Variants in autophagy‐related genes and clinical characteristics in melanoma: a population‐based study
Abstract Autophagy has been linked with melanoma risk and survival, but no polymorphisms in autophagy‐related (ATG) genes have been investigated in relation to melanoma progression. We examined five single‐nucleotide polymorphisms (SNPs) in three ATG genes (ATG5; ATG10; and ATG16L) with known or sus...
Ausführliche Beschreibung
Autor*in: |
Kirsten A. M. White [verfasserIn] Li Luo [verfasserIn] Todd A. Thompson [verfasserIn] Salina Torres [verfasserIn] Chien‐An Andy Hu [verfasserIn] Nancy E. Thomas [verfasserIn] Jenna Lilyquist [verfasserIn] Hoda Anton‐Culver [verfasserIn] Stephen B. Gruber [verfasserIn] Lynn From [verfasserIn] Klaus J. Busam [verfasserIn] Irene Orlow [verfasserIn] Peter A. Kanetsky [verfasserIn] Loraine D. Marrett [verfasserIn] Richard P. Gallagher [verfasserIn] Lidia Sacchetto [verfasserIn] Stefano Rosso [verfasserIn] Terence Dwyer [verfasserIn] Anne E. Cust [verfasserIn] Colin B. Begg [verfasserIn] Marianne Berwick [verfasserIn] The GEM Study Group [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2016 |
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Übergeordnetes Werk: |
In: Cancer Medicine - Wiley, 2012, 5(2016), 11, Seite 3336-3345 |
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Übergeordnetes Werk: |
volume:5 ; year:2016 ; number:11 ; pages:3336-3345 |
Links: |
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DOI / URN: |
10.1002/cam4.929 |
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Katalog-ID: |
DOAJ068327072 |
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245 | 1 | 0 | |a Variants in autophagy‐related genes and clinical characteristics in melanoma: a population‐based study |
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520 | |a Abstract Autophagy has been linked with melanoma risk and survival, but no polymorphisms in autophagy‐related (ATG) genes have been investigated in relation to melanoma progression. We examined five single‐nucleotide polymorphisms (SNPs) in three ATG genes (ATG5; ATG10; and ATG16L) with known or suspected impact on autophagic flux in an international population‐based case–control study of melanoma. DNA from 911 melanoma patients was genotyped. An association was identified between (GG) (rs2241880) and earlier stage at diagnosis (OR 0.47; 95% Confidence Intervals (CI) = 0.27–0.81, P = 0.02) and a decrease in Breslow thickness (P = 0.03). The ATG16L heterozygous genotype (AG) (rs2241880) was associated with younger age at diagnosis (P = 0.02). Two SNPs in ATG5 were found to be associated with increased stage (rs2245214 CG, OR 1.47; 95% CI = 1.11–1.94, P = 0.03; rs510432 CC, OR 1.84; 95% CI = 1.12–3.02, P = 0.05). Finally, we identified inverse associations between ATG5 (GG rs2245214) and melanomas on the scalp or neck (OR 0.20, 95% CI = 0.05–0.86, P = 0.03); ATG10 (CC) (rs1864182) and brisk tumor infiltrating lymphocytes (TILs) (OR 0.42; 95% CI = 0.21–0.88, P = 0.02), and ATG5 (CC) (rs510432) with nonbrisk TILs (OR 0.55; 95% CI = 0.34–0.87, P = 0.01). Our data suggest that ATG SNPs might be differentially associated with specific host and tumor characteristics including age at diagnosis, TILs, and stage. These associations may be critical to understanding the role of autophagy in cancer, and further investigation will help characterize the contribution of these variants to melanoma progression. | ||
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653 | 0 | |a Neoplasms. Tumors. Oncology. Including cancer and carcinogens | |
700 | 0 | |a Li Luo |e verfasserin |4 aut | |
700 | 0 | |a Todd A. Thompson |e verfasserin |4 aut | |
700 | 0 | |a Salina Torres |e verfasserin |4 aut | |
700 | 0 | |a Chien‐An Andy Hu |e verfasserin |4 aut | |
700 | 0 | |a Nancy E. Thomas |e verfasserin |4 aut | |
700 | 0 | |a Jenna Lilyquist |e verfasserin |4 aut | |
700 | 0 | |a Hoda Anton‐Culver |e verfasserin |4 aut | |
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700 | 0 | |a Marianne Berwick |e verfasserin |4 aut | |
700 | 0 | |a The GEM Study Group |e verfasserin |4 aut | |
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10.1002/cam4.929 doi (DE-627)DOAJ068327072 (DE-599)DOAJde730952c22246768b0e5f672a3112b6 DE-627 ger DE-627 rakwb eng RC254-282 Kirsten A. M. White verfasserin aut Variants in autophagy‐related genes and clinical characteristics in melanoma: a population‐based study 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Autophagy has been linked with melanoma risk and survival, but no polymorphisms in autophagy‐related (ATG) genes have been investigated in relation to melanoma progression. We examined five single‐nucleotide polymorphisms (SNPs) in three ATG genes (ATG5; ATG10; and ATG16L) with known or suspected impact on autophagic flux in an international population‐based case–control study of melanoma. DNA from 911 melanoma patients was genotyped. An association was identified between (GG) (rs2241880) and earlier stage at diagnosis (OR 0.47; 95% Confidence Intervals (CI) = 0.27–0.81, P = 0.02) and a decrease in Breslow thickness (P = 0.03). The ATG16L heterozygous genotype (AG) (rs2241880) was associated with younger age at diagnosis (P = 0.02). Two SNPs in ATG5 were found to be associated with increased stage (rs2245214 CG, OR 1.47; 95% CI = 1.11–1.94, P = 0.03; rs510432 CC, OR 1.84; 95% CI = 1.12–3.02, P = 0.05). Finally, we identified inverse associations between ATG5 (GG rs2245214) and melanomas on the scalp or neck (OR 0.20, 95% CI = 0.05–0.86, P = 0.03); ATG10 (CC) (rs1864182) and brisk tumor infiltrating lymphocytes (TILs) (OR 0.42; 95% CI = 0.21–0.88, P = 0.02), and ATG5 (CC) (rs510432) with nonbrisk TILs (OR 0.55; 95% CI = 0.34–0.87, P = 0.01). Our data suggest that ATG SNPs might be differentially associated with specific host and tumor characteristics including age at diagnosis, TILs, and stage. These associations may be critical to understanding the role of autophagy in cancer, and further investigation will help characterize the contribution of these variants to melanoma progression. ATG16L1 autophagy melanoma polymorphism SNP Neoplasms. Tumors. Oncology. Including cancer and carcinogens Li Luo verfasserin aut Todd A. Thompson verfasserin aut Salina Torres verfasserin aut Chien‐An Andy Hu verfasserin aut Nancy E. Thomas verfasserin aut Jenna Lilyquist verfasserin aut Hoda Anton‐Culver verfasserin aut Stephen B. Gruber verfasserin aut Lynn From verfasserin aut Klaus J. Busam verfasserin aut Irene Orlow verfasserin aut Peter A. Kanetsky verfasserin aut Loraine D. Marrett verfasserin aut Richard P. Gallagher verfasserin aut Lidia Sacchetto verfasserin aut Stefano Rosso verfasserin aut Terence Dwyer verfasserin aut Anne E. Cust verfasserin aut Colin B. Begg verfasserin aut Marianne Berwick verfasserin aut The GEM Study Group verfasserin aut In Cancer Medicine Wiley, 2012 5(2016), 11, Seite 3336-3345 (DE-627)71860153X (DE-600)2659751-2 20457634 nnns volume:5 year:2016 number:11 pages:3336-3345 https://doi.org/10.1002/cam4.929 kostenfrei https://doaj.org/article/de730952c22246768b0e5f672a3112b6 kostenfrei https://doi.org/10.1002/cam4.929 kostenfrei https://doaj.org/toc/2045-7634 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 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_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_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2016 11 3336-3345 |
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10.1002/cam4.929 doi (DE-627)DOAJ068327072 (DE-599)DOAJde730952c22246768b0e5f672a3112b6 DE-627 ger DE-627 rakwb eng RC254-282 Kirsten A. M. White verfasserin aut Variants in autophagy‐related genes and clinical characteristics in melanoma: a population‐based study 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Autophagy has been linked with melanoma risk and survival, but no polymorphisms in autophagy‐related (ATG) genes have been investigated in relation to melanoma progression. We examined five single‐nucleotide polymorphisms (SNPs) in three ATG genes (ATG5; ATG10; and ATG16L) with known or suspected impact on autophagic flux in an international population‐based case–control study of melanoma. DNA from 911 melanoma patients was genotyped. An association was identified between (GG) (rs2241880) and earlier stage at diagnosis (OR 0.47; 95% Confidence Intervals (CI) = 0.27–0.81, P = 0.02) and a decrease in Breslow thickness (P = 0.03). The ATG16L heterozygous genotype (AG) (rs2241880) was associated with younger age at diagnosis (P = 0.02). Two SNPs in ATG5 were found to be associated with increased stage (rs2245214 CG, OR 1.47; 95% CI = 1.11–1.94, P = 0.03; rs510432 CC, OR 1.84; 95% CI = 1.12–3.02, P = 0.05). Finally, we identified inverse associations between ATG5 (GG rs2245214) and melanomas on the scalp or neck (OR 0.20, 95% CI = 0.05–0.86, P = 0.03); ATG10 (CC) (rs1864182) and brisk tumor infiltrating lymphocytes (TILs) (OR 0.42; 95% CI = 0.21–0.88, P = 0.02), and ATG5 (CC) (rs510432) with nonbrisk TILs (OR 0.55; 95% CI = 0.34–0.87, P = 0.01). Our data suggest that ATG SNPs might be differentially associated with specific host and tumor characteristics including age at diagnosis, TILs, and stage. These associations may be critical to understanding the role of autophagy in cancer, and further investigation will help characterize the contribution of these variants to melanoma progression. ATG16L1 autophagy melanoma polymorphism SNP Neoplasms. Tumors. Oncology. Including cancer and carcinogens Li Luo verfasserin aut Todd A. Thompson verfasserin aut Salina Torres verfasserin aut Chien‐An Andy Hu verfasserin aut Nancy E. Thomas verfasserin aut Jenna Lilyquist verfasserin aut Hoda Anton‐Culver verfasserin aut Stephen B. Gruber verfasserin aut Lynn From verfasserin aut Klaus J. Busam verfasserin aut Irene Orlow verfasserin aut Peter A. Kanetsky verfasserin aut Loraine D. Marrett verfasserin aut Richard P. Gallagher verfasserin aut Lidia Sacchetto verfasserin aut Stefano Rosso verfasserin aut Terence Dwyer verfasserin aut Anne E. Cust verfasserin aut Colin B. Begg verfasserin aut Marianne Berwick verfasserin aut The GEM Study Group verfasserin aut In Cancer Medicine Wiley, 2012 5(2016), 11, Seite 3336-3345 (DE-627)71860153X (DE-600)2659751-2 20457634 nnns volume:5 year:2016 number:11 pages:3336-3345 https://doi.org/10.1002/cam4.929 kostenfrei https://doaj.org/article/de730952c22246768b0e5f672a3112b6 kostenfrei https://doi.org/10.1002/cam4.929 kostenfrei https://doaj.org/toc/2045-7634 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 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_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_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2016 11 3336-3345 |
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10.1002/cam4.929 doi (DE-627)DOAJ068327072 (DE-599)DOAJde730952c22246768b0e5f672a3112b6 DE-627 ger DE-627 rakwb eng RC254-282 Kirsten A. M. White verfasserin aut Variants in autophagy‐related genes and clinical characteristics in melanoma: a population‐based study 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Autophagy has been linked with melanoma risk and survival, but no polymorphisms in autophagy‐related (ATG) genes have been investigated in relation to melanoma progression. We examined five single‐nucleotide polymorphisms (SNPs) in three ATG genes (ATG5; ATG10; and ATG16L) with known or suspected impact on autophagic flux in an international population‐based case–control study of melanoma. DNA from 911 melanoma patients was genotyped. An association was identified between (GG) (rs2241880) and earlier stage at diagnosis (OR 0.47; 95% Confidence Intervals (CI) = 0.27–0.81, P = 0.02) and a decrease in Breslow thickness (P = 0.03). The ATG16L heterozygous genotype (AG) (rs2241880) was associated with younger age at diagnosis (P = 0.02). Two SNPs in ATG5 were found to be associated with increased stage (rs2245214 CG, OR 1.47; 95% CI = 1.11–1.94, P = 0.03; rs510432 CC, OR 1.84; 95% CI = 1.12–3.02, P = 0.05). Finally, we identified inverse associations between ATG5 (GG rs2245214) and melanomas on the scalp or neck (OR 0.20, 95% CI = 0.05–0.86, P = 0.03); ATG10 (CC) (rs1864182) and brisk tumor infiltrating lymphocytes (TILs) (OR 0.42; 95% CI = 0.21–0.88, P = 0.02), and ATG5 (CC) (rs510432) with nonbrisk TILs (OR 0.55; 95% CI = 0.34–0.87, P = 0.01). Our data suggest that ATG SNPs might be differentially associated with specific host and tumor characteristics including age at diagnosis, TILs, and stage. These associations may be critical to understanding the role of autophagy in cancer, and further investigation will help characterize the contribution of these variants to melanoma progression. ATG16L1 autophagy melanoma polymorphism SNP Neoplasms. Tumors. Oncology. Including cancer and carcinogens Li Luo verfasserin aut Todd A. Thompson verfasserin aut Salina Torres verfasserin aut Chien‐An Andy Hu verfasserin aut Nancy E. Thomas verfasserin aut Jenna Lilyquist verfasserin aut Hoda Anton‐Culver verfasserin aut Stephen B. Gruber verfasserin aut Lynn From verfasserin aut Klaus J. Busam verfasserin aut Irene Orlow verfasserin aut Peter A. Kanetsky verfasserin aut Loraine D. Marrett verfasserin aut Richard P. Gallagher verfasserin aut Lidia Sacchetto verfasserin aut Stefano Rosso verfasserin aut Terence Dwyer verfasserin aut Anne E. Cust verfasserin aut Colin B. Begg verfasserin aut Marianne Berwick verfasserin aut The GEM Study Group verfasserin aut In Cancer Medicine Wiley, 2012 5(2016), 11, Seite 3336-3345 (DE-627)71860153X (DE-600)2659751-2 20457634 nnns volume:5 year:2016 number:11 pages:3336-3345 https://doi.org/10.1002/cam4.929 kostenfrei https://doaj.org/article/de730952c22246768b0e5f672a3112b6 kostenfrei https://doi.org/10.1002/cam4.929 kostenfrei https://doaj.org/toc/2045-7634 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 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_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_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2016 11 3336-3345 |
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10.1002/cam4.929 doi (DE-627)DOAJ068327072 (DE-599)DOAJde730952c22246768b0e5f672a3112b6 DE-627 ger DE-627 rakwb eng RC254-282 Kirsten A. M. White verfasserin aut Variants in autophagy‐related genes and clinical characteristics in melanoma: a population‐based study 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Autophagy has been linked with melanoma risk and survival, but no polymorphisms in autophagy‐related (ATG) genes have been investigated in relation to melanoma progression. We examined five single‐nucleotide polymorphisms (SNPs) in three ATG genes (ATG5; ATG10; and ATG16L) with known or suspected impact on autophagic flux in an international population‐based case–control study of melanoma. DNA from 911 melanoma patients was genotyped. An association was identified between (GG) (rs2241880) and earlier stage at diagnosis (OR 0.47; 95% Confidence Intervals (CI) = 0.27–0.81, P = 0.02) and a decrease in Breslow thickness (P = 0.03). The ATG16L heterozygous genotype (AG) (rs2241880) was associated with younger age at diagnosis (P = 0.02). Two SNPs in ATG5 were found to be associated with increased stage (rs2245214 CG, OR 1.47; 95% CI = 1.11–1.94, P = 0.03; rs510432 CC, OR 1.84; 95% CI = 1.12–3.02, P = 0.05). Finally, we identified inverse associations between ATG5 (GG rs2245214) and melanomas on the scalp or neck (OR 0.20, 95% CI = 0.05–0.86, P = 0.03); ATG10 (CC) (rs1864182) and brisk tumor infiltrating lymphocytes (TILs) (OR 0.42; 95% CI = 0.21–0.88, P = 0.02), and ATG5 (CC) (rs510432) with nonbrisk TILs (OR 0.55; 95% CI = 0.34–0.87, P = 0.01). Our data suggest that ATG SNPs might be differentially associated with specific host and tumor characteristics including age at diagnosis, TILs, and stage. These associations may be critical to understanding the role of autophagy in cancer, and further investigation will help characterize the contribution of these variants to melanoma progression. ATG16L1 autophagy melanoma polymorphism SNP Neoplasms. Tumors. Oncology. Including cancer and carcinogens Li Luo verfasserin aut Todd A. Thompson verfasserin aut Salina Torres verfasserin aut Chien‐An Andy Hu verfasserin aut Nancy E. Thomas verfasserin aut Jenna Lilyquist verfasserin aut Hoda Anton‐Culver verfasserin aut Stephen B. Gruber verfasserin aut Lynn From verfasserin aut Klaus J. Busam verfasserin aut Irene Orlow verfasserin aut Peter A. Kanetsky verfasserin aut Loraine D. Marrett verfasserin aut Richard P. Gallagher verfasserin aut Lidia Sacchetto verfasserin aut Stefano Rosso verfasserin aut Terence Dwyer verfasserin aut Anne E. Cust verfasserin aut Colin B. Begg verfasserin aut Marianne Berwick verfasserin aut The GEM Study Group verfasserin aut In Cancer Medicine Wiley, 2012 5(2016), 11, Seite 3336-3345 (DE-627)71860153X (DE-600)2659751-2 20457634 nnns volume:5 year:2016 number:11 pages:3336-3345 https://doi.org/10.1002/cam4.929 kostenfrei https://doaj.org/article/de730952c22246768b0e5f672a3112b6 kostenfrei https://doi.org/10.1002/cam4.929 kostenfrei https://doaj.org/toc/2045-7634 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 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_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_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2016 11 3336-3345 |
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10.1002/cam4.929 doi (DE-627)DOAJ068327072 (DE-599)DOAJde730952c22246768b0e5f672a3112b6 DE-627 ger DE-627 rakwb eng RC254-282 Kirsten A. M. White verfasserin aut Variants in autophagy‐related genes and clinical characteristics in melanoma: a population‐based study 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Autophagy has been linked with melanoma risk and survival, but no polymorphisms in autophagy‐related (ATG) genes have been investigated in relation to melanoma progression. We examined five single‐nucleotide polymorphisms (SNPs) in three ATG genes (ATG5; ATG10; and ATG16L) with known or suspected impact on autophagic flux in an international population‐based case–control study of melanoma. DNA from 911 melanoma patients was genotyped. An association was identified between (GG) (rs2241880) and earlier stage at diagnosis (OR 0.47; 95% Confidence Intervals (CI) = 0.27–0.81, P = 0.02) and a decrease in Breslow thickness (P = 0.03). The ATG16L heterozygous genotype (AG) (rs2241880) was associated with younger age at diagnosis (P = 0.02). Two SNPs in ATG5 were found to be associated with increased stage (rs2245214 CG, OR 1.47; 95% CI = 1.11–1.94, P = 0.03; rs510432 CC, OR 1.84; 95% CI = 1.12–3.02, P = 0.05). Finally, we identified inverse associations between ATG5 (GG rs2245214) and melanomas on the scalp or neck (OR 0.20, 95% CI = 0.05–0.86, P = 0.03); ATG10 (CC) (rs1864182) and brisk tumor infiltrating lymphocytes (TILs) (OR 0.42; 95% CI = 0.21–0.88, P = 0.02), and ATG5 (CC) (rs510432) with nonbrisk TILs (OR 0.55; 95% CI = 0.34–0.87, P = 0.01). Our data suggest that ATG SNPs might be differentially associated with specific host and tumor characteristics including age at diagnosis, TILs, and stage. These associations may be critical to understanding the role of autophagy in cancer, and further investigation will help characterize the contribution of these variants to melanoma progression. ATG16L1 autophagy melanoma polymorphism SNP Neoplasms. Tumors. Oncology. Including cancer and carcinogens Li Luo verfasserin aut Todd A. Thompson verfasserin aut Salina Torres verfasserin aut Chien‐An Andy Hu verfasserin aut Nancy E. Thomas verfasserin aut Jenna Lilyquist verfasserin aut Hoda Anton‐Culver verfasserin aut Stephen B. Gruber verfasserin aut Lynn From verfasserin aut Klaus J. Busam verfasserin aut Irene Orlow verfasserin aut Peter A. Kanetsky verfasserin aut Loraine D. Marrett verfasserin aut Richard P. Gallagher verfasserin aut Lidia Sacchetto verfasserin aut Stefano Rosso verfasserin aut Terence Dwyer verfasserin aut Anne E. Cust verfasserin aut Colin B. Begg verfasserin aut Marianne Berwick verfasserin aut The GEM Study Group verfasserin aut In Cancer Medicine Wiley, 2012 5(2016), 11, Seite 3336-3345 (DE-627)71860153X (DE-600)2659751-2 20457634 nnns volume:5 year:2016 number:11 pages:3336-3345 https://doi.org/10.1002/cam4.929 kostenfrei https://doaj.org/article/de730952c22246768b0e5f672a3112b6 kostenfrei https://doi.org/10.1002/cam4.929 kostenfrei https://doaj.org/toc/2045-7634 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_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 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_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_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2016 11 3336-3345 |
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Kirsten A. M. White @@aut@@ Li Luo @@aut@@ Todd A. Thompson @@aut@@ Salina Torres @@aut@@ Chien‐An Andy Hu @@aut@@ Nancy E. Thomas @@aut@@ Jenna Lilyquist @@aut@@ Hoda Anton‐Culver @@aut@@ Stephen B. Gruber @@aut@@ Lynn From @@aut@@ Klaus J. Busam @@aut@@ Irene Orlow @@aut@@ Peter A. Kanetsky @@aut@@ Loraine D. Marrett @@aut@@ Richard P. Gallagher @@aut@@ Lidia Sacchetto @@aut@@ Stefano Rosso @@aut@@ Terence Dwyer @@aut@@ Anne E. Cust @@aut@@ Colin B. Begg @@aut@@ Marianne Berwick @@aut@@ The GEM Study Group @@aut@@ |
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We examined five single‐nucleotide polymorphisms (SNPs) in three ATG genes (ATG5; ATG10; and ATG16L) with known or suspected impact on autophagic flux in an international population‐based case–control study of melanoma. DNA from 911 melanoma patients was genotyped. An association was identified between (GG) (rs2241880) and earlier stage at diagnosis (OR 0.47; 95% Confidence Intervals (CI) = 0.27–0.81, P = 0.02) and a decrease in Breslow thickness (P = 0.03). The ATG16L heterozygous genotype (AG) (rs2241880) was associated with younger age at diagnosis (P = 0.02). Two SNPs in ATG5 were found to be associated with increased stage (rs2245214 CG, OR 1.47; 95% CI = 1.11–1.94, P = 0.03; rs510432 CC, OR 1.84; 95% CI = 1.12–3.02, P = 0.05). Finally, we identified inverse associations between ATG5 (GG rs2245214) and melanomas on the scalp or neck (OR 0.20, 95% CI = 0.05–0.86, P = 0.03); ATG10 (CC) (rs1864182) and brisk tumor infiltrating lymphocytes (TILs) (OR 0.42; 95% CI = 0.21–0.88, P = 0.02), and ATG5 (CC) (rs510432) with nonbrisk TILs (OR 0.55; 95% CI = 0.34–0.87, P = 0.01). Our data suggest that ATG SNPs might be differentially associated with specific host and tumor characteristics including age at diagnosis, TILs, and stage. 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Kirsten A. M. White |
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Kirsten A. M. White misc RC254-282 misc ATG16L1 misc autophagy misc melanoma misc polymorphism misc SNP misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens Variants in autophagy‐related genes and clinical characteristics in melanoma: a population‐based study |
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RC254-282 Variants in autophagy‐related genes and clinical characteristics in melanoma: a population‐based study ATG16L1 autophagy melanoma polymorphism SNP |
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Kirsten A. M. White Li Luo Todd A. Thompson Salina Torres Chien‐An Andy Hu Nancy E. Thomas Jenna Lilyquist Hoda Anton‐Culver Stephen B. Gruber Lynn From Klaus J. Busam Irene Orlow Peter A. Kanetsky Loraine D. Marrett Richard P. Gallagher Lidia Sacchetto Stefano Rosso Terence Dwyer Anne E. Cust Colin B. Begg Marianne Berwick The GEM Study Group |
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variants in autophagy‐related genes and clinical characteristics in melanoma: a population‐based study |
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Variants in autophagy‐related genes and clinical characteristics in melanoma: a population‐based study |
abstract |
Abstract Autophagy has been linked with melanoma risk and survival, but no polymorphisms in autophagy‐related (ATG) genes have been investigated in relation to melanoma progression. We examined five single‐nucleotide polymorphisms (SNPs) in three ATG genes (ATG5; ATG10; and ATG16L) with known or suspected impact on autophagic flux in an international population‐based case–control study of melanoma. DNA from 911 melanoma patients was genotyped. An association was identified between (GG) (rs2241880) and earlier stage at diagnosis (OR 0.47; 95% Confidence Intervals (CI) = 0.27–0.81, P = 0.02) and a decrease in Breslow thickness (P = 0.03). The ATG16L heterozygous genotype (AG) (rs2241880) was associated with younger age at diagnosis (P = 0.02). Two SNPs in ATG5 were found to be associated with increased stage (rs2245214 CG, OR 1.47; 95% CI = 1.11–1.94, P = 0.03; rs510432 CC, OR 1.84; 95% CI = 1.12–3.02, P = 0.05). Finally, we identified inverse associations between ATG5 (GG rs2245214) and melanomas on the scalp or neck (OR 0.20, 95% CI = 0.05–0.86, P = 0.03); ATG10 (CC) (rs1864182) and brisk tumor infiltrating lymphocytes (TILs) (OR 0.42; 95% CI = 0.21–0.88, P = 0.02), and ATG5 (CC) (rs510432) with nonbrisk TILs (OR 0.55; 95% CI = 0.34–0.87, P = 0.01). Our data suggest that ATG SNPs might be differentially associated with specific host and tumor characteristics including age at diagnosis, TILs, and stage. These associations may be critical to understanding the role of autophagy in cancer, and further investigation will help characterize the contribution of these variants to melanoma progression. |
abstractGer |
Abstract Autophagy has been linked with melanoma risk and survival, but no polymorphisms in autophagy‐related (ATG) genes have been investigated in relation to melanoma progression. We examined five single‐nucleotide polymorphisms (SNPs) in three ATG genes (ATG5; ATG10; and ATG16L) with known or suspected impact on autophagic flux in an international population‐based case–control study of melanoma. DNA from 911 melanoma patients was genotyped. An association was identified between (GG) (rs2241880) and earlier stage at diagnosis (OR 0.47; 95% Confidence Intervals (CI) = 0.27–0.81, P = 0.02) and a decrease in Breslow thickness (P = 0.03). The ATG16L heterozygous genotype (AG) (rs2241880) was associated with younger age at diagnosis (P = 0.02). Two SNPs in ATG5 were found to be associated with increased stage (rs2245214 CG, OR 1.47; 95% CI = 1.11–1.94, P = 0.03; rs510432 CC, OR 1.84; 95% CI = 1.12–3.02, P = 0.05). Finally, we identified inverse associations between ATG5 (GG rs2245214) and melanomas on the scalp or neck (OR 0.20, 95% CI = 0.05–0.86, P = 0.03); ATG10 (CC) (rs1864182) and brisk tumor infiltrating lymphocytes (TILs) (OR 0.42; 95% CI = 0.21–0.88, P = 0.02), and ATG5 (CC) (rs510432) with nonbrisk TILs (OR 0.55; 95% CI = 0.34–0.87, P = 0.01). Our data suggest that ATG SNPs might be differentially associated with specific host and tumor characteristics including age at diagnosis, TILs, and stage. These associations may be critical to understanding the role of autophagy in cancer, and further investigation will help characterize the contribution of these variants to melanoma progression. |
abstract_unstemmed |
Abstract Autophagy has been linked with melanoma risk and survival, but no polymorphisms in autophagy‐related (ATG) genes have been investigated in relation to melanoma progression. We examined five single‐nucleotide polymorphisms (SNPs) in three ATG genes (ATG5; ATG10; and ATG16L) with known or suspected impact on autophagic flux in an international population‐based case–control study of melanoma. DNA from 911 melanoma patients was genotyped. An association was identified between (GG) (rs2241880) and earlier stage at diagnosis (OR 0.47; 95% Confidence Intervals (CI) = 0.27–0.81, P = 0.02) and a decrease in Breslow thickness (P = 0.03). The ATG16L heterozygous genotype (AG) (rs2241880) was associated with younger age at diagnosis (P = 0.02). Two SNPs in ATG5 were found to be associated with increased stage (rs2245214 CG, OR 1.47; 95% CI = 1.11–1.94, P = 0.03; rs510432 CC, OR 1.84; 95% CI = 1.12–3.02, P = 0.05). Finally, we identified inverse associations between ATG5 (GG rs2245214) and melanomas on the scalp or neck (OR 0.20, 95% CI = 0.05–0.86, P = 0.03); ATG10 (CC) (rs1864182) and brisk tumor infiltrating lymphocytes (TILs) (OR 0.42; 95% CI = 0.21–0.88, P = 0.02), and ATG5 (CC) (rs510432) with nonbrisk TILs (OR 0.55; 95% CI = 0.34–0.87, P = 0.01). Our data suggest that ATG SNPs might be differentially associated with specific host and tumor characteristics including age at diagnosis, TILs, and stage. These associations may be critical to understanding the role of autophagy in cancer, and further investigation will help characterize the contribution of these variants to melanoma progression. |
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container_issue |
11 |
title_short |
Variants in autophagy‐related genes and clinical characteristics in melanoma: a population‐based study |
url |
https://doi.org/10.1002/cam4.929 https://doaj.org/article/de730952c22246768b0e5f672a3112b6 https://doaj.org/toc/2045-7634 |
remote_bool |
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author2 |
Li Luo Todd A. Thompson Salina Torres Chien‐An Andy Hu Nancy E. Thomas Jenna Lilyquist Hoda Anton‐Culver Stephen B. Gruber Lynn From Klaus J. Busam Irene Orlow Peter A. Kanetsky Loraine D. Marrett Richard P. Gallagher Lidia Sacchetto Stefano Rosso Terence Dwyer Anne E. Cust Colin B. Begg Marianne Berwick The GEM Study Group |
author2Str |
Li Luo Todd A. Thompson Salina Torres Chien‐An Andy Hu Nancy E. Thomas Jenna Lilyquist Hoda Anton‐Culver Stephen B. Gruber Lynn From Klaus J. Busam Irene Orlow Peter A. Kanetsky Loraine D. Marrett Richard P. Gallagher Lidia Sacchetto Stefano Rosso Terence Dwyer Anne E. Cust Colin B. Begg Marianne Berwick The GEM Study Group |
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doi_str |
10.1002/cam4.929 |
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RC254-282 |
up_date |
2024-07-03T17:08:20.256Z |
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|
score |
7.399805 |