Targeting the UPS as therapy in multiple myeloma

Abstract The coordinated regulation of cellular protein synthesis and degradation is essential for normal cellular functioning. The ubiquitin proteasome system mediates the intracellular protein degradation that is required for normal cellular homeostasis. The 26S proteasome is a multi-enzyme protea...
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Autor*in:	Chauhan, Dharminder [verfasserIn] Bianchi, Giada Anderson, Kenneth C

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2008

Schlagwörter:	Bortezomib Lenalidomide Proteasome Inhibitor HDAC Inhibitor Ubiquitin Proteasome System

Anmerkung:	© Chauhan et al; licensee BioMed Central Ltd. 2008

Übergeordnetes Werk:	Enthalten in: BMC biochemistry - London : BioMed Central, 2000, 9(2008), Suppl 1 vom: 21. Okt.
Übergeordnetes Werk:	volume:9 ; year:2008 ; number:Suppl 1 ; day:21 ; month:10

Links:	Volltext

DOI / URN:	10.1186/1471-2091-9-S1-S1

Katalog-ID:	SPR02681580X

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520			\|a Abstract The coordinated regulation of cellular protein synthesis and degradation is essential for normal cellular functioning. The ubiquitin proteasome system mediates the intracellular protein degradation that is required for normal cellular homeostasis. The 26S proteasome is a multi-enzyme protease that degrades redundant proteins; conversely, inhibition of proteasomal degradation results in intracellular aggregation of unwanted proteins and cell death. This observation led to the development of proteasome inhibitors as therapeutics for use in cancer. The clinical applicability of targeting proteasomes is exemplified by the recent FDA approval of the first proteasome inhibitor, bortezomib, for the treatment of relapsed/refractory multiple myeloma. Although bortezomib represents a major advance in the treatment of this disease, it can be associated with toxicity and the development of drug resistance. Importantly, extensive preclinical studies suggest that combination therapies can both circumvent drug resistance and reduce toxicity. In addition, promising novel proteasome inhibitors, which are distinct from bortezomib, and exhibit equipotent anti-multiple myeloma activities, are undergoing clinical evaluation in order to improve patient outcome in multiple myeloma. Publication history Republished from Current BioData's Targeted Proteins database (TPdb; http://www.targetedproteinsdb.com).
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allfields	10.1186/1471-2091-9-S1-S1 doi (DE-627)SPR02681580X (SPR)1471-2091-9-S1-S1-e DE-627 ger DE-627 rakwb eng Chauhan, Dharminder verfasserin aut Targeting the UPS as therapy in multiple myeloma 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Chauhan et al; licensee BioMed Central Ltd. 2008 Abstract The coordinated regulation of cellular protein synthesis and degradation is essential for normal cellular functioning. The ubiquitin proteasome system mediates the intracellular protein degradation that is required for normal cellular homeostasis. The 26S proteasome is a multi-enzyme protease that degrades redundant proteins; conversely, inhibition of proteasomal degradation results in intracellular aggregation of unwanted proteins and cell death. This observation led to the development of proteasome inhibitors as therapeutics for use in cancer. The clinical applicability of targeting proteasomes is exemplified by the recent FDA approval of the first proteasome inhibitor, bortezomib, for the treatment of relapsed/refractory multiple myeloma. Although bortezomib represents a major advance in the treatment of this disease, it can be associated with toxicity and the development of drug resistance. Importantly, extensive preclinical studies suggest that combination therapies can both circumvent drug resistance and reduce toxicity. In addition, promising novel proteasome inhibitors, which are distinct from bortezomib, and exhibit equipotent anti-multiple myeloma activities, are undergoing clinical evaluation in order to improve patient outcome in multiple myeloma. Publication history Republished from Current BioData's Targeted Proteins database (TPdb; http://www.targetedproteinsdb.com). Bortezomib (dpeaa)DE-He213 Lenalidomide (dpeaa)DE-He213 Proteasome Inhibitor (dpeaa)DE-He213 HDAC Inhibitor (dpeaa)DE-He213 Ubiquitin Proteasome System (dpeaa)DE-He213 Bianchi, Giada aut Anderson, Kenneth C aut Enthalten in BMC biochemistry London : BioMed Central, 2000 9(2008), Suppl 1 vom: 21. Okt. (DE-627)326179399 (DE-600)2041216-2 1471-2091 nnns volume:9 year:2008 number:Suppl 1 day:21 month:10 https://dx.doi.org/10.1186/1471-2091-9-S1-S1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2008 Suppl 1 21 10
spelling	10.1186/1471-2091-9-S1-S1 doi (DE-627)SPR02681580X (SPR)1471-2091-9-S1-S1-e DE-627 ger DE-627 rakwb eng Chauhan, Dharminder verfasserin aut Targeting the UPS as therapy in multiple myeloma 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Chauhan et al; licensee BioMed Central Ltd. 2008 Abstract The coordinated regulation of cellular protein synthesis and degradation is essential for normal cellular functioning. The ubiquitin proteasome system mediates the intracellular protein degradation that is required for normal cellular homeostasis. The 26S proteasome is a multi-enzyme protease that degrades redundant proteins; conversely, inhibition of proteasomal degradation results in intracellular aggregation of unwanted proteins and cell death. This observation led to the development of proteasome inhibitors as therapeutics for use in cancer. The clinical applicability of targeting proteasomes is exemplified by the recent FDA approval of the first proteasome inhibitor, bortezomib, for the treatment of relapsed/refractory multiple myeloma. Although bortezomib represents a major advance in the treatment of this disease, it can be associated with toxicity and the development of drug resistance. Importantly, extensive preclinical studies suggest that combination therapies can both circumvent drug resistance and reduce toxicity. In addition, promising novel proteasome inhibitors, which are distinct from bortezomib, and exhibit equipotent anti-multiple myeloma activities, are undergoing clinical evaluation in order to improve patient outcome in multiple myeloma. Publication history Republished from Current BioData's Targeted Proteins database (TPdb; http://www.targetedproteinsdb.com). Bortezomib (dpeaa)DE-He213 Lenalidomide (dpeaa)DE-He213 Proteasome Inhibitor (dpeaa)DE-He213 HDAC Inhibitor (dpeaa)DE-He213 Ubiquitin Proteasome System (dpeaa)DE-He213 Bianchi, Giada aut Anderson, Kenneth C aut Enthalten in BMC biochemistry London : BioMed Central, 2000 9(2008), Suppl 1 vom: 21. Okt. (DE-627)326179399 (DE-600)2041216-2 1471-2091 nnns volume:9 year:2008 number:Suppl 1 day:21 month:10 https://dx.doi.org/10.1186/1471-2091-9-S1-S1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2008 Suppl 1 21 10
allfields_unstemmed	10.1186/1471-2091-9-S1-S1 doi (DE-627)SPR02681580X (SPR)1471-2091-9-S1-S1-e DE-627 ger DE-627 rakwb eng Chauhan, Dharminder verfasserin aut Targeting the UPS as therapy in multiple myeloma 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Chauhan et al; licensee BioMed Central Ltd. 2008 Abstract The coordinated regulation of cellular protein synthesis and degradation is essential for normal cellular functioning. The ubiquitin proteasome system mediates the intracellular protein degradation that is required for normal cellular homeostasis. The 26S proteasome is a multi-enzyme protease that degrades redundant proteins; conversely, inhibition of proteasomal degradation results in intracellular aggregation of unwanted proteins and cell death. This observation led to the development of proteasome inhibitors as therapeutics for use in cancer. The clinical applicability of targeting proteasomes is exemplified by the recent FDA approval of the first proteasome inhibitor, bortezomib, for the treatment of relapsed/refractory multiple myeloma. Although bortezomib represents a major advance in the treatment of this disease, it can be associated with toxicity and the development of drug resistance. Importantly, extensive preclinical studies suggest that combination therapies can both circumvent drug resistance and reduce toxicity. In addition, promising novel proteasome inhibitors, which are distinct from bortezomib, and exhibit equipotent anti-multiple myeloma activities, are undergoing clinical evaluation in order to improve patient outcome in multiple myeloma. Publication history Republished from Current BioData's Targeted Proteins database (TPdb; http://www.targetedproteinsdb.com). Bortezomib (dpeaa)DE-He213 Lenalidomide (dpeaa)DE-He213 Proteasome Inhibitor (dpeaa)DE-He213 HDAC Inhibitor (dpeaa)DE-He213 Ubiquitin Proteasome System (dpeaa)DE-He213 Bianchi, Giada aut Anderson, Kenneth C aut Enthalten in BMC biochemistry London : BioMed Central, 2000 9(2008), Suppl 1 vom: 21. Okt. (DE-627)326179399 (DE-600)2041216-2 1471-2091 nnns volume:9 year:2008 number:Suppl 1 day:21 month:10 https://dx.doi.org/10.1186/1471-2091-9-S1-S1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2008 Suppl 1 21 10
allfieldsGer	10.1186/1471-2091-9-S1-S1 doi (DE-627)SPR02681580X (SPR)1471-2091-9-S1-S1-e DE-627 ger DE-627 rakwb eng Chauhan, Dharminder verfasserin aut Targeting the UPS as therapy in multiple myeloma 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Chauhan et al; licensee BioMed Central Ltd. 2008 Abstract The coordinated regulation of cellular protein synthesis and degradation is essential for normal cellular functioning. The ubiquitin proteasome system mediates the intracellular protein degradation that is required for normal cellular homeostasis. The 26S proteasome is a multi-enzyme protease that degrades redundant proteins; conversely, inhibition of proteasomal degradation results in intracellular aggregation of unwanted proteins and cell death. This observation led to the development of proteasome inhibitors as therapeutics for use in cancer. The clinical applicability of targeting proteasomes is exemplified by the recent FDA approval of the first proteasome inhibitor, bortezomib, for the treatment of relapsed/refractory multiple myeloma. Although bortezomib represents a major advance in the treatment of this disease, it can be associated with toxicity and the development of drug resistance. Importantly, extensive preclinical studies suggest that combination therapies can both circumvent drug resistance and reduce toxicity. In addition, promising novel proteasome inhibitors, which are distinct from bortezomib, and exhibit equipotent anti-multiple myeloma activities, are undergoing clinical evaluation in order to improve patient outcome in multiple myeloma. Publication history Republished from Current BioData's Targeted Proteins database (TPdb; http://www.targetedproteinsdb.com). Bortezomib (dpeaa)DE-He213 Lenalidomide (dpeaa)DE-He213 Proteasome Inhibitor (dpeaa)DE-He213 HDAC Inhibitor (dpeaa)DE-He213 Ubiquitin Proteasome System (dpeaa)DE-He213 Bianchi, Giada aut Anderson, Kenneth C aut Enthalten in BMC biochemistry London : BioMed Central, 2000 9(2008), Suppl 1 vom: 21. Okt. (DE-627)326179399 (DE-600)2041216-2 1471-2091 nnns volume:9 year:2008 number:Suppl 1 day:21 month:10 https://dx.doi.org/10.1186/1471-2091-9-S1-S1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2008 Suppl 1 21 10
allfieldsSound	10.1186/1471-2091-9-S1-S1 doi (DE-627)SPR02681580X (SPR)1471-2091-9-S1-S1-e DE-627 ger DE-627 rakwb eng Chauhan, Dharminder verfasserin aut Targeting the UPS as therapy in multiple myeloma 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Chauhan et al; licensee BioMed Central Ltd. 2008 Abstract The coordinated regulation of cellular protein synthesis and degradation is essential for normal cellular functioning. The ubiquitin proteasome system mediates the intracellular protein degradation that is required for normal cellular homeostasis. The 26S proteasome is a multi-enzyme protease that degrades redundant proteins; conversely, inhibition of proteasomal degradation results in intracellular aggregation of unwanted proteins and cell death. This observation led to the development of proteasome inhibitors as therapeutics for use in cancer. The clinical applicability of targeting proteasomes is exemplified by the recent FDA approval of the first proteasome inhibitor, bortezomib, for the treatment of relapsed/refractory multiple myeloma. Although bortezomib represents a major advance in the treatment of this disease, it can be associated with toxicity and the development of drug resistance. Importantly, extensive preclinical studies suggest that combination therapies can both circumvent drug resistance and reduce toxicity. In addition, promising novel proteasome inhibitors, which are distinct from bortezomib, and exhibit equipotent anti-multiple myeloma activities, are undergoing clinical evaluation in order to improve patient outcome in multiple myeloma. Publication history Republished from Current BioData's Targeted Proteins database (TPdb; http://www.targetedproteinsdb.com). Bortezomib (dpeaa)DE-He213 Lenalidomide (dpeaa)DE-He213 Proteasome Inhibitor (dpeaa)DE-He213 HDAC Inhibitor (dpeaa)DE-He213 Ubiquitin Proteasome System (dpeaa)DE-He213 Bianchi, Giada aut Anderson, Kenneth C aut Enthalten in BMC biochemistry London : BioMed Central, 2000 9(2008), Suppl 1 vom: 21. Okt. (DE-627)326179399 (DE-600)2041216-2 1471-2091 nnns volume:9 year:2008 number:Suppl 1 day:21 month:10 https://dx.doi.org/10.1186/1471-2091-9-S1-S1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2008 Suppl 1 21 10
language	English
source	Enthalten in BMC biochemistry 9(2008), Suppl 1 vom: 21. Okt. volume:9 year:2008 number:Suppl 1 day:21 month:10
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author	Chauhan, Dharminder
spellingShingle	Chauhan, Dharminder misc Bortezomib misc Lenalidomide misc Proteasome Inhibitor misc HDAC Inhibitor misc Ubiquitin Proteasome System Targeting the UPS as therapy in multiple myeloma
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topic_title	Targeting the UPS as therapy in multiple myeloma Bortezomib (dpeaa)DE-He213 Lenalidomide (dpeaa)DE-He213 Proteasome Inhibitor (dpeaa)DE-He213 HDAC Inhibitor (dpeaa)DE-He213 Ubiquitin Proteasome System (dpeaa)DE-He213
topic	misc Bortezomib misc Lenalidomide misc Proteasome Inhibitor misc HDAC Inhibitor misc Ubiquitin Proteasome System
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title	Targeting the UPS as therapy in multiple myeloma
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title_sort	targeting the ups as therapy in multiple myeloma
title_auth	Targeting the UPS as therapy in multiple myeloma
abstract	Abstract The coordinated regulation of cellular protein synthesis and degradation is essential for normal cellular functioning. The ubiquitin proteasome system mediates the intracellular protein degradation that is required for normal cellular homeostasis. The 26S proteasome is a multi-enzyme protease that degrades redundant proteins; conversely, inhibition of proteasomal degradation results in intracellular aggregation of unwanted proteins and cell death. This observation led to the development of proteasome inhibitors as therapeutics for use in cancer. The clinical applicability of targeting proteasomes is exemplified by the recent FDA approval of the first proteasome inhibitor, bortezomib, for the treatment of relapsed/refractory multiple myeloma. Although bortezomib represents a major advance in the treatment of this disease, it can be associated with toxicity and the development of drug resistance. Importantly, extensive preclinical studies suggest that combination therapies can both circumvent drug resistance and reduce toxicity. In addition, promising novel proteasome inhibitors, which are distinct from bortezomib, and exhibit equipotent anti-multiple myeloma activities, are undergoing clinical evaluation in order to improve patient outcome in multiple myeloma. Publication history Republished from Current BioData's Targeted Proteins database (TPdb; http://www.targetedproteinsdb.com). © Chauhan et al; licensee BioMed Central Ltd. 2008
abstractGer	Abstract The coordinated regulation of cellular protein synthesis and degradation is essential for normal cellular functioning. The ubiquitin proteasome system mediates the intracellular protein degradation that is required for normal cellular homeostasis. The 26S proteasome is a multi-enzyme protease that degrades redundant proteins; conversely, inhibition of proteasomal degradation results in intracellular aggregation of unwanted proteins and cell death. This observation led to the development of proteasome inhibitors as therapeutics for use in cancer. The clinical applicability of targeting proteasomes is exemplified by the recent FDA approval of the first proteasome inhibitor, bortezomib, for the treatment of relapsed/refractory multiple myeloma. Although bortezomib represents a major advance in the treatment of this disease, it can be associated with toxicity and the development of drug resistance. Importantly, extensive preclinical studies suggest that combination therapies can both circumvent drug resistance and reduce toxicity. In addition, promising novel proteasome inhibitors, which are distinct from bortezomib, and exhibit equipotent anti-multiple myeloma activities, are undergoing clinical evaluation in order to improve patient outcome in multiple myeloma. Publication history Republished from Current BioData's Targeted Proteins database (TPdb; http://www.targetedproteinsdb.com). © Chauhan et al; licensee BioMed Central Ltd. 2008
abstract_unstemmed	Abstract The coordinated regulation of cellular protein synthesis and degradation is essential for normal cellular functioning. The ubiquitin proteasome system mediates the intracellular protein degradation that is required for normal cellular homeostasis. The 26S proteasome is a multi-enzyme protease that degrades redundant proteins; conversely, inhibition of proteasomal degradation results in intracellular aggregation of unwanted proteins and cell death. This observation led to the development of proteasome inhibitors as therapeutics for use in cancer. The clinical applicability of targeting proteasomes is exemplified by the recent FDA approval of the first proteasome inhibitor, bortezomib, for the treatment of relapsed/refractory multiple myeloma. Although bortezomib represents a major advance in the treatment of this disease, it can be associated with toxicity and the development of drug resistance. Importantly, extensive preclinical studies suggest that combination therapies can both circumvent drug resistance and reduce toxicity. In addition, promising novel proteasome inhibitors, which are distinct from bortezomib, and exhibit equipotent anti-multiple myeloma activities, are undergoing clinical evaluation in order to improve patient outcome in multiple myeloma. Publication history Republished from Current BioData's Targeted Proteins database (TPdb; http://www.targetedproteinsdb.com). © Chauhan et al; licensee BioMed Central Ltd. 2008
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