High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it<

<p<Abstract</p< <p<Background</p< <p<The strong association between aberrant HDAC activity and the occurrence of cancer has led to the development of a variety of HDAC inhibitors (HDIs), which emerge as promising new targeted anticancer therapeutics.</p< <p<...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Neuhaus Peter [verfasserIn] Bahra Marcus [verfasserIn] Müller Berit [verfasserIn] Noske Aurelia [verfasserIn] Darb-Esfahani Silvia [verfasserIn] Buckendahl Ann-Christin [verfasserIn] Budczies Jan [verfasserIn] Denkert Carsten [verfasserIn] Lehmann Annika [verfasserIn] Dietel Manfred [verfasserIn] Kristiansen Glen [verfasserIn] Weichert Wilko [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2009

Übergeordnetes Werk:	In: BMC Cancer - BMC, 2003, 9(2009), 1, p 395
Übergeordnetes Werk:	volume:9 ; year:2009 ; number:1, p 395

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1471-2407-9-395

Katalog-ID:	DOAJ078467721

Internformat


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520			\|a <p<Abstract</p< <p<Background</p< <p<The strong association between aberrant HDAC activity and the occurrence of cancer has led to the development of a variety of HDAC inhibitors (HDIs), which emerge as promising new targeted anticancer therapeutics.</p< <p<Methods</p< <p<Due to the pivotal role of RelA/p65 in the tumorigenesis of pancreatic neoplasia we examined the expression of class I HDACs 1, 2 and 3 in a large cohort of human pancreatic carcinomas and correlated our findings with RelA/p65 expression status. Furthermore, we investigated the impact of the HDIs SAHA and VPA on RelA/p65 activity in pancreatic cancer cell culture models.</p< <p<Results</p< <p<Class I HDACs were strongly expressed in a subset of pancreatic adenocarcinomas and high expression was significantly correlated with increased nuclear translocation of RelA/p65 (p = 0.024). The link of HDAC activity and RelA/p65 in this tumor entity was confirmed <it<in vitro</it<, where RelA/p65 nuclear translocation as well as RelA/p65 DNA binding activity could be markedly diminished by HDI treatment.</p< <p<Conclusion</p< <p<The RelA/p65 inhibitory effects of SAHA and VPA <it<in vitro </it<and the close relationship of class I HDACs and RelA/p65 <it<in vivo </it<suggest that treatment with HDIs could serve as a promising approach to suppress NF-κB activity which in turn may lead to enhanced apoptosis and chemosensitization of pancreatic cancers.</p<
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author_variant	n p np b m bm m b mb n a na d e s des b a c bac b j bj d c dc l a la d m dm k g kg w w ww
matchkey_str	article:14712407:2009----::ihlsidcciiynepesoaesoitdihea6atvtoipnrai
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publishDate	2009
allfields	10.1186/1471-2407-9-395 doi (DE-627)DOAJ078467721 (DE-599)DOAJ291d60845cf24ac1a4b5ec732828b797 DE-627 ger DE-627 rakwb eng RC254-282 Neuhaus Peter verfasserin aut High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it< 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The strong association between aberrant HDAC activity and the occurrence of cancer has led to the development of a variety of HDAC inhibitors (HDIs), which emerge as promising new targeted anticancer therapeutics.</p< <p<Methods</p< <p<Due to the pivotal role of RelA/p65 in the tumorigenesis of pancreatic neoplasia we examined the expression of class I HDACs 1, 2 and 3 in a large cohort of human pancreatic carcinomas and correlated our findings with RelA/p65 expression status. Furthermore, we investigated the impact of the HDIs SAHA and VPA on RelA/p65 activity in pancreatic cancer cell culture models.</p< <p<Results</p< <p<Class I HDACs were strongly expressed in a subset of pancreatic adenocarcinomas and high expression was significantly correlated with increased nuclear translocation of RelA/p65 (p = 0.024). The link of HDAC activity and RelA/p65 in this tumor entity was confirmed <it<in vitro</it<, where RelA/p65 nuclear translocation as well as RelA/p65 DNA binding activity could be markedly diminished by HDI treatment.</p< <p<Conclusion</p< <p<The RelA/p65 inhibitory effects of SAHA and VPA <it<in vitro </it<and the close relationship of class I HDACs and RelA/p65 <it<in vivo </it<suggest that treatment with HDIs could serve as a promising approach to suppress NF-κB activity which in turn may lead to enhanced apoptosis and chemosensitization of pancreatic cancers.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Bahra Marcus verfasserin aut Müller Berit verfasserin aut Noske Aurelia verfasserin aut Darb-Esfahani Silvia verfasserin aut Buckendahl Ann-Christin verfasserin aut Budczies Jan verfasserin aut Denkert Carsten verfasserin aut Lehmann Annika verfasserin aut Dietel Manfred verfasserin aut Kristiansen Glen verfasserin aut Weichert Wilko verfasserin aut In BMC Cancer BMC, 2003 9(2009), 1, p 395 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:9 year:2009 number:1, p 395 https://doi.org/10.1186/1471-2407-9-395 kostenfrei https://doaj.org/article/291d60845cf24ac1a4b5ec732828b797 kostenfrei http://www.biomedcentral.com/1471-2407/9/395 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 2009 1, p 395
spelling	10.1186/1471-2407-9-395 doi (DE-627)DOAJ078467721 (DE-599)DOAJ291d60845cf24ac1a4b5ec732828b797 DE-627 ger DE-627 rakwb eng RC254-282 Neuhaus Peter verfasserin aut High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it< 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The strong association between aberrant HDAC activity and the occurrence of cancer has led to the development of a variety of HDAC inhibitors (HDIs), which emerge as promising new targeted anticancer therapeutics.</p< <p<Methods</p< <p<Due to the pivotal role of RelA/p65 in the tumorigenesis of pancreatic neoplasia we examined the expression of class I HDACs 1, 2 and 3 in a large cohort of human pancreatic carcinomas and correlated our findings with RelA/p65 expression status. Furthermore, we investigated the impact of the HDIs SAHA and VPA on RelA/p65 activity in pancreatic cancer cell culture models.</p< <p<Results</p< <p<Class I HDACs were strongly expressed in a subset of pancreatic adenocarcinomas and high expression was significantly correlated with increased nuclear translocation of RelA/p65 (p = 0.024). The link of HDAC activity and RelA/p65 in this tumor entity was confirmed <it<in vitro</it<, where RelA/p65 nuclear translocation as well as RelA/p65 DNA binding activity could be markedly diminished by HDI treatment.</p< <p<Conclusion</p< <p<The RelA/p65 inhibitory effects of SAHA and VPA <it<in vitro </it<and the close relationship of class I HDACs and RelA/p65 <it<in vivo </it<suggest that treatment with HDIs could serve as a promising approach to suppress NF-κB activity which in turn may lead to enhanced apoptosis and chemosensitization of pancreatic cancers.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Bahra Marcus verfasserin aut Müller Berit verfasserin aut Noske Aurelia verfasserin aut Darb-Esfahani Silvia verfasserin aut Buckendahl Ann-Christin verfasserin aut Budczies Jan verfasserin aut Denkert Carsten verfasserin aut Lehmann Annika verfasserin aut Dietel Manfred verfasserin aut Kristiansen Glen verfasserin aut Weichert Wilko verfasserin aut In BMC Cancer BMC, 2003 9(2009), 1, p 395 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:9 year:2009 number:1, p 395 https://doi.org/10.1186/1471-2407-9-395 kostenfrei https://doaj.org/article/291d60845cf24ac1a4b5ec732828b797 kostenfrei http://www.biomedcentral.com/1471-2407/9/395 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 2009 1, p 395
allfields_unstemmed	10.1186/1471-2407-9-395 doi (DE-627)DOAJ078467721 (DE-599)DOAJ291d60845cf24ac1a4b5ec732828b797 DE-627 ger DE-627 rakwb eng RC254-282 Neuhaus Peter verfasserin aut High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it< 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The strong association between aberrant HDAC activity and the occurrence of cancer has led to the development of a variety of HDAC inhibitors (HDIs), which emerge as promising new targeted anticancer therapeutics.</p< <p<Methods</p< <p<Due to the pivotal role of RelA/p65 in the tumorigenesis of pancreatic neoplasia we examined the expression of class I HDACs 1, 2 and 3 in a large cohort of human pancreatic carcinomas and correlated our findings with RelA/p65 expression status. Furthermore, we investigated the impact of the HDIs SAHA and VPA on RelA/p65 activity in pancreatic cancer cell culture models.</p< <p<Results</p< <p<Class I HDACs were strongly expressed in a subset of pancreatic adenocarcinomas and high expression was significantly correlated with increased nuclear translocation of RelA/p65 (p = 0.024). The link of HDAC activity and RelA/p65 in this tumor entity was confirmed <it<in vitro</it<, where RelA/p65 nuclear translocation as well as RelA/p65 DNA binding activity could be markedly diminished by HDI treatment.</p< <p<Conclusion</p< <p<The RelA/p65 inhibitory effects of SAHA and VPA <it<in vitro </it<and the close relationship of class I HDACs and RelA/p65 <it<in vivo </it<suggest that treatment with HDIs could serve as a promising approach to suppress NF-κB activity which in turn may lead to enhanced apoptosis and chemosensitization of pancreatic cancers.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Bahra Marcus verfasserin aut Müller Berit verfasserin aut Noske Aurelia verfasserin aut Darb-Esfahani Silvia verfasserin aut Buckendahl Ann-Christin verfasserin aut Budczies Jan verfasserin aut Denkert Carsten verfasserin aut Lehmann Annika verfasserin aut Dietel Manfred verfasserin aut Kristiansen Glen verfasserin aut Weichert Wilko verfasserin aut In BMC Cancer BMC, 2003 9(2009), 1, p 395 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:9 year:2009 number:1, p 395 https://doi.org/10.1186/1471-2407-9-395 kostenfrei https://doaj.org/article/291d60845cf24ac1a4b5ec732828b797 kostenfrei http://www.biomedcentral.com/1471-2407/9/395 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 2009 1, p 395
allfieldsGer	10.1186/1471-2407-9-395 doi (DE-627)DOAJ078467721 (DE-599)DOAJ291d60845cf24ac1a4b5ec732828b797 DE-627 ger DE-627 rakwb eng RC254-282 Neuhaus Peter verfasserin aut High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it< 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The strong association between aberrant HDAC activity and the occurrence of cancer has led to the development of a variety of HDAC inhibitors (HDIs), which emerge as promising new targeted anticancer therapeutics.</p< <p<Methods</p< <p<Due to the pivotal role of RelA/p65 in the tumorigenesis of pancreatic neoplasia we examined the expression of class I HDACs 1, 2 and 3 in a large cohort of human pancreatic carcinomas and correlated our findings with RelA/p65 expression status. Furthermore, we investigated the impact of the HDIs SAHA and VPA on RelA/p65 activity in pancreatic cancer cell culture models.</p< <p<Results</p< <p<Class I HDACs were strongly expressed in a subset of pancreatic adenocarcinomas and high expression was significantly correlated with increased nuclear translocation of RelA/p65 (p = 0.024). The link of HDAC activity and RelA/p65 in this tumor entity was confirmed <it<in vitro</it<, where RelA/p65 nuclear translocation as well as RelA/p65 DNA binding activity could be markedly diminished by HDI treatment.</p< <p<Conclusion</p< <p<The RelA/p65 inhibitory effects of SAHA and VPA <it<in vitro </it<and the close relationship of class I HDACs and RelA/p65 <it<in vivo </it<suggest that treatment with HDIs could serve as a promising approach to suppress NF-κB activity which in turn may lead to enhanced apoptosis and chemosensitization of pancreatic cancers.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Bahra Marcus verfasserin aut Müller Berit verfasserin aut Noske Aurelia verfasserin aut Darb-Esfahani Silvia verfasserin aut Buckendahl Ann-Christin verfasserin aut Budczies Jan verfasserin aut Denkert Carsten verfasserin aut Lehmann Annika verfasserin aut Dietel Manfred verfasserin aut Kristiansen Glen verfasserin aut Weichert Wilko verfasserin aut In BMC Cancer BMC, 2003 9(2009), 1, p 395 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:9 year:2009 number:1, p 395 https://doi.org/10.1186/1471-2407-9-395 kostenfrei https://doaj.org/article/291d60845cf24ac1a4b5ec732828b797 kostenfrei http://www.biomedcentral.com/1471-2407/9/395 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 2009 1, p 395
allfieldsSound	10.1186/1471-2407-9-395 doi (DE-627)DOAJ078467721 (DE-599)DOAJ291d60845cf24ac1a4b5ec732828b797 DE-627 ger DE-627 rakwb eng RC254-282 Neuhaus Peter verfasserin aut High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it< 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The strong association between aberrant HDAC activity and the occurrence of cancer has led to the development of a variety of HDAC inhibitors (HDIs), which emerge as promising new targeted anticancer therapeutics.</p< <p<Methods</p< <p<Due to the pivotal role of RelA/p65 in the tumorigenesis of pancreatic neoplasia we examined the expression of class I HDACs 1, 2 and 3 in a large cohort of human pancreatic carcinomas and correlated our findings with RelA/p65 expression status. Furthermore, we investigated the impact of the HDIs SAHA and VPA on RelA/p65 activity in pancreatic cancer cell culture models.</p< <p<Results</p< <p<Class I HDACs were strongly expressed in a subset of pancreatic adenocarcinomas and high expression was significantly correlated with increased nuclear translocation of RelA/p65 (p = 0.024). The link of HDAC activity and RelA/p65 in this tumor entity was confirmed <it<in vitro</it<, where RelA/p65 nuclear translocation as well as RelA/p65 DNA binding activity could be markedly diminished by HDI treatment.</p< <p<Conclusion</p< <p<The RelA/p65 inhibitory effects of SAHA and VPA <it<in vitro </it<and the close relationship of class I HDACs and RelA/p65 <it<in vivo </it<suggest that treatment with HDIs could serve as a promising approach to suppress NF-κB activity which in turn may lead to enhanced apoptosis and chemosensitization of pancreatic cancers.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Bahra Marcus verfasserin aut Müller Berit verfasserin aut Noske Aurelia verfasserin aut Darb-Esfahani Silvia verfasserin aut Buckendahl Ann-Christin verfasserin aut Budczies Jan verfasserin aut Denkert Carsten verfasserin aut Lehmann Annika verfasserin aut Dietel Manfred verfasserin aut Kristiansen Glen verfasserin aut Weichert Wilko verfasserin aut In BMC Cancer BMC, 2003 9(2009), 1, p 395 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:9 year:2009 number:1, p 395 https://doi.org/10.1186/1471-2407-9-395 kostenfrei https://doaj.org/article/291d60845cf24ac1a4b5ec732828b797 kostenfrei http://www.biomedcentral.com/1471-2407/9/395 kostenfrei https://doaj.org/toc/1471-2407 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 2009 1, p 395
language	English
source	In BMC Cancer 9(2009), 1, p 395 volume:9 year:2009 number:1, p 395
sourceStr	In BMC Cancer 9(2009), 1, p 395 volume:9 year:2009 number:1, p 395
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Neoplasms. Tumors. Oncology. Including cancer and carcinogens
isfreeaccess_bool	true
container_title	BMC Cancer
authorswithroles_txt_mv	Neuhaus Peter @@aut@@ Bahra Marcus @@aut@@ Müller Berit @@aut@@ Noske Aurelia @@aut@@ Darb-Esfahani Silvia @@aut@@ Buckendahl Ann-Christin @@aut@@ Budczies Jan @@aut@@ Denkert Carsten @@aut@@ Lehmann Annika @@aut@@ Dietel Manfred @@aut@@ Kristiansen Glen @@aut@@ Weichert Wilko @@aut@@
publishDateDaySort_date	2009-01-01T00:00:00Z
hierarchy_top_id	326643710
id	DOAJ078467721
language_de	englisch
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callnumber-first	R - Medicine
author	Neuhaus Peter
spellingShingle	Neuhaus Peter misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it<
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topic_title	RC254-282 High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it<
topic	misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it<
ctrlnum	(DE-627)DOAJ078467721 (DE-599)DOAJ291d60845cf24ac1a4b5ec732828b797
title_full	High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it<
author_sort	Neuhaus Peter
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author_browse	Neuhaus Peter Bahra Marcus Müller Berit Noske Aurelia Darb-Esfahani Silvia Buckendahl Ann-Christin Budczies Jan Denkert Carsten Lehmann Annika Dietel Manfred Kristiansen Glen Weichert Wilko
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title_sort	high class i hdac activity and expression are associated with rela/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it<
callnumber	RC254-282
title_auth	High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it<
abstract	<p<Abstract</p< <p<Background</p< <p<The strong association between aberrant HDAC activity and the occurrence of cancer has led to the development of a variety of HDAC inhibitors (HDIs), which emerge as promising new targeted anticancer therapeutics.</p< <p<Methods</p< <p<Due to the pivotal role of RelA/p65 in the tumorigenesis of pancreatic neoplasia we examined the expression of class I HDACs 1, 2 and 3 in a large cohort of human pancreatic carcinomas and correlated our findings with RelA/p65 expression status. Furthermore, we investigated the impact of the HDIs SAHA and VPA on RelA/p65 activity in pancreatic cancer cell culture models.</p< <p<Results</p< <p<Class I HDACs were strongly expressed in a subset of pancreatic adenocarcinomas and high expression was significantly correlated with increased nuclear translocation of RelA/p65 (p = 0.024). The link of HDAC activity and RelA/p65 in this tumor entity was confirmed <it<in vitro</it<, where RelA/p65 nuclear translocation as well as RelA/p65 DNA binding activity could be markedly diminished by HDI treatment.</p< <p<Conclusion</p< <p<The RelA/p65 inhibitory effects of SAHA and VPA <it<in vitro </it<and the close relationship of class I HDACs and RelA/p65 <it<in vivo </it<suggest that treatment with HDIs could serve as a promising approach to suppress NF-κB activity which in turn may lead to enhanced apoptosis and chemosensitization of pancreatic cancers.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<The strong association between aberrant HDAC activity and the occurrence of cancer has led to the development of a variety of HDAC inhibitors (HDIs), which emerge as promising new targeted anticancer therapeutics.</p< <p<Methods</p< <p<Due to the pivotal role of RelA/p65 in the tumorigenesis of pancreatic neoplasia we examined the expression of class I HDACs 1, 2 and 3 in a large cohort of human pancreatic carcinomas and correlated our findings with RelA/p65 expression status. Furthermore, we investigated the impact of the HDIs SAHA and VPA on RelA/p65 activity in pancreatic cancer cell culture models.</p< <p<Results</p< <p<Class I HDACs were strongly expressed in a subset of pancreatic adenocarcinomas and high expression was significantly correlated with increased nuclear translocation of RelA/p65 (p = 0.024). The link of HDAC activity and RelA/p65 in this tumor entity was confirmed <it<in vitro</it<, where RelA/p65 nuclear translocation as well as RelA/p65 DNA binding activity could be markedly diminished by HDI treatment.</p< <p<Conclusion</p< <p<The RelA/p65 inhibitory effects of SAHA and VPA <it<in vitro </it<and the close relationship of class I HDACs and RelA/p65 <it<in vivo </it<suggest that treatment with HDIs could serve as a promising approach to suppress NF-κB activity which in turn may lead to enhanced apoptosis and chemosensitization of pancreatic cancers.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<The strong association between aberrant HDAC activity and the occurrence of cancer has led to the development of a variety of HDAC inhibitors (HDIs), which emerge as promising new targeted anticancer therapeutics.</p< <p<Methods</p< <p<Due to the pivotal role of RelA/p65 in the tumorigenesis of pancreatic neoplasia we examined the expression of class I HDACs 1, 2 and 3 in a large cohort of human pancreatic carcinomas and correlated our findings with RelA/p65 expression status. Furthermore, we investigated the impact of the HDIs SAHA and VPA on RelA/p65 activity in pancreatic cancer cell culture models.</p< <p<Results</p< <p<Class I HDACs were strongly expressed in a subset of pancreatic adenocarcinomas and high expression was significantly correlated with increased nuclear translocation of RelA/p65 (p = 0.024). The link of HDAC activity and RelA/p65 in this tumor entity was confirmed <it<in vitro</it<, where RelA/p65 nuclear translocation as well as RelA/p65 DNA binding activity could be markedly diminished by HDI treatment.</p< <p<Conclusion</p< <p<The RelA/p65 inhibitory effects of SAHA and VPA <it<in vitro </it<and the close relationship of class I HDACs and RelA/p65 <it<in vivo </it<suggest that treatment with HDIs could serve as a promising approach to suppress NF-κB activity which in turn may lead to enhanced apoptosis and chemosensitization of pancreatic cancers.</p<
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title_short	High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it<
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High class I HDAC activity and expression are associated with RelA/p65 activation in pancreatic cancer <it<in vitro </it<and <it<in vivo</it<

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