Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer
Background Activation-induced cytidine deaminase (AID) is expressed in B lymphocytes and triggers antibody diversification. Recent reports have indicated that the constitutive expression of AID in mice causes not only lymphomas, but also cancers of some organs including the lung, prompting us to inv...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Shinmura, Kazuya [verfasserIn] Igarashi, Hisaki [verfasserIn] Goto, Masanori [verfasserIn] Tao, Hong [verfasserIn] Yamada, Hidetaka [verfasserIn] Matsuura, Shun [verfasserIn] Tajima, Mari [verfasserIn] Matsuda, Tomonari [verfasserIn] Yamane, Arito [verfasserIn] Funai, Kazuhito [verfasserIn] Tanahashi, Masayuki [verfasserIn] Niwa, Hiroshi [verfasserIn] Ogawa, Hiroshi [verfasserIn] Sugimura, Haruhiko [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2011 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Annals of surgical oncology - Berlin [u.a.] : Springer, 1994, 18(2011), 7 vom: 03. Feb., Seite 2084-2092 |
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| Übergeordnetes Werk: |
volume:18 ; year:2011 ; number:7 ; day:03 ; month:02 ; pages:2084-2092 |
| Links: |
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| DOI / URN: |
10.1245/s10434-011-1568-8 |
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| Katalog-ID: |
SPR009944400 |
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| 100 | 1 | |a Shinmura, Kazuya |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer |
| 264 | 1 | |c 2011 | |
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| 520 | |a Background Activation-induced cytidine deaminase (AID) is expressed in B lymphocytes and triggers antibody diversification. Recent reports have indicated that the constitutive expression of AID in mice causes not only lymphomas, but also cancers of some organs including the lung, prompting us to investigate the expression and effect of AID on human lung cancer. Materials and Methods We examined AID mRNA expression in 17 lung cancer cell lines and 51 primary lung cancers using a quantitative RT-PCR analysis. Next, we established H1299 lung cancer cells stably overexpressing AID and performed a supF forward mutation assay. We then examined AID protein expression and p53 mutation in 129 primary lung cancers by an immunohistochemical analysis and PCR-SSCP and sequencing analyses, respectively. Results Aberrant mRNA expression of AID was detected in 29% (5 of 17) of the lung cancer cell lines and 31% (16 of 51) of the primary lung cancers. AID-overexpressing H1299 clones showed a 5.0- to 6.1-fold higher mutation frequency than an empty vector-transfected H1299 clone, and about half of the AID-induced mutations were base substitutions, indicating that AID induces gene mutations in lung cancer cells. Furthermore, an association was found between the AID protein expression level and the p53 mutation status in an analysis of 129 primary lung cancers. A further expression analysis revealed that a portion of AID is localized at the centrosomes. Conclusion Our current findings suggest that the aberrant expression of AID may be involved in a subset of human lung cancers as a result of its mutation-inducing activity. | ||
| 650 | 4 | |a Lung Cancer |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Lung Cancer Cell Line |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Human Lung Cancer |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Primary Lung Cancer |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Lung Carcinogenesis |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Igarashi, Hisaki |e verfasserin |4 aut | |
| 700 | 1 | |a Goto, Masanori |e verfasserin |4 aut | |
| 700 | 1 | |a Tao, Hong |e verfasserin |4 aut | |
| 700 | 1 | |a Yamada, Hidetaka |e verfasserin |4 aut | |
| 700 | 1 | |a Matsuura, Shun |e verfasserin |4 aut | |
| 700 | 1 | |a Tajima, Mari |e verfasserin |4 aut | |
| 700 | 1 | |a Matsuda, Tomonari |e verfasserin |4 aut | |
| 700 | 1 | |a Yamane, Arito |e verfasserin |4 aut | |
| 700 | 1 | |a Funai, Kazuhito |e verfasserin |4 aut | |
| 700 | 1 | |a Tanahashi, Masayuki |e verfasserin |4 aut | |
| 700 | 1 | |a Niwa, Hiroshi |e verfasserin |4 aut | |
| 700 | 1 | |a Ogawa, Hiroshi |e verfasserin |4 aut | |
| 700 | 1 | |a Sugimura, Haruhiko |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Annals of surgical oncology |d Berlin [u.a.] : Springer, 1994 |g 18(2011), 7 vom: 03. Feb., Seite 2084-2092 |w (DE-627)343969947 |w (DE-600)2074021-9 |x 1534-4681 |7 nnns |
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10.1245/s10434-011-1568-8 doi (DE-627)SPR009944400 (SPR)s10434-011-1568-8-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.65 bkl Shinmura, Kazuya verfasserin aut Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Activation-induced cytidine deaminase (AID) is expressed in B lymphocytes and triggers antibody diversification. Recent reports have indicated that the constitutive expression of AID in mice causes not only lymphomas, but also cancers of some organs including the lung, prompting us to investigate the expression and effect of AID on human lung cancer. Materials and Methods We examined AID mRNA expression in 17 lung cancer cell lines and 51 primary lung cancers using a quantitative RT-PCR analysis. Next, we established H1299 lung cancer cells stably overexpressing AID and performed a supF forward mutation assay. We then examined AID protein expression and p53 mutation in 129 primary lung cancers by an immunohistochemical analysis and PCR-SSCP and sequencing analyses, respectively. Results Aberrant mRNA expression of AID was detected in 29% (5 of 17) of the lung cancer cell lines and 31% (16 of 51) of the primary lung cancers. AID-overexpressing H1299 clones showed a 5.0- to 6.1-fold higher mutation frequency than an empty vector-transfected H1299 clone, and about half of the AID-induced mutations were base substitutions, indicating that AID induces gene mutations in lung cancer cells. Furthermore, an association was found between the AID protein expression level and the p53 mutation status in an analysis of 129 primary lung cancers. A further expression analysis revealed that a portion of AID is localized at the centrosomes. Conclusion Our current findings suggest that the aberrant expression of AID may be involved in a subset of human lung cancers as a result of its mutation-inducing activity. Lung Cancer (dpeaa)DE-He213 Lung Cancer Cell Line (dpeaa)DE-He213 Human Lung Cancer (dpeaa)DE-He213 Primary Lung Cancer (dpeaa)DE-He213 Lung Carcinogenesis (dpeaa)DE-He213 Igarashi, Hisaki verfasserin aut Goto, Masanori verfasserin aut Tao, Hong verfasserin aut Yamada, Hidetaka verfasserin aut Matsuura, Shun verfasserin aut Tajima, Mari verfasserin aut Matsuda, Tomonari verfasserin aut Yamane, Arito verfasserin aut Funai, Kazuhito verfasserin aut Tanahashi, Masayuki verfasserin aut Niwa, Hiroshi verfasserin aut Ogawa, Hiroshi verfasserin aut Sugimura, Haruhiko verfasserin aut Enthalten in Annals of surgical oncology Berlin [u.a.] : Springer, 1994 18(2011), 7 vom: 03. Feb., Seite 2084-2092 (DE-627)343969947 (DE-600)2074021-9 1534-4681 nnns volume:18 year:2011 number:7 day:03 month:02 pages:2084-2092 https://dx.doi.org/10.1245/s10434-011-1568-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 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_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.65 ASE AR 18 2011 7 03 02 2084-2092 |
| spelling |
10.1245/s10434-011-1568-8 doi (DE-627)SPR009944400 (SPR)s10434-011-1568-8-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.65 bkl Shinmura, Kazuya verfasserin aut Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Activation-induced cytidine deaminase (AID) is expressed in B lymphocytes and triggers antibody diversification. Recent reports have indicated that the constitutive expression of AID in mice causes not only lymphomas, but also cancers of some organs including the lung, prompting us to investigate the expression and effect of AID on human lung cancer. Materials and Methods We examined AID mRNA expression in 17 lung cancer cell lines and 51 primary lung cancers using a quantitative RT-PCR analysis. Next, we established H1299 lung cancer cells stably overexpressing AID and performed a supF forward mutation assay. We then examined AID protein expression and p53 mutation in 129 primary lung cancers by an immunohistochemical analysis and PCR-SSCP and sequencing analyses, respectively. Results Aberrant mRNA expression of AID was detected in 29% (5 of 17) of the lung cancer cell lines and 31% (16 of 51) of the primary lung cancers. AID-overexpressing H1299 clones showed a 5.0- to 6.1-fold higher mutation frequency than an empty vector-transfected H1299 clone, and about half of the AID-induced mutations were base substitutions, indicating that AID induces gene mutations in lung cancer cells. Furthermore, an association was found between the AID protein expression level and the p53 mutation status in an analysis of 129 primary lung cancers. A further expression analysis revealed that a portion of AID is localized at the centrosomes. Conclusion Our current findings suggest that the aberrant expression of AID may be involved in a subset of human lung cancers as a result of its mutation-inducing activity. Lung Cancer (dpeaa)DE-He213 Lung Cancer Cell Line (dpeaa)DE-He213 Human Lung Cancer (dpeaa)DE-He213 Primary Lung Cancer (dpeaa)DE-He213 Lung Carcinogenesis (dpeaa)DE-He213 Igarashi, Hisaki verfasserin aut Goto, Masanori verfasserin aut Tao, Hong verfasserin aut Yamada, Hidetaka verfasserin aut Matsuura, Shun verfasserin aut Tajima, Mari verfasserin aut Matsuda, Tomonari verfasserin aut Yamane, Arito verfasserin aut Funai, Kazuhito verfasserin aut Tanahashi, Masayuki verfasserin aut Niwa, Hiroshi verfasserin aut Ogawa, Hiroshi verfasserin aut Sugimura, Haruhiko verfasserin aut Enthalten in Annals of surgical oncology Berlin [u.a.] : Springer, 1994 18(2011), 7 vom: 03. Feb., Seite 2084-2092 (DE-627)343969947 (DE-600)2074021-9 1534-4681 nnns volume:18 year:2011 number:7 day:03 month:02 pages:2084-2092 https://dx.doi.org/10.1245/s10434-011-1568-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 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_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.65 ASE AR 18 2011 7 03 02 2084-2092 |
| allfields_unstemmed |
10.1245/s10434-011-1568-8 doi (DE-627)SPR009944400 (SPR)s10434-011-1568-8-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.65 bkl Shinmura, Kazuya verfasserin aut Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Activation-induced cytidine deaminase (AID) is expressed in B lymphocytes and triggers antibody diversification. Recent reports have indicated that the constitutive expression of AID in mice causes not only lymphomas, but also cancers of some organs including the lung, prompting us to investigate the expression and effect of AID on human lung cancer. Materials and Methods We examined AID mRNA expression in 17 lung cancer cell lines and 51 primary lung cancers using a quantitative RT-PCR analysis. Next, we established H1299 lung cancer cells stably overexpressing AID and performed a supF forward mutation assay. We then examined AID protein expression and p53 mutation in 129 primary lung cancers by an immunohistochemical analysis and PCR-SSCP and sequencing analyses, respectively. Results Aberrant mRNA expression of AID was detected in 29% (5 of 17) of the lung cancer cell lines and 31% (16 of 51) of the primary lung cancers. AID-overexpressing H1299 clones showed a 5.0- to 6.1-fold higher mutation frequency than an empty vector-transfected H1299 clone, and about half of the AID-induced mutations were base substitutions, indicating that AID induces gene mutations in lung cancer cells. Furthermore, an association was found between the AID protein expression level and the p53 mutation status in an analysis of 129 primary lung cancers. A further expression analysis revealed that a portion of AID is localized at the centrosomes. Conclusion Our current findings suggest that the aberrant expression of AID may be involved in a subset of human lung cancers as a result of its mutation-inducing activity. Lung Cancer (dpeaa)DE-He213 Lung Cancer Cell Line (dpeaa)DE-He213 Human Lung Cancer (dpeaa)DE-He213 Primary Lung Cancer (dpeaa)DE-He213 Lung Carcinogenesis (dpeaa)DE-He213 Igarashi, Hisaki verfasserin aut Goto, Masanori verfasserin aut Tao, Hong verfasserin aut Yamada, Hidetaka verfasserin aut Matsuura, Shun verfasserin aut Tajima, Mari verfasserin aut Matsuda, Tomonari verfasserin aut Yamane, Arito verfasserin aut Funai, Kazuhito verfasserin aut Tanahashi, Masayuki verfasserin aut Niwa, Hiroshi verfasserin aut Ogawa, Hiroshi verfasserin aut Sugimura, Haruhiko verfasserin aut Enthalten in Annals of surgical oncology Berlin [u.a.] : Springer, 1994 18(2011), 7 vom: 03. Feb., Seite 2084-2092 (DE-627)343969947 (DE-600)2074021-9 1534-4681 nnns volume:18 year:2011 number:7 day:03 month:02 pages:2084-2092 https://dx.doi.org/10.1245/s10434-011-1568-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 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_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.65 ASE AR 18 2011 7 03 02 2084-2092 |
| allfieldsGer |
10.1245/s10434-011-1568-8 doi (DE-627)SPR009944400 (SPR)s10434-011-1568-8-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.65 bkl Shinmura, Kazuya verfasserin aut Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Activation-induced cytidine deaminase (AID) is expressed in B lymphocytes and triggers antibody diversification. Recent reports have indicated that the constitutive expression of AID in mice causes not only lymphomas, but also cancers of some organs including the lung, prompting us to investigate the expression and effect of AID on human lung cancer. Materials and Methods We examined AID mRNA expression in 17 lung cancer cell lines and 51 primary lung cancers using a quantitative RT-PCR analysis. Next, we established H1299 lung cancer cells stably overexpressing AID and performed a supF forward mutation assay. We then examined AID protein expression and p53 mutation in 129 primary lung cancers by an immunohistochemical analysis and PCR-SSCP and sequencing analyses, respectively. Results Aberrant mRNA expression of AID was detected in 29% (5 of 17) of the lung cancer cell lines and 31% (16 of 51) of the primary lung cancers. AID-overexpressing H1299 clones showed a 5.0- to 6.1-fold higher mutation frequency than an empty vector-transfected H1299 clone, and about half of the AID-induced mutations were base substitutions, indicating that AID induces gene mutations in lung cancer cells. Furthermore, an association was found between the AID protein expression level and the p53 mutation status in an analysis of 129 primary lung cancers. A further expression analysis revealed that a portion of AID is localized at the centrosomes. Conclusion Our current findings suggest that the aberrant expression of AID may be involved in a subset of human lung cancers as a result of its mutation-inducing activity. Lung Cancer (dpeaa)DE-He213 Lung Cancer Cell Line (dpeaa)DE-He213 Human Lung Cancer (dpeaa)DE-He213 Primary Lung Cancer (dpeaa)DE-He213 Lung Carcinogenesis (dpeaa)DE-He213 Igarashi, Hisaki verfasserin aut Goto, Masanori verfasserin aut Tao, Hong verfasserin aut Yamada, Hidetaka verfasserin aut Matsuura, Shun verfasserin aut Tajima, Mari verfasserin aut Matsuda, Tomonari verfasserin aut Yamane, Arito verfasserin aut Funai, Kazuhito verfasserin aut Tanahashi, Masayuki verfasserin aut Niwa, Hiroshi verfasserin aut Ogawa, Hiroshi verfasserin aut Sugimura, Haruhiko verfasserin aut Enthalten in Annals of surgical oncology Berlin [u.a.] : Springer, 1994 18(2011), 7 vom: 03. Feb., Seite 2084-2092 (DE-627)343969947 (DE-600)2074021-9 1534-4681 nnns volume:18 year:2011 number:7 day:03 month:02 pages:2084-2092 https://dx.doi.org/10.1245/s10434-011-1568-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 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_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.65 ASE AR 18 2011 7 03 02 2084-2092 |
| allfieldsSound |
10.1245/s10434-011-1568-8 doi (DE-627)SPR009944400 (SPR)s10434-011-1568-8-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl 44.65 bkl Shinmura, Kazuya verfasserin aut Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Activation-induced cytidine deaminase (AID) is expressed in B lymphocytes and triggers antibody diversification. Recent reports have indicated that the constitutive expression of AID in mice causes not only lymphomas, but also cancers of some organs including the lung, prompting us to investigate the expression and effect of AID on human lung cancer. Materials and Methods We examined AID mRNA expression in 17 lung cancer cell lines and 51 primary lung cancers using a quantitative RT-PCR analysis. Next, we established H1299 lung cancer cells stably overexpressing AID and performed a supF forward mutation assay. We then examined AID protein expression and p53 mutation in 129 primary lung cancers by an immunohistochemical analysis and PCR-SSCP and sequencing analyses, respectively. Results Aberrant mRNA expression of AID was detected in 29% (5 of 17) of the lung cancer cell lines and 31% (16 of 51) of the primary lung cancers. AID-overexpressing H1299 clones showed a 5.0- to 6.1-fold higher mutation frequency than an empty vector-transfected H1299 clone, and about half of the AID-induced mutations were base substitutions, indicating that AID induces gene mutations in lung cancer cells. Furthermore, an association was found between the AID protein expression level and the p53 mutation status in an analysis of 129 primary lung cancers. A further expression analysis revealed that a portion of AID is localized at the centrosomes. Conclusion Our current findings suggest that the aberrant expression of AID may be involved in a subset of human lung cancers as a result of its mutation-inducing activity. Lung Cancer (dpeaa)DE-He213 Lung Cancer Cell Line (dpeaa)DE-He213 Human Lung Cancer (dpeaa)DE-He213 Primary Lung Cancer (dpeaa)DE-He213 Lung Carcinogenesis (dpeaa)DE-He213 Igarashi, Hisaki verfasserin aut Goto, Masanori verfasserin aut Tao, Hong verfasserin aut Yamada, Hidetaka verfasserin aut Matsuura, Shun verfasserin aut Tajima, Mari verfasserin aut Matsuda, Tomonari verfasserin aut Yamane, Arito verfasserin aut Funai, Kazuhito verfasserin aut Tanahashi, Masayuki verfasserin aut Niwa, Hiroshi verfasserin aut Ogawa, Hiroshi verfasserin aut Sugimura, Haruhiko verfasserin aut Enthalten in Annals of surgical oncology Berlin [u.a.] : Springer, 1994 18(2011), 7 vom: 03. Feb., Seite 2084-2092 (DE-627)343969947 (DE-600)2074021-9 1534-4681 nnns volume:18 year:2011 number:7 day:03 month:02 pages:2084-2092 https://dx.doi.org/10.1245/s10434-011-1568-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 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_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE 44.65 ASE AR 18 2011 7 03 02 2084-2092 |
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Enthalten in Annals of surgical oncology 18(2011), 7 vom: 03. Feb., Seite 2084-2092 volume:18 year:2011 number:7 day:03 month:02 pages:2084-2092 |
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Shinmura, Kazuya @@aut@@ Igarashi, Hisaki @@aut@@ Goto, Masanori @@aut@@ Tao, Hong @@aut@@ Yamada, Hidetaka @@aut@@ Matsuura, Shun @@aut@@ Tajima, Mari @@aut@@ Matsuda, Tomonari @@aut@@ Yamane, Arito @@aut@@ Funai, Kazuhito @@aut@@ Tanahashi, Masayuki @@aut@@ Niwa, Hiroshi @@aut@@ Ogawa, Hiroshi @@aut@@ Sugimura, Haruhiko @@aut@@ |
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2011-02-03T00:00:00Z |
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Shinmura, Kazuya |
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Shinmura, Kazuya ddc 610 bkl 44.81 bkl 44.65 misc Lung Cancer misc Lung Cancer Cell Line misc Human Lung Cancer misc Primary Lung Cancer misc Lung Carcinogenesis Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer |
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610 ASE 44.81 bkl 44.65 bkl Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer Lung Cancer (dpeaa)DE-He213 Lung Cancer Cell Line (dpeaa)DE-He213 Human Lung Cancer (dpeaa)DE-He213 Primary Lung Cancer (dpeaa)DE-He213 Lung Carcinogenesis (dpeaa)DE-He213 |
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ddc 610 bkl 44.81 bkl 44.65 misc Lung Cancer misc Lung Cancer Cell Line misc Human Lung Cancer misc Primary Lung Cancer misc Lung Carcinogenesis |
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ddc 610 bkl 44.81 bkl 44.65 misc Lung Cancer misc Lung Cancer Cell Line misc Human Lung Cancer misc Primary Lung Cancer misc Lung Carcinogenesis |
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ddc 610 bkl 44.81 bkl 44.65 misc Lung Cancer misc Lung Cancer Cell Line misc Human Lung Cancer misc Primary Lung Cancer misc Lung Carcinogenesis |
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Annals of surgical oncology |
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Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer |
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Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer |
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Shinmura, Kazuya |
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Annals of surgical oncology |
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Shinmura, Kazuya Igarashi, Hisaki Goto, Masanori Tao, Hong Yamada, Hidetaka Matsuura, Shun Tajima, Mari Matsuda, Tomonari Yamane, Arito Funai, Kazuhito Tanahashi, Masayuki Niwa, Hiroshi Ogawa, Hiroshi Sugimura, Haruhiko |
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Shinmura, Kazuya |
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10.1245/s10434-011-1568-8 |
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aberrant expression and mutation-inducing activity of aid in human lung cancer |
| title_auth |
Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer |
| abstract |
Background Activation-induced cytidine deaminase (AID) is expressed in B lymphocytes and triggers antibody diversification. Recent reports have indicated that the constitutive expression of AID in mice causes not only lymphomas, but also cancers of some organs including the lung, prompting us to investigate the expression and effect of AID on human lung cancer. Materials and Methods We examined AID mRNA expression in 17 lung cancer cell lines and 51 primary lung cancers using a quantitative RT-PCR analysis. Next, we established H1299 lung cancer cells stably overexpressing AID and performed a supF forward mutation assay. We then examined AID protein expression and p53 mutation in 129 primary lung cancers by an immunohistochemical analysis and PCR-SSCP and sequencing analyses, respectively. Results Aberrant mRNA expression of AID was detected in 29% (5 of 17) of the lung cancer cell lines and 31% (16 of 51) of the primary lung cancers. AID-overexpressing H1299 clones showed a 5.0- to 6.1-fold higher mutation frequency than an empty vector-transfected H1299 clone, and about half of the AID-induced mutations were base substitutions, indicating that AID induces gene mutations in lung cancer cells. Furthermore, an association was found between the AID protein expression level and the p53 mutation status in an analysis of 129 primary lung cancers. A further expression analysis revealed that a portion of AID is localized at the centrosomes. Conclusion Our current findings suggest that the aberrant expression of AID may be involved in a subset of human lung cancers as a result of its mutation-inducing activity. |
| abstractGer |
Background Activation-induced cytidine deaminase (AID) is expressed in B lymphocytes and triggers antibody diversification. Recent reports have indicated that the constitutive expression of AID in mice causes not only lymphomas, but also cancers of some organs including the lung, prompting us to investigate the expression and effect of AID on human lung cancer. Materials and Methods We examined AID mRNA expression in 17 lung cancer cell lines and 51 primary lung cancers using a quantitative RT-PCR analysis. Next, we established H1299 lung cancer cells stably overexpressing AID and performed a supF forward mutation assay. We then examined AID protein expression and p53 mutation in 129 primary lung cancers by an immunohistochemical analysis and PCR-SSCP and sequencing analyses, respectively. Results Aberrant mRNA expression of AID was detected in 29% (5 of 17) of the lung cancer cell lines and 31% (16 of 51) of the primary lung cancers. AID-overexpressing H1299 clones showed a 5.0- to 6.1-fold higher mutation frequency than an empty vector-transfected H1299 clone, and about half of the AID-induced mutations were base substitutions, indicating that AID induces gene mutations in lung cancer cells. Furthermore, an association was found between the AID protein expression level and the p53 mutation status in an analysis of 129 primary lung cancers. A further expression analysis revealed that a portion of AID is localized at the centrosomes. Conclusion Our current findings suggest that the aberrant expression of AID may be involved in a subset of human lung cancers as a result of its mutation-inducing activity. |
| abstract_unstemmed |
Background Activation-induced cytidine deaminase (AID) is expressed in B lymphocytes and triggers antibody diversification. Recent reports have indicated that the constitutive expression of AID in mice causes not only lymphomas, but also cancers of some organs including the lung, prompting us to investigate the expression and effect of AID on human lung cancer. Materials and Methods We examined AID mRNA expression in 17 lung cancer cell lines and 51 primary lung cancers using a quantitative RT-PCR analysis. Next, we established H1299 lung cancer cells stably overexpressing AID and performed a supF forward mutation assay. We then examined AID protein expression and p53 mutation in 129 primary lung cancers by an immunohistochemical analysis and PCR-SSCP and sequencing analyses, respectively. Results Aberrant mRNA expression of AID was detected in 29% (5 of 17) of the lung cancer cell lines and 31% (16 of 51) of the primary lung cancers. AID-overexpressing H1299 clones showed a 5.0- to 6.1-fold higher mutation frequency than an empty vector-transfected H1299 clone, and about half of the AID-induced mutations were base substitutions, indicating that AID induces gene mutations in lung cancer cells. Furthermore, an association was found between the AID protein expression level and the p53 mutation status in an analysis of 129 primary lung cancers. A further expression analysis revealed that a portion of AID is localized at the centrosomes. Conclusion Our current findings suggest that the aberrant expression of AID may be involved in a subset of human lung cancers as a result of its mutation-inducing activity. |
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Aberrant Expression and Mutation-Inducing Activity of AID in Human Lung Cancer |
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Igarashi, Hisaki Goto, Masanori Tao, Hong Yamada, Hidetaka Matsuura, Shun Tajima, Mari Matsuda, Tomonari Yamane, Arito Funai, Kazuhito Tanahashi, Masayuki Niwa, Hiroshi Ogawa, Hiroshi Sugimura, Haruhiko |
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Igarashi, Hisaki Goto, Masanori Tao, Hong Yamada, Hidetaka Matsuura, Shun Tajima, Mari Matsuda, Tomonari Yamane, Arito Funai, Kazuhito Tanahashi, Masayuki Niwa, Hiroshi Ogawa, Hiroshi Sugimura, Haruhiko |
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Recent reports have indicated that the constitutive expression of AID in mice causes not only lymphomas, but also cancers of some organs including the lung, prompting us to investigate the expression and effect of AID on human lung cancer. Materials and Methods We examined AID mRNA expression in 17 lung cancer cell lines and 51 primary lung cancers using a quantitative RT-PCR analysis. Next, we established H1299 lung cancer cells stably overexpressing AID and performed a supF forward mutation assay. We then examined AID protein expression and p53 mutation in 129 primary lung cancers by an immunohistochemical analysis and PCR-SSCP and sequencing analyses, respectively. Results Aberrant mRNA expression of AID was detected in 29% (5 of 17) of the lung cancer cell lines and 31% (16 of 51) of the primary lung cancers. AID-overexpressing H1299 clones showed a 5.0- to 6.1-fold higher mutation frequency than an empty vector-transfected H1299 clone, and about half of the AID-induced mutations were base substitutions, indicating that AID induces gene mutations in lung cancer cells. Furthermore, an association was found between the AID protein expression level and the p53 mutation status in an analysis of 129 primary lung cancers. A further expression analysis revealed that a portion of AID is localized at the centrosomes. 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