Molecular oncology of lung cancer

Abstract Progress in genetic engineering has made it possible to elucidate the molecular biological abnormalities in lung cancer. Mutations in KRAS and P53 genes, loss of specific alleles, and DNA methylation of the tumor suppressor genes were the major abnormalities investigated between 1980 and th...
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Autor*in:	Toyooka, Shinichi [verfasserIn] Mitsudomi, Tetsuya Soh, Junichi Aokage, Keiju Yamane, Masaomi Oto, Takahiro Kiura, Katsuyuki Miyoshi, Shinichiro

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2011

Anmerkung:	© The Japanese Association for Thoracic Surgery 2011

Übergeordnetes Werk:	Enthalten in: The Japanese journal of thoracic and cardiovascular surgery - Tōkyō : Springer Japan, 1998, 59(2011), 8 vom: 18. Aug.
Übergeordnetes Werk:	volume:59 ; year:2011 ; number:8 ; day:18 ; month:08

Links:	Volltext

DOI / URN:	10.1007/s11748-010-0743-3

Katalog-ID:	SPR022500235

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allfields	10.1007/s11748-010-0743-3 doi (DE-627)SPR022500235 (SPR)s11748-010-0743-3-e DE-627 ger DE-627 rakwb eng Toyooka, Shinichi verfasserin aut Molecular oncology of lung cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Association for Thoracic Surgery 2011 Abstract Progress in genetic engineering has made it possible to elucidate the molecular biological abnormalities in lung cancer. Mutations in KRAS and P53 genes, loss of specific alleles, and DNA methylation of the tumor suppressor genes were the major abnormalities investigated between 1980 and the 2000s. In 2004, mutations in the epidermal growth factor receptor (EGFR) gene that cause oncogene addiction were discovered in non-small-cell lung cancers (NSCLCs), especially in adenocarcinomas. Because they are strongly associated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), a great deal of knowledge has been acquired in regard to both EGFR and other genes in the EGFR family and their downstream genes. Moreover, in 2007 the existence of the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene was discovered in NSCLC; and the same as EGFR-TKIs, ALK inhibitors are being found to be highly effective in lung cancers that have this translocation. These discoveries graphically illustrate that molecular biological findings are directly linked to the development of clinical oncology and to improving the survival rates of lung cancer patients. Here, we review the remarkable progress in molecular biological knowledge acquired thus far in regard to lung cancer, especially NSCLC, and the future possibilities. Mitsudomi, Tetsuya aut Soh, Junichi aut Aokage, Keiju aut Yamane, Masaomi aut Oto, Takahiro aut Kiura, Katsuyuki aut Miyoshi, Shinichiro aut Enthalten in The Japanese journal of thoracic and cardiovascular surgery Tōkyō : Springer Japan, 1998 59(2011), 8 vom: 18. Aug. (DE-627)539545104 (DE-600)2381600-4 1863-2092 nnns volume:59 year:2011 number:8 day:18 month:08 https://dx.doi.org/10.1007/s11748-010-0743-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 AR 59 2011 8 18 08
spelling	10.1007/s11748-010-0743-3 doi (DE-627)SPR022500235 (SPR)s11748-010-0743-3-e DE-627 ger DE-627 rakwb eng Toyooka, Shinichi verfasserin aut Molecular oncology of lung cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Association for Thoracic Surgery 2011 Abstract Progress in genetic engineering has made it possible to elucidate the molecular biological abnormalities in lung cancer. Mutations in KRAS and P53 genes, loss of specific alleles, and DNA methylation of the tumor suppressor genes were the major abnormalities investigated between 1980 and the 2000s. In 2004, mutations in the epidermal growth factor receptor (EGFR) gene that cause oncogene addiction were discovered in non-small-cell lung cancers (NSCLCs), especially in adenocarcinomas. Because they are strongly associated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), a great deal of knowledge has been acquired in regard to both EGFR and other genes in the EGFR family and their downstream genes. Moreover, in 2007 the existence of the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene was discovered in NSCLC; and the same as EGFR-TKIs, ALK inhibitors are being found to be highly effective in lung cancers that have this translocation. These discoveries graphically illustrate that molecular biological findings are directly linked to the development of clinical oncology and to improving the survival rates of lung cancer patients. Here, we review the remarkable progress in molecular biological knowledge acquired thus far in regard to lung cancer, especially NSCLC, and the future possibilities. Mitsudomi, Tetsuya aut Soh, Junichi aut Aokage, Keiju aut Yamane, Masaomi aut Oto, Takahiro aut Kiura, Katsuyuki aut Miyoshi, Shinichiro aut Enthalten in The Japanese journal of thoracic and cardiovascular surgery Tōkyō : Springer Japan, 1998 59(2011), 8 vom: 18. Aug. (DE-627)539545104 (DE-600)2381600-4 1863-2092 nnns volume:59 year:2011 number:8 day:18 month:08 https://dx.doi.org/10.1007/s11748-010-0743-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 AR 59 2011 8 18 08
allfields_unstemmed	10.1007/s11748-010-0743-3 doi (DE-627)SPR022500235 (SPR)s11748-010-0743-3-e DE-627 ger DE-627 rakwb eng Toyooka, Shinichi verfasserin aut Molecular oncology of lung cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Association for Thoracic Surgery 2011 Abstract Progress in genetic engineering has made it possible to elucidate the molecular biological abnormalities in lung cancer. Mutations in KRAS and P53 genes, loss of specific alleles, and DNA methylation of the tumor suppressor genes were the major abnormalities investigated between 1980 and the 2000s. In 2004, mutations in the epidermal growth factor receptor (EGFR) gene that cause oncogene addiction were discovered in non-small-cell lung cancers (NSCLCs), especially in adenocarcinomas. Because they are strongly associated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), a great deal of knowledge has been acquired in regard to both EGFR and other genes in the EGFR family and their downstream genes. Moreover, in 2007 the existence of the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene was discovered in NSCLC; and the same as EGFR-TKIs, ALK inhibitors are being found to be highly effective in lung cancers that have this translocation. These discoveries graphically illustrate that molecular biological findings are directly linked to the development of clinical oncology and to improving the survival rates of lung cancer patients. Here, we review the remarkable progress in molecular biological knowledge acquired thus far in regard to lung cancer, especially NSCLC, and the future possibilities. Mitsudomi, Tetsuya aut Soh, Junichi aut Aokage, Keiju aut Yamane, Masaomi aut Oto, Takahiro aut Kiura, Katsuyuki aut Miyoshi, Shinichiro aut Enthalten in The Japanese journal of thoracic and cardiovascular surgery Tōkyō : Springer Japan, 1998 59(2011), 8 vom: 18. Aug. (DE-627)539545104 (DE-600)2381600-4 1863-2092 nnns volume:59 year:2011 number:8 day:18 month:08 https://dx.doi.org/10.1007/s11748-010-0743-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 AR 59 2011 8 18 08
allfieldsGer	10.1007/s11748-010-0743-3 doi (DE-627)SPR022500235 (SPR)s11748-010-0743-3-e DE-627 ger DE-627 rakwb eng Toyooka, Shinichi verfasserin aut Molecular oncology of lung cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Association for Thoracic Surgery 2011 Abstract Progress in genetic engineering has made it possible to elucidate the molecular biological abnormalities in lung cancer. Mutations in KRAS and P53 genes, loss of specific alleles, and DNA methylation of the tumor suppressor genes were the major abnormalities investigated between 1980 and the 2000s. In 2004, mutations in the epidermal growth factor receptor (EGFR) gene that cause oncogene addiction were discovered in non-small-cell lung cancers (NSCLCs), especially in adenocarcinomas. Because they are strongly associated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), a great deal of knowledge has been acquired in regard to both EGFR and other genes in the EGFR family and their downstream genes. Moreover, in 2007 the existence of the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene was discovered in NSCLC; and the same as EGFR-TKIs, ALK inhibitors are being found to be highly effective in lung cancers that have this translocation. These discoveries graphically illustrate that molecular biological findings are directly linked to the development of clinical oncology and to improving the survival rates of lung cancer patients. Here, we review the remarkable progress in molecular biological knowledge acquired thus far in regard to lung cancer, especially NSCLC, and the future possibilities. Mitsudomi, Tetsuya aut Soh, Junichi aut Aokage, Keiju aut Yamane, Masaomi aut Oto, Takahiro aut Kiura, Katsuyuki aut Miyoshi, Shinichiro aut Enthalten in The Japanese journal of thoracic and cardiovascular surgery Tōkyō : Springer Japan, 1998 59(2011), 8 vom: 18. Aug. (DE-627)539545104 (DE-600)2381600-4 1863-2092 nnns volume:59 year:2011 number:8 day:18 month:08 https://dx.doi.org/10.1007/s11748-010-0743-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 AR 59 2011 8 18 08
allfieldsSound	10.1007/s11748-010-0743-3 doi (DE-627)SPR022500235 (SPR)s11748-010-0743-3-e DE-627 ger DE-627 rakwb eng Toyooka, Shinichi verfasserin aut Molecular oncology of lung cancer 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Association for Thoracic Surgery 2011 Abstract Progress in genetic engineering has made it possible to elucidate the molecular biological abnormalities in lung cancer. Mutations in KRAS and P53 genes, loss of specific alleles, and DNA methylation of the tumor suppressor genes were the major abnormalities investigated between 1980 and the 2000s. In 2004, mutations in the epidermal growth factor receptor (EGFR) gene that cause oncogene addiction were discovered in non-small-cell lung cancers (NSCLCs), especially in adenocarcinomas. Because they are strongly associated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), a great deal of knowledge has been acquired in regard to both EGFR and other genes in the EGFR family and their downstream genes. Moreover, in 2007 the existence of the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene was discovered in NSCLC; and the same as EGFR-TKIs, ALK inhibitors are being found to be highly effective in lung cancers that have this translocation. These discoveries graphically illustrate that molecular biological findings are directly linked to the development of clinical oncology and to improving the survival rates of lung cancer patients. Here, we review the remarkable progress in molecular biological knowledge acquired thus far in regard to lung cancer, especially NSCLC, and the future possibilities. Mitsudomi, Tetsuya aut Soh, Junichi aut Aokage, Keiju aut Yamane, Masaomi aut Oto, Takahiro aut Kiura, Katsuyuki aut Miyoshi, Shinichiro aut Enthalten in The Japanese journal of thoracic and cardiovascular surgery Tōkyō : Springer Japan, 1998 59(2011), 8 vom: 18. Aug. (DE-627)539545104 (DE-600)2381600-4 1863-2092 nnns volume:59 year:2011 number:8 day:18 month:08 https://dx.doi.org/10.1007/s11748-010-0743-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_120 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 AR 59 2011 8 18 08
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title	Molecular oncology of lung cancer
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abstract	Abstract Progress in genetic engineering has made it possible to elucidate the molecular biological abnormalities in lung cancer. Mutations in KRAS and P53 genes, loss of specific alleles, and DNA methylation of the tumor suppressor genes were the major abnormalities investigated between 1980 and the 2000s. In 2004, mutations in the epidermal growth factor receptor (EGFR) gene that cause oncogene addiction were discovered in non-small-cell lung cancers (NSCLCs), especially in adenocarcinomas. Because they are strongly associated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), a great deal of knowledge has been acquired in regard to both EGFR and other genes in the EGFR family and their downstream genes. Moreover, in 2007 the existence of the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene was discovered in NSCLC; and the same as EGFR-TKIs, ALK inhibitors are being found to be highly effective in lung cancers that have this translocation. These discoveries graphically illustrate that molecular biological findings are directly linked to the development of clinical oncology and to improving the survival rates of lung cancer patients. Here, we review the remarkable progress in molecular biological knowledge acquired thus far in regard to lung cancer, especially NSCLC, and the future possibilities. © The Japanese Association for Thoracic Surgery 2011
abstractGer	Abstract Progress in genetic engineering has made it possible to elucidate the molecular biological abnormalities in lung cancer. Mutations in KRAS and P53 genes, loss of specific alleles, and DNA methylation of the tumor suppressor genes were the major abnormalities investigated between 1980 and the 2000s. In 2004, mutations in the epidermal growth factor receptor (EGFR) gene that cause oncogene addiction were discovered in non-small-cell lung cancers (NSCLCs), especially in adenocarcinomas. Because they are strongly associated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), a great deal of knowledge has been acquired in regard to both EGFR and other genes in the EGFR family and their downstream genes. Moreover, in 2007 the existence of the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene was discovered in NSCLC; and the same as EGFR-TKIs, ALK inhibitors are being found to be highly effective in lung cancers that have this translocation. These discoveries graphically illustrate that molecular biological findings are directly linked to the development of clinical oncology and to improving the survival rates of lung cancer patients. Here, we review the remarkable progress in molecular biological knowledge acquired thus far in regard to lung cancer, especially NSCLC, and the future possibilities. © The Japanese Association for Thoracic Surgery 2011
abstract_unstemmed	Abstract Progress in genetic engineering has made it possible to elucidate the molecular biological abnormalities in lung cancer. Mutations in KRAS and P53 genes, loss of specific alleles, and DNA methylation of the tumor suppressor genes were the major abnormalities investigated between 1980 and the 2000s. In 2004, mutations in the epidermal growth factor receptor (EGFR) gene that cause oncogene addiction were discovered in non-small-cell lung cancers (NSCLCs), especially in adenocarcinomas. Because they are strongly associated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), a great deal of knowledge has been acquired in regard to both EGFR and other genes in the EGFR family and their downstream genes. Moreover, in 2007 the existence of the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene was discovered in NSCLC; and the same as EGFR-TKIs, ALK inhibitors are being found to be highly effective in lung cancers that have this translocation. These discoveries graphically illustrate that molecular biological findings are directly linked to the development of clinical oncology and to improving the survival rates of lung cancer patients. Here, we review the remarkable progress in molecular biological knowledge acquired thus far in regard to lung cancer, especially NSCLC, and the future possibilities. © The Japanese Association for Thoracic Surgery 2011
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title_short	Molecular oncology of lung cancer
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