Opposite role of Bax and BCL-2 in the anti-tumoral responses of the immune system

<p<Abstract</p< <p<Background</p< <p<The relative role of anti apoptotic (i.e. Bcl-2) or pro-apoptotic (e.g. Bax) proteins in tumor progression is still not completely understood.</p< <p<Methods</p< <p<The rat glioma cell line A15A5 was stably tr...
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Autor*in:	Bougras Gwenola [verfasserIn] Cartron Pierre-François [verfasserIn] Gautier Fabien [verfasserIn] Martin Stéphane [verfasserIn] LeCabellec Marité [verfasserIn] Meflah Khaled [verfasserIn] Gregoire Marc [verfasserIn] Vallette François M [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2004

Übergeordnetes Werk:	In: BMC Cancer - BMC, 2003, 4(2004), 1, p 54
Übergeordnetes Werk:	volume:4 ; year:2004 ; number:1, p 54

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1471-2407-4-54

Katalog-ID:	DOAJ065300610

Internformat


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520			\|a <p<Abstract</p< <p<Background</p< <p<The relative role of anti apoptotic (i.e. Bcl-2) or pro-apoptotic (e.g. Bax) proteins in tumor progression is still not completely understood.</p< <p<Methods</p< <p<The rat glioma cell line A15A5 was stably transfected with human <it<Bcl-2 </it<and <it<Bax </it<transgenes and the viability of theses cell lines was analyzed in vitro and in vivo.</p< <p<Results</p< <p<<it<In vitro</it<, the transfected cell lines (huBax A15A5 and huBcl-2 A15A5) exhibited different sensitivities toward apoptotic stimuli. huBax A15A5 cells were more sensitive and huBcl-2 A15A5 cells more resistant to apoptosis than mock-transfected A15A5 cells (pCMV A15A5). However, <it<in vivo, </it<in syngenic rat BDIX, these cell lines behaved differently, as no tumor growth was observed with huBax A15A5 cells while huBcl-2 A15A5 cells formed large tumors. The immune system appeared to be involved in the rejection of huBax A15A5 cells since i) huBax A15A5 cells were tumorogenic in <it<nude </it<mice, ii) an accumulation of CD8+ T-lymphocytes was observed at the site of injection of huBax A15A5 cells and iii) BDIX rats, which had received huBax A15A5 cells developed an immune protection against pCMV A15A5 and huBcl-2 A15A5 cells.</p< <p<Conclusions</p< <p<We show that the expression of Bax and Bcl-2 controls the sensitivity of the cancer cells toward the immune system. This sensitization is most likely to be due to an increase in immune induced cell death and/or the amplification of an anti tumour immune response</p<
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700	0		\|a Meflah Khaled \|e verfasserin \|4 aut
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allfields	10.1186/1471-2407-4-54 doi (DE-627)DOAJ065300610 (DE-599)DOAJ1746146df2e04b27ba03352f1a25baa6 DE-627 ger DE-627 rakwb eng RC254-282 Bougras Gwenola verfasserin aut Opposite role of Bax and BCL-2 in the anti-tumoral responses of the immune system 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The relative role of anti apoptotic (i.e. Bcl-2) or pro-apoptotic (e.g. Bax) proteins in tumor progression is still not completely understood.</p< <p<Methods</p< <p<The rat glioma cell line A15A5 was stably transfected with human <it<Bcl-2 </it<and <it<Bax </it<transgenes and the viability of theses cell lines was analyzed in vitro and in vivo.</p< <p<Results</p< <p<<it<In vitro</it<, the transfected cell lines (huBax A15A5 and huBcl-2 A15A5) exhibited different sensitivities toward apoptotic stimuli. huBax A15A5 cells were more sensitive and huBcl-2 A15A5 cells more resistant to apoptosis than mock-transfected A15A5 cells (pCMV A15A5). However, <it<in vivo, </it<in syngenic rat BDIX, these cell lines behaved differently, as no tumor growth was observed with huBax A15A5 cells while huBcl-2 A15A5 cells formed large tumors. The immune system appeared to be involved in the rejection of huBax A15A5 cells since i) huBax A15A5 cells were tumorogenic in <it<nude </it<mice, ii) an accumulation of CD8+ T-lymphocytes was observed at the site of injection of huBax A15A5 cells and iii) BDIX rats, which had received huBax A15A5 cells developed an immune protection against pCMV A15A5 and huBcl-2 A15A5 cells.</p< <p<Conclusions</p< <p<We show that the expression of Bax and Bcl-2 controls the sensitivity of the cancer cells toward the immune system. This sensitization is most likely to be due to an increase in immune induced cell death and/or the amplification of an anti tumour immune response</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cartron Pierre-François verfasserin aut Gautier Fabien verfasserin aut Martin Stéphane verfasserin aut LeCabellec Marité verfasserin aut Meflah Khaled verfasserin aut Gregoire Marc verfasserin aut Vallette François M verfasserin aut In BMC Cancer BMC, 2003 4(2004), 1, p 54 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:4 year:2004 number:1, p 54 https://doi.org/10.1186/1471-2407-4-54 kostenfrei https://doaj.org/article/1746146df2e04b27ba03352f1a25baa6 kostenfrei http://www.biomedcentral.com/1471-2407/4/54 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 4 2004 1, p 54
spelling	10.1186/1471-2407-4-54 doi (DE-627)DOAJ065300610 (DE-599)DOAJ1746146df2e04b27ba03352f1a25baa6 DE-627 ger DE-627 rakwb eng RC254-282 Bougras Gwenola verfasserin aut Opposite role of Bax and BCL-2 in the anti-tumoral responses of the immune system 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The relative role of anti apoptotic (i.e. Bcl-2) or pro-apoptotic (e.g. Bax) proteins in tumor progression is still not completely understood.</p< <p<Methods</p< <p<The rat glioma cell line A15A5 was stably transfected with human <it<Bcl-2 </it<and <it<Bax </it<transgenes and the viability of theses cell lines was analyzed in vitro and in vivo.</p< <p<Results</p< <p<<it<In vitro</it<, the transfected cell lines (huBax A15A5 and huBcl-2 A15A5) exhibited different sensitivities toward apoptotic stimuli. huBax A15A5 cells were more sensitive and huBcl-2 A15A5 cells more resistant to apoptosis than mock-transfected A15A5 cells (pCMV A15A5). However, <it<in vivo, </it<in syngenic rat BDIX, these cell lines behaved differently, as no tumor growth was observed with huBax A15A5 cells while huBcl-2 A15A5 cells formed large tumors. The immune system appeared to be involved in the rejection of huBax A15A5 cells since i) huBax A15A5 cells were tumorogenic in <it<nude </it<mice, ii) an accumulation of CD8+ T-lymphocytes was observed at the site of injection of huBax A15A5 cells and iii) BDIX rats, which had received huBax A15A5 cells developed an immune protection against pCMV A15A5 and huBcl-2 A15A5 cells.</p< <p<Conclusions</p< <p<We show that the expression of Bax and Bcl-2 controls the sensitivity of the cancer cells toward the immune system. This sensitization is most likely to be due to an increase in immune induced cell death and/or the amplification of an anti tumour immune response</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cartron Pierre-François verfasserin aut Gautier Fabien verfasserin aut Martin Stéphane verfasserin aut LeCabellec Marité verfasserin aut Meflah Khaled verfasserin aut Gregoire Marc verfasserin aut Vallette François M verfasserin aut In BMC Cancer BMC, 2003 4(2004), 1, p 54 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:4 year:2004 number:1, p 54 https://doi.org/10.1186/1471-2407-4-54 kostenfrei https://doaj.org/article/1746146df2e04b27ba03352f1a25baa6 kostenfrei http://www.biomedcentral.com/1471-2407/4/54 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 4 2004 1, p 54
allfields_unstemmed	10.1186/1471-2407-4-54 doi (DE-627)DOAJ065300610 (DE-599)DOAJ1746146df2e04b27ba03352f1a25baa6 DE-627 ger DE-627 rakwb eng RC254-282 Bougras Gwenola verfasserin aut Opposite role of Bax and BCL-2 in the anti-tumoral responses of the immune system 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The relative role of anti apoptotic (i.e. Bcl-2) or pro-apoptotic (e.g. Bax) proteins in tumor progression is still not completely understood.</p< <p<Methods</p< <p<The rat glioma cell line A15A5 was stably transfected with human <it<Bcl-2 </it<and <it<Bax </it<transgenes and the viability of theses cell lines was analyzed in vitro and in vivo.</p< <p<Results</p< <p<<it<In vitro</it<, the transfected cell lines (huBax A15A5 and huBcl-2 A15A5) exhibited different sensitivities toward apoptotic stimuli. huBax A15A5 cells were more sensitive and huBcl-2 A15A5 cells more resistant to apoptosis than mock-transfected A15A5 cells (pCMV A15A5). However, <it<in vivo, </it<in syngenic rat BDIX, these cell lines behaved differently, as no tumor growth was observed with huBax A15A5 cells while huBcl-2 A15A5 cells formed large tumors. The immune system appeared to be involved in the rejection of huBax A15A5 cells since i) huBax A15A5 cells were tumorogenic in <it<nude </it<mice, ii) an accumulation of CD8+ T-lymphocytes was observed at the site of injection of huBax A15A5 cells and iii) BDIX rats, which had received huBax A15A5 cells developed an immune protection against pCMV A15A5 and huBcl-2 A15A5 cells.</p< <p<Conclusions</p< <p<We show that the expression of Bax and Bcl-2 controls the sensitivity of the cancer cells toward the immune system. This sensitization is most likely to be due to an increase in immune induced cell death and/or the amplification of an anti tumour immune response</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cartron Pierre-François verfasserin aut Gautier Fabien verfasserin aut Martin Stéphane verfasserin aut LeCabellec Marité verfasserin aut Meflah Khaled verfasserin aut Gregoire Marc verfasserin aut Vallette François M verfasserin aut In BMC Cancer BMC, 2003 4(2004), 1, p 54 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:4 year:2004 number:1, p 54 https://doi.org/10.1186/1471-2407-4-54 kostenfrei https://doaj.org/article/1746146df2e04b27ba03352f1a25baa6 kostenfrei http://www.biomedcentral.com/1471-2407/4/54 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 4 2004 1, p 54
allfieldsGer	10.1186/1471-2407-4-54 doi (DE-627)DOAJ065300610 (DE-599)DOAJ1746146df2e04b27ba03352f1a25baa6 DE-627 ger DE-627 rakwb eng RC254-282 Bougras Gwenola verfasserin aut Opposite role of Bax and BCL-2 in the anti-tumoral responses of the immune system 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The relative role of anti apoptotic (i.e. Bcl-2) or pro-apoptotic (e.g. Bax) proteins in tumor progression is still not completely understood.</p< <p<Methods</p< <p<The rat glioma cell line A15A5 was stably transfected with human <it<Bcl-2 </it<and <it<Bax </it<transgenes and the viability of theses cell lines was analyzed in vitro and in vivo.</p< <p<Results</p< <p<<it<In vitro</it<, the transfected cell lines (huBax A15A5 and huBcl-2 A15A5) exhibited different sensitivities toward apoptotic stimuli. huBax A15A5 cells were more sensitive and huBcl-2 A15A5 cells more resistant to apoptosis than mock-transfected A15A5 cells (pCMV A15A5). However, <it<in vivo, </it<in syngenic rat BDIX, these cell lines behaved differently, as no tumor growth was observed with huBax A15A5 cells while huBcl-2 A15A5 cells formed large tumors. The immune system appeared to be involved in the rejection of huBax A15A5 cells since i) huBax A15A5 cells were tumorogenic in <it<nude </it<mice, ii) an accumulation of CD8+ T-lymphocytes was observed at the site of injection of huBax A15A5 cells and iii) BDIX rats, which had received huBax A15A5 cells developed an immune protection against pCMV A15A5 and huBcl-2 A15A5 cells.</p< <p<Conclusions</p< <p<We show that the expression of Bax and Bcl-2 controls the sensitivity of the cancer cells toward the immune system. This sensitization is most likely to be due to an increase in immune induced cell death and/or the amplification of an anti tumour immune response</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cartron Pierre-François verfasserin aut Gautier Fabien verfasserin aut Martin Stéphane verfasserin aut LeCabellec Marité verfasserin aut Meflah Khaled verfasserin aut Gregoire Marc verfasserin aut Vallette François M verfasserin aut In BMC Cancer BMC, 2003 4(2004), 1, p 54 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:4 year:2004 number:1, p 54 https://doi.org/10.1186/1471-2407-4-54 kostenfrei https://doaj.org/article/1746146df2e04b27ba03352f1a25baa6 kostenfrei http://www.biomedcentral.com/1471-2407/4/54 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 4 2004 1, p 54
allfieldsSound	10.1186/1471-2407-4-54 doi (DE-627)DOAJ065300610 (DE-599)DOAJ1746146df2e04b27ba03352f1a25baa6 DE-627 ger DE-627 rakwb eng RC254-282 Bougras Gwenola verfasserin aut Opposite role of Bax and BCL-2 in the anti-tumoral responses of the immune system 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The relative role of anti apoptotic (i.e. Bcl-2) or pro-apoptotic (e.g. Bax) proteins in tumor progression is still not completely understood.</p< <p<Methods</p< <p<The rat glioma cell line A15A5 was stably transfected with human <it<Bcl-2 </it<and <it<Bax </it<transgenes and the viability of theses cell lines was analyzed in vitro and in vivo.</p< <p<Results</p< <p<<it<In vitro</it<, the transfected cell lines (huBax A15A5 and huBcl-2 A15A5) exhibited different sensitivities toward apoptotic stimuli. huBax A15A5 cells were more sensitive and huBcl-2 A15A5 cells more resistant to apoptosis than mock-transfected A15A5 cells (pCMV A15A5). However, <it<in vivo, </it<in syngenic rat BDIX, these cell lines behaved differently, as no tumor growth was observed with huBax A15A5 cells while huBcl-2 A15A5 cells formed large tumors. The immune system appeared to be involved in the rejection of huBax A15A5 cells since i) huBax A15A5 cells were tumorogenic in <it<nude </it<mice, ii) an accumulation of CD8+ T-lymphocytes was observed at the site of injection of huBax A15A5 cells and iii) BDIX rats, which had received huBax A15A5 cells developed an immune protection against pCMV A15A5 and huBcl-2 A15A5 cells.</p< <p<Conclusions</p< <p<We show that the expression of Bax and Bcl-2 controls the sensitivity of the cancer cells toward the immune system. This sensitization is most likely to be due to an increase in immune induced cell death and/or the amplification of an anti tumour immune response</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cartron Pierre-François verfasserin aut Gautier Fabien verfasserin aut Martin Stéphane verfasserin aut LeCabellec Marité verfasserin aut Meflah Khaled verfasserin aut Gregoire Marc verfasserin aut Vallette François M verfasserin aut In BMC Cancer BMC, 2003 4(2004), 1, p 54 (DE-627)326643710 (DE-600)2041352-X 14712407 nnns volume:4 year:2004 number:1, p 54 https://doi.org/10.1186/1471-2407-4-54 kostenfrei https://doaj.org/article/1746146df2e04b27ba03352f1a25baa6 kostenfrei http://www.biomedcentral.com/1471-2407/4/54 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 4 2004 1, p 54
language	English
source	In BMC Cancer 4(2004), 1, p 54 volume:4 year:2004 number:1, p 54
sourceStr	In BMC Cancer 4(2004), 1, p 54 volume:4 year:2004 number:1, p 54
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	Bougras Gwenola @@aut@@ Cartron Pierre-François @@aut@@ Gautier Fabien @@aut@@ Martin Stéphane @@aut@@ LeCabellec Marité @@aut@@ Meflah Khaled @@aut@@ Gregoire Marc @@aut@@ Vallette François M @@aut@@
publishDateDaySort_date	2004-01-01T00:00:00Z
hierarchy_top_id	326643710
id	DOAJ065300610
language_de	englisch
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callnumber-first	R - Medicine
author	Bougras Gwenola
spellingShingle	Bougras Gwenola misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens Opposite role of Bax and BCL-2 in the anti-tumoral responses of the immune system
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topic_title	RC254-282 Opposite role of Bax and BCL-2 in the anti-tumoral responses of the immune system
topic	misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_browse	misc RC254-282 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	Opposite role of Bax and BCL-2 in the anti-tumoral responses of the immune system
ctrlnum	(DE-627)DOAJ065300610 (DE-599)DOAJ1746146df2e04b27ba03352f1a25baa6
title_full	Opposite role of Bax and BCL-2 in the anti-tumoral responses of the immune system
author_sort	Bougras Gwenola
journal	BMC Cancer
journalStr	BMC Cancer
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lang_code	eng
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author_browse	Bougras Gwenola Cartron Pierre-François Gautier Fabien Martin Stéphane LeCabellec Marité Meflah Khaled Gregoire Marc Vallette François M
container_volume	4
class	RC254-282
format_se	Elektronische Aufsätze
author-letter	Bougras Gwenola
doi_str_mv	10.1186/1471-2407-4-54
author2-role	verfasserin
title_sort	opposite role of bax and bcl-2 in the anti-tumoral responses of the immune system
callnumber	RC254-282
title_auth	Opposite role of Bax and BCL-2 in the anti-tumoral responses of the immune system
abstract	<p<Abstract</p< <p<Background</p< <p<The relative role of anti apoptotic (i.e. Bcl-2) or pro-apoptotic (e.g. Bax) proteins in tumor progression is still not completely understood.</p< <p<Methods</p< <p<The rat glioma cell line A15A5 was stably transfected with human <it<Bcl-2 </it<and <it<Bax </it<transgenes and the viability of theses cell lines was analyzed in vitro and in vivo.</p< <p<Results</p< <p<<it<In vitro</it<, the transfected cell lines (huBax A15A5 and huBcl-2 A15A5) exhibited different sensitivities toward apoptotic stimuli. huBax A15A5 cells were more sensitive and huBcl-2 A15A5 cells more resistant to apoptosis than mock-transfected A15A5 cells (pCMV A15A5). However, <it<in vivo, </it<in syngenic rat BDIX, these cell lines behaved differently, as no tumor growth was observed with huBax A15A5 cells while huBcl-2 A15A5 cells formed large tumors. The immune system appeared to be involved in the rejection of huBax A15A5 cells since i) huBax A15A5 cells were tumorogenic in <it<nude </it<mice, ii) an accumulation of CD8+ T-lymphocytes was observed at the site of injection of huBax A15A5 cells and iii) BDIX rats, which had received huBax A15A5 cells developed an immune protection against pCMV A15A5 and huBcl-2 A15A5 cells.</p< <p<Conclusions</p< <p<We show that the expression of Bax and Bcl-2 controls the sensitivity of the cancer cells toward the immune system. This sensitization is most likely to be due to an increase in immune induced cell death and/or the amplification of an anti tumour immune response</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<The relative role of anti apoptotic (i.e. Bcl-2) or pro-apoptotic (e.g. Bax) proteins in tumor progression is still not completely understood.</p< <p<Methods</p< <p<The rat glioma cell line A15A5 was stably transfected with human <it<Bcl-2 </it<and <it<Bax </it<transgenes and the viability of theses cell lines was analyzed in vitro and in vivo.</p< <p<Results</p< <p<<it<In vitro</it<, the transfected cell lines (huBax A15A5 and huBcl-2 A15A5) exhibited different sensitivities toward apoptotic stimuli. huBax A15A5 cells were more sensitive and huBcl-2 A15A5 cells more resistant to apoptosis than mock-transfected A15A5 cells (pCMV A15A5). However, <it<in vivo, </it<in syngenic rat BDIX, these cell lines behaved differently, as no tumor growth was observed with huBax A15A5 cells while huBcl-2 A15A5 cells formed large tumors. The immune system appeared to be involved in the rejection of huBax A15A5 cells since i) huBax A15A5 cells were tumorogenic in <it<nude </it<mice, ii) an accumulation of CD8+ T-lymphocytes was observed at the site of injection of huBax A15A5 cells and iii) BDIX rats, which had received huBax A15A5 cells developed an immune protection against pCMV A15A5 and huBcl-2 A15A5 cells.</p< <p<Conclusions</p< <p<We show that the expression of Bax and Bcl-2 controls the sensitivity of the cancer cells toward the immune system. This sensitization is most likely to be due to an increase in immune induced cell death and/or the amplification of an anti tumour immune response</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<The relative role of anti apoptotic (i.e. Bcl-2) or pro-apoptotic (e.g. Bax) proteins in tumor progression is still not completely understood.</p< <p<Methods</p< <p<The rat glioma cell line A15A5 was stably transfected with human <it<Bcl-2 </it<and <it<Bax </it<transgenes and the viability of theses cell lines was analyzed in vitro and in vivo.</p< <p<Results</p< <p<<it<In vitro</it<, the transfected cell lines (huBax A15A5 and huBcl-2 A15A5) exhibited different sensitivities toward apoptotic stimuli. huBax A15A5 cells were more sensitive and huBcl-2 A15A5 cells more resistant to apoptosis than mock-transfected A15A5 cells (pCMV A15A5). However, <it<in vivo, </it<in syngenic rat BDIX, these cell lines behaved differently, as no tumor growth was observed with huBax A15A5 cells while huBcl-2 A15A5 cells formed large tumors. The immune system appeared to be involved in the rejection of huBax A15A5 cells since i) huBax A15A5 cells were tumorogenic in <it<nude </it<mice, ii) an accumulation of CD8+ T-lymphocytes was observed at the site of injection of huBax A15A5 cells and iii) BDIX rats, which had received huBax A15A5 cells developed an immune protection against pCMV A15A5 and huBcl-2 A15A5 cells.</p< <p<Conclusions</p< <p<We show that the expression of Bax and Bcl-2 controls the sensitivity of the cancer cells toward the immune system. This sensitization is most likely to be due to an increase in immune induced cell death and/or the amplification of an anti tumour immune response</p<
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title_short	Opposite role of Bax and BCL-2 in the anti-tumoral responses of the immune system
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Opposite role of Bax and BCL-2 in the anti-tumoral responses of the immune system

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