfasserin aut Yu Chen verfasserin aut Filippo G. Giancotti verfasserin aut In Cell Reports Elsevier, 2015 39(2022), 1, Seite 110595- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:39 year:2022 number:1 pages:110595- https://doi.org/10.1016/j.celrep.2022.110595 kostenfrei https://doaj.org/article/577c4a7ae5774bfabb0ebff830f751f6 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124722003436 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 39 2022 1 110595-
allfieldsSound	10.1016/j.celrep.2022.110595 doi (DE-627)DOAJ050941992 (DE-599)DOAJ577c4a7ae5774bfabb0ebff830f751f6 DE-627 ger DE-627 rakwb eng QH301-705.5 Hyunho Han verfasserin aut Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC (MSPC), and neuroendocrine PC (NEPC). A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. These results define MSPC, trace its origin to therapy-induced lineage plasticity, and reveal its sensitivity to HER2/3 inhibition. CP: Cancer Biology (General) Yan Wang verfasserin aut Josue Curto verfasserin aut Sreeharsha Gurrapu verfasserin aut Sara Laudato verfasserin aut Alekya Rumandla verfasserin aut Goutam Chakraborty verfasserin aut Xiaobo Wang verfasserin aut Hong Chen verfasserin aut Yan Jiang verfasserin aut Dhiraj Kumar verfasserin aut Emily G. Caggiano verfasserin aut Monica Capogiri verfasserin aut Boyu Zhang verfasserin aut Yan Ji verfasserin aut Sankar N. Maity verfasserin aut Min Hu verfasserin aut Shanshan Bai verfasserin aut Ana M. Aparicio verfasserin aut Eleni Efstathiou verfasserin aut Christopher J. Logothetis verfasserin aut Nicholas Navin verfasserin aut Nora M. Navone verfasserin aut Yu Chen verfasserin aut Filippo G. Giancotti verfasserin aut In Cell Reports Elsevier, 2015 39(2022), 1, Seite 110595- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:39 year:2022 number:1 pages:110595- https://doi.org/10.1016/j.celrep.2022.110595 kostenfrei https://doaj.org/article/577c4a7ae5774bfabb0ebff830f751f6 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124722003436 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 39 2022 1 110595-
language	English
source	In Cell Reports 39(2022), 1, Seite 110595- volume:39 year:2022 number:1 pages:110595-
sourceStr	In Cell Reports 39(2022), 1, Seite 110595- volume:39 year:2022 number:1 pages:110595-
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	CP: Cancer Biology (General)
isfreeaccess_bool	true
container_title	Cell Reports
authorswithroles_txt_mv	Hyunho Han @@aut@@ Yan Wang @@aut@@ Josue Curto @@aut@@ Sreeharsha Gurrapu @@aut@@ Sara Laudato @@aut@@ Alekya Rumandla @@aut@@ Goutam Chakraborty @@aut@@ Xiaobo Wang @@aut@@ Hong Chen @@aut@@ Yan Jiang @@aut@@ Dhiraj Kumar @@aut@@ Emily G. Caggiano @@aut@@ Monica Capogiri @@aut@@ Boyu Zhang @@aut@@ Yan Ji @@aut@@ Sankar N. Maity @@aut@@ Min Hu @@aut@@ Shanshan Bai @@aut@@ Ana M. Aparicio @@aut@@ Eleni Efstathiou @@aut@@ Christopher J. Logothetis @@aut@@ Nicholas Navin @@aut@@ Nora M. Navone @@aut@@ Yu Chen @@aut@@ Filippo G. Giancotti @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	684964562
id	DOAJ050941992
language_de	englisch
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callnumber-first	Q - Science
author	Hyunho Han
spellingShingle	Hyunho Han misc QH301-705.5 misc CP: Cancer misc Biology (General) Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis
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topic_title	QH301-705.5 Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis CP: Cancer
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title	Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis
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title_full	Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis
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author_browse	Hyunho Han Yan Wang Josue Curto Sreeharsha Gurrapu Sara Laudato Alekya Rumandla Goutam Chakraborty Xiaobo Wang Hong Chen Yan Jiang Dhiraj Kumar Emily G. Caggiano Monica Capogiri Boyu Zhang Yan Ji Sankar N. Maity Min Hu Shanshan Bai Ana M. Aparicio Eleni Efstathiou Christopher J. Logothetis Nicholas Navin Nora M. Navone Yu Chen Filippo G. Giancotti
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title_sort	mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis
callnumber	QH301-705.5
title_auth	Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis
abstract	Summary: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC (MSPC), and neuroendocrine PC (NEPC). A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. These results define MSPC, trace its origin to therapy-induced lineage plasticity, and reveal its sensitivity to HER2/3 inhibition.
abstractGer	Summary: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC (MSPC), and neuroendocrine PC (NEPC). A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. These results define MSPC, trace its origin to therapy-induced lineage plasticity, and reveal its sensitivity to HER2/3 inhibition.
abstract_unstemmed	Summary: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC (MSPC), and neuroendocrine PC (NEPC). A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. These results define MSPC, trace its origin to therapy-induced lineage plasticity, and reveal its sensitivity to HER2/3 inhibition.
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title_short	Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis
url	https://doi.org/10.1016/j.celrep.2022.110595 https://doaj.org/article/577c4a7ae5774bfabb0ebff830f751f6 http://www.sciencedirect.com/science/article/pii/S2211124722003436 https://doaj.org/toc/2211-1247
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author2	Yan Wang Josue Curto Sreeharsha Gurrapu Sara Laudato Alekya Rumandla Goutam Chakraborty Xiaobo Wang Hong Chen Yan Jiang Dhiraj Kumar Emily G. Caggiano Monica Capogiri Boyu Zhang Yan Ji Sankar N. Maity Min Hu Shanshan Bai Ana M. Aparicio Eleni Efstathiou Christopher J. Logothetis Nicholas Navin Nora M. Navone Yu Chen Filippo G. Giancotti
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up_date	2024-07-03T17:35:22.274Z
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A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. 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Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis

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