Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway

The molecular hallmarks of inflammation-mediated lung carcinogenesis have not been fully clarified, mainly due to the scarcity of appropriate animal models. We have used a silica-induced multistep lung carcinogenesis model driven by chronic inflammation to study the evolution of molecular markers, g...
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Autor*in:	David Blanco [verfasserIn] Silvestre Vicent [verfasserIn] Mario F. Fraga [verfasserIn] Ignacio Fernandez-Garcia [verfasserIn] Javier Freire [verfasserIn] Amaia Lujambio [verfasserIn] Manel Esteller [verfasserIn] Carlos Ortiz-de-Solorzano [verfasserIn] Ruben Pio [verfasserIn] Fernando Lecanda [verfasserIn] Luis M. Montuenga [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2007

Schlagwörter:	lung cancer inflammation animal model preneoplastic lesions DNA damage response

Übergeordnetes Werk:	In: Neoplasia: An International Journal for Oncology Research - Elsevier, 2008, 9(2007), 10, Seite 840-852
Übergeordnetes Werk:	volume:9 ; year:2007 ; number:10 ; pages:840-852

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1593/neo.07517

Katalog-ID:	DOAJ077697103

Internformat


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520			\|a The molecular hallmarks of inflammation-mediated lung carcinogenesis have not been fully clarified, mainly due to the scarcity of appropriate animal models. We have used a silica-induced multistep lung carcinogenesis model driven by chronic inflammation to study the evolution of molecular markers, genetic alterations. We analyzed markers of DNA damage response (DDR), proliferative stress, telomeric stress: δ-H2AX, p16, p53, TERT. Lung cancer-related epigenetic, genetic alterations, including promoter hypermethylation status of p16(CDKN2A), APC, CDH13, Rassf1, Nore1A, as well as mutations of Tp53, epidermal growth factor receptor, K-ras, N-ras, c-H-ras, have been also studied. Our results showed DDR pathway activation in preneoplastic lesions, in association with inducible nitric oxide synthase, p53 induction. p16 was also induced in early tumorigenic progression, was inactivated in bronchiolar dysplasias, tumors. Remarkably, lack of mutations of Ras, epidermal growth factor receptor, a very low frequency of Tp53 mutations suggest that they are not required for tumorigenesis in this model. In contrast, epigenetic alterations in p16(CDKN2A), CDH13, APC, but not in Rassf1, Nore1A, were clearly observed. These data suggest the existence of a specific molecular signature of inflammation-driven lung carcinogenesis that shares some, but not all, of the molecular landmarks of chemically induced lung cancer.
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650		4	\|a preneoplastic lesions
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653		0	\|a Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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700	0		\|a Mario F. Fraga \|e verfasserin \|4 aut
700	0		\|a Ignacio Fernandez-Garcia \|e verfasserin \|4 aut
700	0		\|a Javier Freire \|e verfasserin \|4 aut
700	0		\|a Amaia Lujambio \|e verfasserin \|4 aut
700	0		\|a Manel Esteller \|e verfasserin \|4 aut
700	0		\|a Carlos Ortiz-de-Solorzano \|e verfasserin \|4 aut
700	0		\|a Ruben Pio \|e verfasserin \|4 aut
700	0		\|a Fernando Lecanda \|e verfasserin \|4 aut
700	0		\|a Luis M. Montuenga \|e verfasserin \|4 aut
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allfields	10.1593/neo.07517 doi (DE-627)DOAJ077697103 (DE-599)DOAJ56003e2bccc9405f9f690ca6e8cafd0c DE-627 ger DE-627 rakwb eng RC254-282 David Blanco verfasserin aut Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The molecular hallmarks of inflammation-mediated lung carcinogenesis have not been fully clarified, mainly due to the scarcity of appropriate animal models. We have used a silica-induced multistep lung carcinogenesis model driven by chronic inflammation to study the evolution of molecular markers, genetic alterations. We analyzed markers of DNA damage response (DDR), proliferative stress, telomeric stress: δ-H2AX, p16, p53, TERT. Lung cancer-related epigenetic, genetic alterations, including promoter hypermethylation status of p16(CDKN2A), APC, CDH13, Rassf1, Nore1A, as well as mutations of Tp53, epidermal growth factor receptor, K-ras, N-ras, c-H-ras, have been also studied. Our results showed DDR pathway activation in preneoplastic lesions, in association with inducible nitric oxide synthase, p53 induction. p16 was also induced in early tumorigenic progression, was inactivated in bronchiolar dysplasias, tumors. Remarkably, lack of mutations of Ras, epidermal growth factor receptor, a very low frequency of Tp53 mutations suggest that they are not required for tumorigenesis in this model. In contrast, epigenetic alterations in p16(CDKN2A), CDH13, APC, but not in Rassf1, Nore1A, were clearly observed. These data suggest the existence of a specific molecular signature of inflammation-driven lung carcinogenesis that shares some, but not all, of the molecular landmarks of chemically induced lung cancer. lung cancer inflammation animal model preneoplastic lesions DNA damage response Neoplasms. Tumors. Oncology. Including cancer and carcinogens Silvestre Vicent verfasserin aut Mario F. Fraga verfasserin aut Ignacio Fernandez-Garcia verfasserin aut Javier Freire verfasserin aut Amaia Lujambio verfasserin aut Manel Esteller verfasserin aut Carlos Ortiz-de-Solorzano verfasserin aut Ruben Pio verfasserin aut Fernando Lecanda verfasserin aut Luis M. Montuenga verfasserin aut In Neoplasia: An International Journal for Oncology Research Elsevier, 2008 9(2007), 10, Seite 840-852 (DE-627)320468690 (DE-600)2008231-9 14765586 nnns volume:9 year:2007 number:10 pages:840-852 https://doi.org/10.1593/neo.07517 kostenfrei https://doaj.org/article/56003e2bccc9405f9f690ca6e8cafd0c kostenfrei http://www.sciencedirect.com/science/article/pii/S1476558607800649 kostenfrei https://doaj.org/toc/1476-5586 Journal toc kostenfrei https://doaj.org/toc/1522-8002 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 9 2007 10 840-852
spelling	10.1593/neo.07517 doi (DE-627)DOAJ077697103 (DE-599)DOAJ56003e2bccc9405f9f690ca6e8cafd0c DE-627 ger DE-627 rakwb eng RC254-282 David Blanco verfasserin aut Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The molecular hallmarks of inflammation-mediated lung carcinogenesis have not been fully clarified, mainly due to the scarcity of appropriate animal models. We have used a silica-induced multistep lung carcinogenesis model driven by chronic inflammation to study the evolution of molecular markers, genetic alterations. We analyzed markers of DNA damage response (DDR), proliferative stress, telomeric stress: δ-H2AX, p16, p53, TERT. Lung cancer-related epigenetic, genetic alterations, including promoter hypermethylation status of p16(CDKN2A), APC, CDH13, Rassf1, Nore1A, as well as mutations of Tp53, epidermal growth factor receptor, K-ras, N-ras, c-H-ras, have been also studied. Our results showed DDR pathway activation in preneoplastic lesions, in association with inducible nitric oxide synthase, p53 induction. p16 was also induced in early tumorigenic progression, was inactivated in bronchiolar dysplasias, tumors. Remarkably, lack of mutations of Ras, epidermal growth factor receptor, a very low frequency of Tp53 mutations suggest that they are not required for tumorigenesis in this model. In contrast, epigenetic alterations in p16(CDKN2A), CDH13, APC, but not in Rassf1, Nore1A, were clearly observed. These data suggest the existence of a specific molecular signature of inflammation-driven lung carcinogenesis that shares some, but not all, of the molecular landmarks of chemically induced lung cancer. lung cancer inflammation animal model preneoplastic lesions DNA damage response Neoplasms. Tumors. Oncology. Including cancer and carcinogens Silvestre Vicent verfasserin aut Mario F. Fraga verfasserin aut Ignacio Fernandez-Garcia verfasserin aut Javier Freire verfasserin aut Amaia Lujambio verfasserin aut Manel Esteller verfasserin aut Carlos Ortiz-de-Solorzano verfasserin aut Ruben Pio verfasserin aut Fernando Lecanda verfasserin aut Luis M. Montuenga verfasserin aut In Neoplasia: An International Journal for Oncology Research Elsevier, 2008 9(2007), 10, Seite 840-852 (DE-627)320468690 (DE-600)2008231-9 14765586 nnns volume:9 year:2007 number:10 pages:840-852 https://doi.org/10.1593/neo.07517 kostenfrei https://doaj.org/article/56003e2bccc9405f9f690ca6e8cafd0c kostenfrei http://www.sciencedirect.com/science/article/pii/S1476558607800649 kostenfrei https://doaj.org/toc/1476-5586 Journal toc kostenfrei https://doaj.org/toc/1522-8002 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 9 2007 10 840-852
allfields_unstemmed	10.1593/neo.07517 doi (DE-627)DOAJ077697103 (DE-599)DOAJ56003e2bccc9405f9f690ca6e8cafd0c DE-627 ger DE-627 rakwb eng RC254-282 David Blanco verfasserin aut Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The molecular hallmarks of inflammation-mediated lung carcinogenesis have not been fully clarified, mainly due to the scarcity of appropriate animal models. We have used a silica-induced multistep lung carcinogenesis model driven by chronic inflammation to study the evolution of molecular markers, genetic alterations. We analyzed markers of DNA damage response (DDR), proliferative stress, telomeric stress: δ-H2AX, p16, p53, TERT. Lung cancer-related epigenetic, genetic alterations, including promoter hypermethylation status of p16(CDKN2A), APC, CDH13, Rassf1, Nore1A, as well as mutations of Tp53, epidermal growth factor receptor, K-ras, N-ras, c-H-ras, have been also studied. Our results showed DDR pathway activation in preneoplastic lesions, in association with inducible nitric oxide synthase, p53 induction. p16 was also induced in early tumorigenic progression, was inactivated in bronchiolar dysplasias, tumors. Remarkably, lack of mutations of Ras, epidermal growth factor receptor, a very low frequency of Tp53 mutations suggest that they are not required for tumorigenesis in this model. In contrast, epigenetic alterations in p16(CDKN2A), CDH13, APC, but not in Rassf1, Nore1A, were clearly observed. These data suggest the existence of a specific molecular signature of inflammation-driven lung carcinogenesis that shares some, but not all, of the molecular landmarks of chemically induced lung cancer. lung cancer inflammation animal model preneoplastic lesions DNA damage response Neoplasms. Tumors. Oncology. Including cancer and carcinogens Silvestre Vicent verfasserin aut Mario F. Fraga verfasserin aut Ignacio Fernandez-Garcia verfasserin aut Javier Freire verfasserin aut Amaia Lujambio verfasserin aut Manel Esteller verfasserin aut Carlos Ortiz-de-Solorzano verfasserin aut Ruben Pio verfasserin aut Fernando Lecanda verfasserin aut Luis M. Montuenga verfasserin aut In Neoplasia: An International Journal for Oncology Research Elsevier, 2008 9(2007), 10, Seite 840-852 (DE-627)320468690 (DE-600)2008231-9 14765586 nnns volume:9 year:2007 number:10 pages:840-852 https://doi.org/10.1593/neo.07517 kostenfrei https://doaj.org/article/56003e2bccc9405f9f690ca6e8cafd0c kostenfrei http://www.sciencedirect.com/science/article/pii/S1476558607800649 kostenfrei https://doaj.org/toc/1476-5586 Journal toc kostenfrei https://doaj.org/toc/1522-8002 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 9 2007 10 840-852
allfieldsGer	10.1593/neo.07517 doi (DE-627)DOAJ077697103 (DE-599)DOAJ56003e2bccc9405f9f690ca6e8cafd0c DE-627 ger DE-627 rakwb eng RC254-282 David Blanco verfasserin aut Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The molecular hallmarks of inflammation-mediated lung carcinogenesis have not been fully clarified, mainly due to the scarcity of appropriate animal models. We have used a silica-induced multistep lung carcinogenesis model driven by chronic inflammation to study the evolution of molecular markers, genetic alterations. We analyzed markers of DNA damage response (DDR), proliferative stress, telomeric stress: δ-H2AX, p16, p53, TERT. Lung cancer-related epigenetic, genetic alterations, including promoter hypermethylation status of p16(CDKN2A), APC, CDH13, Rassf1, Nore1A, as well as mutations of Tp53, epidermal growth factor receptor, K-ras, N-ras, c-H-ras, have been also studied. Our results showed DDR pathway activation in preneoplastic lesions, in association with inducible nitric oxide synthase, p53 induction. p16 was also induced in early tumorigenic progression, was inactivated in bronchiolar dysplasias, tumors. Remarkably, lack of mutations of Ras, epidermal growth factor receptor, a very low frequency of Tp53 mutations suggest that they are not required for tumorigenesis in this model. In contrast, epigenetic alterations in p16(CDKN2A), CDH13, APC, but not in Rassf1, Nore1A, were clearly observed. These data suggest the existence of a specific molecular signature of inflammation-driven lung carcinogenesis that shares some, but not all, of the molecular landmarks of chemically induced lung cancer. lung cancer inflammation animal model preneoplastic lesions DNA damage response Neoplasms. Tumors. Oncology. Including cancer and carcinogens Silvestre Vicent verfasserin aut Mario F. Fraga verfasserin aut Ignacio Fernandez-Garcia verfasserin aut Javier Freire verfasserin aut Amaia Lujambio verfasserin aut Manel Esteller verfasserin aut Carlos Ortiz-de-Solorzano verfasserin aut Ruben Pio verfasserin aut Fernando Lecanda verfasserin aut Luis M. Montuenga verfasserin aut In Neoplasia: An International Journal for Oncology Research Elsevier, 2008 9(2007), 10, Seite 840-852 (DE-627)320468690 (DE-600)2008231-9 14765586 nnns volume:9 year:2007 number:10 pages:840-852 https://doi.org/10.1593/neo.07517 kostenfrei https://doaj.org/article/56003e2bccc9405f9f690ca6e8cafd0c kostenfrei http://www.sciencedirect.com/science/article/pii/S1476558607800649 kostenfrei https://doaj.org/toc/1476-5586 Journal toc kostenfrei https://doaj.org/toc/1522-8002 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 9 2007 10 840-852
allfieldsSound	10.1593/neo.07517 doi (DE-627)DOAJ077697103 (DE-599)DOAJ56003e2bccc9405f9f690ca6e8cafd0c DE-627 ger DE-627 rakwb eng RC254-282 David Blanco verfasserin aut Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The molecular hallmarks of inflammation-mediated lung carcinogenesis have not been fully clarified, mainly due to the scarcity of appropriate animal models. We have used a silica-induced multistep lung carcinogenesis model driven by chronic inflammation to study the evolution of molecular markers, genetic alterations. We analyzed markers of DNA damage response (DDR), proliferative stress, telomeric stress: δ-H2AX, p16, p53, TERT. Lung cancer-related epigenetic, genetic alterations, including promoter hypermethylation status of p16(CDKN2A), APC, CDH13, Rassf1, Nore1A, as well as mutations of Tp53, epidermal growth factor receptor, K-ras, N-ras, c-H-ras, have been also studied. Our results showed DDR pathway activation in preneoplastic lesions, in association with inducible nitric oxide synthase, p53 induction. p16 was also induced in early tumorigenic progression, was inactivated in bronchiolar dysplasias, tumors. Remarkably, lack of mutations of Ras, epidermal growth factor receptor, a very low frequency of Tp53 mutations suggest that they are not required for tumorigenesis in this model. In contrast, epigenetic alterations in p16(CDKN2A), CDH13, APC, but not in Rassf1, Nore1A, were clearly observed. These data suggest the existence of a specific molecular signature of inflammation-driven lung carcinogenesis that shares some, but not all, of the molecular landmarks of chemically induced lung cancer. lung cancer inflammation animal model preneoplastic lesions DNA damage response Neoplasms. Tumors. Oncology. Including cancer and carcinogens Silvestre Vicent verfasserin aut Mario F. Fraga verfasserin aut Ignacio Fernandez-Garcia verfasserin aut Javier Freire verfasserin aut Amaia Lujambio verfasserin aut Manel Esteller verfasserin aut Carlos Ortiz-de-Solorzano verfasserin aut Ruben Pio verfasserin aut Fernando Lecanda verfasserin aut Luis M. Montuenga verfasserin aut In Neoplasia: An International Journal for Oncology Research Elsevier, 2008 9(2007), 10, Seite 840-852 (DE-627)320468690 (DE-600)2008231-9 14765586 nnns volume:9 year:2007 number:10 pages:840-852 https://doi.org/10.1593/neo.07517 kostenfrei https://doaj.org/article/56003e2bccc9405f9f690ca6e8cafd0c kostenfrei http://www.sciencedirect.com/science/article/pii/S1476558607800649 kostenfrei https://doaj.org/toc/1476-5586 Journal toc kostenfrei https://doaj.org/toc/1522-8002 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 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_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 9 2007 10 840-852
language	English
source	In Neoplasia: An International Journal for Oncology Research 9(2007), 10, Seite 840-852 volume:9 year:2007 number:10 pages:840-852
sourceStr	In Neoplasia: An International Journal for Oncology Research 9(2007), 10, Seite 840-852 volume:9 year:2007 number:10 pages:840-852
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	lung cancer inflammation animal model preneoplastic lesions DNA damage response Neoplasms. Tumors. Oncology. Including cancer and carcinogens
isfreeaccess_bool	true
container_title	Neoplasia: An International Journal for Oncology Research
authorswithroles_txt_mv	David Blanco @@aut@@ Silvestre Vicent @@aut@@ Mario F. Fraga @@aut@@ Ignacio Fernandez-Garcia @@aut@@ Javier Freire @@aut@@ Amaia Lujambio @@aut@@ Manel Esteller @@aut@@ Carlos Ortiz-de-Solorzano @@aut@@ Ruben Pio @@aut@@ Fernando Lecanda @@aut@@ Luis M. Montuenga @@aut@@
publishDateDaySort_date	2007-01-01T00:00:00Z
hierarchy_top_id	320468690
id	DOAJ077697103
language_de	englisch
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callnumber-first	R - Medicine
author	David Blanco
spellingShingle	David Blanco misc RC254-282 misc lung cancer misc inflammation misc animal model misc preneoplastic lesions misc DNA damage response misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway
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topic_title	RC254-282 Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway lung cancer inflammation animal model preneoplastic lesions DNA damage response
topic	misc RC254-282 misc lung cancer misc inflammation misc animal model misc preneoplastic lesions misc DNA damage response misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc lung cancer misc inflammation misc animal model misc preneoplastic lesions misc DNA damage response misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_browse	misc RC254-282 misc lung cancer misc inflammation misc animal model misc preneoplastic lesions misc DNA damage response misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway
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title_full	Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway
author_sort	David Blanco
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author_browse	David Blanco Silvestre Vicent Mario F. Fraga Ignacio Fernandez-Garcia Javier Freire Amaia Lujambio Manel Esteller Carlos Ortiz-de-Solorzano Ruben Pio Fernando Lecanda Luis M. Montuenga
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title_sort	molecular analysis of a multistep lung cancer model induced by chronic inflammation reveals epigenetic regulation of p16, activation of the dna damage response pathway
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title_auth	Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway
abstract	The molecular hallmarks of inflammation-mediated lung carcinogenesis have not been fully clarified, mainly due to the scarcity of appropriate animal models. We have used a silica-induced multistep lung carcinogenesis model driven by chronic inflammation to study the evolution of molecular markers, genetic alterations. We analyzed markers of DNA damage response (DDR), proliferative stress, telomeric stress: δ-H2AX, p16, p53, TERT. Lung cancer-related epigenetic, genetic alterations, including promoter hypermethylation status of p16(CDKN2A), APC, CDH13, Rassf1, Nore1A, as well as mutations of Tp53, epidermal growth factor receptor, K-ras, N-ras, c-H-ras, have been also studied. Our results showed DDR pathway activation in preneoplastic lesions, in association with inducible nitric oxide synthase, p53 induction. p16 was also induced in early tumorigenic progression, was inactivated in bronchiolar dysplasias, tumors. Remarkably, lack of mutations of Ras, epidermal growth factor receptor, a very low frequency of Tp53 mutations suggest that they are not required for tumorigenesis in this model. In contrast, epigenetic alterations in p16(CDKN2A), CDH13, APC, but not in Rassf1, Nore1A, were clearly observed. These data suggest the existence of a specific molecular signature of inflammation-driven lung carcinogenesis that shares some, but not all, of the molecular landmarks of chemically induced lung cancer.
abstractGer	The molecular hallmarks of inflammation-mediated lung carcinogenesis have not been fully clarified, mainly due to the scarcity of appropriate animal models. We have used a silica-induced multistep lung carcinogenesis model driven by chronic inflammation to study the evolution of molecular markers, genetic alterations. We analyzed markers of DNA damage response (DDR), proliferative stress, telomeric stress: δ-H2AX, p16, p53, TERT. Lung cancer-related epigenetic, genetic alterations, including promoter hypermethylation status of p16(CDKN2A), APC, CDH13, Rassf1, Nore1A, as well as mutations of Tp53, epidermal growth factor receptor, K-ras, N-ras, c-H-ras, have been also studied. Our results showed DDR pathway activation in preneoplastic lesions, in association with inducible nitric oxide synthase, p53 induction. p16 was also induced in early tumorigenic progression, was inactivated in bronchiolar dysplasias, tumors. Remarkably, lack of mutations of Ras, epidermal growth factor receptor, a very low frequency of Tp53 mutations suggest that they are not required for tumorigenesis in this model. In contrast, epigenetic alterations in p16(CDKN2A), CDH13, APC, but not in Rassf1, Nore1A, were clearly observed. These data suggest the existence of a specific molecular signature of inflammation-driven lung carcinogenesis that shares some, but not all, of the molecular landmarks of chemically induced lung cancer.
abstract_unstemmed	The molecular hallmarks of inflammation-mediated lung carcinogenesis have not been fully clarified, mainly due to the scarcity of appropriate animal models. We have used a silica-induced multistep lung carcinogenesis model driven by chronic inflammation to study the evolution of molecular markers, genetic alterations. We analyzed markers of DNA damage response (DDR), proliferative stress, telomeric stress: δ-H2AX, p16, p53, TERT. Lung cancer-related epigenetic, genetic alterations, including promoter hypermethylation status of p16(CDKN2A), APC, CDH13, Rassf1, Nore1A, as well as mutations of Tp53, epidermal growth factor receptor, K-ras, N-ras, c-H-ras, have been also studied. Our results showed DDR pathway activation in preneoplastic lesions, in association with inducible nitric oxide synthase, p53 induction. p16 was also induced in early tumorigenic progression, was inactivated in bronchiolar dysplasias, tumors. Remarkably, lack of mutations of Ras, epidermal growth factor receptor, a very low frequency of Tp53 mutations suggest that they are not required for tumorigenesis in this model. In contrast, epigenetic alterations in p16(CDKN2A), CDH13, APC, but not in Rassf1, Nore1A, were clearly observed. These data suggest the existence of a specific molecular signature of inflammation-driven lung carcinogenesis that shares some, but not all, of the molecular landmarks of chemically induced lung cancer.
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title_short	Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway
url	https://doi.org/10.1593/neo.07517 https://doaj.org/article/56003e2bccc9405f9f690ca6e8cafd0c http://www.sciencedirect.com/science/article/pii/S1476558607800649 https://doaj.org/toc/1476-5586 https://doaj.org/toc/1522-8002
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up_date	2024-07-03T13:34:58.197Z
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Molecular Analysis of a Multistep Lung Cancer Model Induced by Chronic Inflammation Reveals Epigenetic Regulation of p16, Activation of the DNA Damage Response Pathway

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