Statins and pancreatic cancer risk: a nested case–control study

Objective To investigate the relationship between statin use and pancreatic cancer risk. Methods A nested case–control study was conducted within the UK GPRD. Cases had a diagnosis of primary malignant neoplasia of the exocrine pancreas. Controls were matched with cases on general practice site, sex...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Bradley, Marie C. [verfasserIn] Hughes, Carmel M. [verfasserIn] Cantwell, Marie M. [verfasserIn] Murray, Liam J. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2010

Schlagwörter:	Statins Pancreatic cancer General practice research database

Übergeordnetes Werk:	Enthalten in: Cancer causes & control - Dordrecht [u.a.] : Springer Science + Business Media B.V., 1990, 21(2010), 12 vom: 10. Aug., Seite 2093-2100
Übergeordnetes Werk:	volume:21 ; year:2010 ; number:12 ; day:10 ; month:08 ; pages:2093-2100

Links:	Volltext

DOI / URN:	10.1007/s10552-010-9628-0

Katalog-ID:	SPR011187484

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520			\|a Objective To investigate the relationship between statin use and pancreatic cancer risk. Methods A nested case–control study was conducted within the UK GPRD. Cases had a diagnosis of primary malignant neoplasia of the exocrine pancreas. Controls were matched with cases on general practice site, sex and year of birth. Exposure of interest was exposure to statins since entry into the GPRD until 1 year before the case diagnosis date. Conditional logistic regression analyses were used to generate ORs and 95% CI associated with statin use compared to non-use. Results A total of 1,141 pancreatic cancer cases and 7,954 controls were identified. Any use of a statin since entry into the GPRD (excluding the year prior to diagnosis) was not associated with the risk of pancreatic cancer OR 0.93 (95% CI, 0.76–1.14). Neither dose nor duration of statin use affected pancreatic cancer risk. When dose and duration of statin use combined were assessed, no evidence of reduced risk was seen for long-term users of high-dose statins OR 0.71 (0.42–1.20). Statin type (simvastatin vs atorvastatin) was not associated with pancreatic cancer risk. Conclusion Statin use at doses for managing hypercholesterolaemia, in a UK population, was not associated with the risk of exocrine pancreatic cancer.
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700	1		\|a Cantwell, Marie M. \|e verfasserin \|4 aut
700	1		\|a Murray, Liam J. \|e verfasserin \|4 aut
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952			\|d 21 \|j 2010 \|e 12 \|b 10 \|c 08 \|h 2093-2100

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matchkey_str	article:15737225:2010----::ttnadacetcacriknsec
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bklnumber	44.81
publishDate	2010
allfields	10.1007/s10552-010-9628-0 doi (DE-627)SPR011187484 (SPR)s10552-010-9628-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Bradley, Marie C. verfasserin aut Statins and pancreatic cancer risk: a nested case–control study 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To investigate the relationship between statin use and pancreatic cancer risk. Methods A nested case–control study was conducted within the UK GPRD. Cases had a diagnosis of primary malignant neoplasia of the exocrine pancreas. Controls were matched with cases on general practice site, sex and year of birth. Exposure of interest was exposure to statins since entry into the GPRD until 1 year before the case diagnosis date. Conditional logistic regression analyses were used to generate ORs and 95% CI associated with statin use compared to non-use. Results A total of 1,141 pancreatic cancer cases and 7,954 controls were identified. Any use of a statin since entry into the GPRD (excluding the year prior to diagnosis) was not associated with the risk of pancreatic cancer OR 0.93 (95% CI, 0.76–1.14). Neither dose nor duration of statin use affected pancreatic cancer risk. When dose and duration of statin use combined were assessed, no evidence of reduced risk was seen for long-term users of high-dose statins OR 0.71 (0.42–1.20). Statin type (simvastatin vs atorvastatin) was not associated with pancreatic cancer risk. Conclusion Statin use at doses for managing hypercholesterolaemia, in a UK population, was not associated with the risk of exocrine pancreatic cancer. Statins (dpeaa)DE-He213 Pancreatic cancer (dpeaa)DE-He213 General practice research database (dpeaa)DE-He213 Hughes, Carmel M. verfasserin aut Cantwell, Marie M. verfasserin aut Murray, Liam J. verfasserin aut Enthalten in Cancer causes & control Dordrecht [u.a.] : Springer Science + Business Media B.V., 1990 21(2010), 12 vom: 10. Aug., Seite 2093-2100 (DE-627)306324288 (DE-600)1496544-6 1573-7225 nnns volume:21 year:2010 number:12 day:10 month:08 pages:2093-2100 https://dx.doi.org/10.1007/s10552-010-9628-0 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_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_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 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_2018 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_2943 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 21 2010 12 10 08 2093-2100
spelling	10.1007/s10552-010-9628-0 doi (DE-627)SPR011187484 (SPR)s10552-010-9628-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Bradley, Marie C. verfasserin aut Statins and pancreatic cancer risk: a nested case–control study 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To investigate the relationship between statin use and pancreatic cancer risk. Methods A nested case–control study was conducted within the UK GPRD. Cases had a diagnosis of primary malignant neoplasia of the exocrine pancreas. Controls were matched with cases on general practice site, sex and year of birth. Exposure of interest was exposure to statins since entry into the GPRD until 1 year before the case diagnosis date. Conditional logistic regression analyses were used to generate ORs and 95% CI associated with statin use compared to non-use. Results A total of 1,141 pancreatic cancer cases and 7,954 controls were identified. Any use of a statin since entry into the GPRD (excluding the year prior to diagnosis) was not associated with the risk of pancreatic cancer OR 0.93 (95% CI, 0.76–1.14). Neither dose nor duration of statin use affected pancreatic cancer risk. When dose and duration of statin use combined were assessed, no evidence of reduced risk was seen for long-term users of high-dose statins OR 0.71 (0.42–1.20). Statin type (simvastatin vs atorvastatin) was not associated with pancreatic cancer risk. Conclusion Statin use at doses for managing hypercholesterolaemia, in a UK population, was not associated with the risk of exocrine pancreatic cancer. Statins (dpeaa)DE-He213 Pancreatic cancer (dpeaa)DE-He213 General practice research database (dpeaa)DE-He213 Hughes, Carmel M. verfasserin aut Cantwell, Marie M. verfasserin aut Murray, Liam J. verfasserin aut Enthalten in Cancer causes & control Dordrecht [u.a.] : Springer Science + Business Media B.V., 1990 21(2010), 12 vom: 10. Aug., Seite 2093-2100 (DE-627)306324288 (DE-600)1496544-6 1573-7225 nnns volume:21 year:2010 number:12 day:10 month:08 pages:2093-2100 https://dx.doi.org/10.1007/s10552-010-9628-0 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_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_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 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_2018 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_2943 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 21 2010 12 10 08 2093-2100
allfields_unstemmed	10.1007/s10552-010-9628-0 doi (DE-627)SPR011187484 (SPR)s10552-010-9628-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Bradley, Marie C. verfasserin aut Statins and pancreatic cancer risk: a nested case–control study 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To investigate the relationship between statin use and pancreatic cancer risk. Methods A nested case–control study was conducted within the UK GPRD. Cases had a diagnosis of primary malignant neoplasia of the exocrine pancreas. Controls were matched with cases on general practice site, sex and year of birth. Exposure of interest was exposure to statins since entry into the GPRD until 1 year before the case diagnosis date. Conditional logistic regression analyses were used to generate ORs and 95% CI associated with statin use compared to non-use. Results A total of 1,141 pancreatic cancer cases and 7,954 controls were identified. Any use of a statin since entry into the GPRD (excluding the year prior to diagnosis) was not associated with the risk of pancreatic cancer OR 0.93 (95% CI, 0.76–1.14). Neither dose nor duration of statin use affected pancreatic cancer risk. When dose and duration of statin use combined were assessed, no evidence of reduced risk was seen for long-term users of high-dose statins OR 0.71 (0.42–1.20). Statin type (simvastatin vs atorvastatin) was not associated with pancreatic cancer risk. Conclusion Statin use at doses for managing hypercholesterolaemia, in a UK population, was not associated with the risk of exocrine pancreatic cancer. Statins (dpeaa)DE-He213 Pancreatic cancer (dpeaa)DE-He213 General practice research database (dpeaa)DE-He213 Hughes, Carmel M. verfasserin aut Cantwell, Marie M. verfasserin aut Murray, Liam J. verfasserin aut Enthalten in Cancer causes & control Dordrecht [u.a.] : Springer Science + Business Media B.V., 1990 21(2010), 12 vom: 10. Aug., Seite 2093-2100 (DE-627)306324288 (DE-600)1496544-6 1573-7225 nnns volume:21 year:2010 number:12 day:10 month:08 pages:2093-2100 https://dx.doi.org/10.1007/s10552-010-9628-0 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_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_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 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_2018 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_2943 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 21 2010 12 10 08 2093-2100
allfieldsGer	10.1007/s10552-010-9628-0 doi (DE-627)SPR011187484 (SPR)s10552-010-9628-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Bradley, Marie C. verfasserin aut Statins and pancreatic cancer risk: a nested case–control study 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To investigate the relationship between statin use and pancreatic cancer risk. Methods A nested case–control study was conducted within the UK GPRD. Cases had a diagnosis of primary malignant neoplasia of the exocrine pancreas. Controls were matched with cases on general practice site, sex and year of birth. Exposure of interest was exposure to statins since entry into the GPRD until 1 year before the case diagnosis date. Conditional logistic regression analyses were used to generate ORs and 95% CI associated with statin use compared to non-use. Results A total of 1,141 pancreatic cancer cases and 7,954 controls were identified. Any use of a statin since entry into the GPRD (excluding the year prior to diagnosis) was not associated with the risk of pancreatic cancer OR 0.93 (95% CI, 0.76–1.14). Neither dose nor duration of statin use affected pancreatic cancer risk. When dose and duration of statin use combined were assessed, no evidence of reduced risk was seen for long-term users of high-dose statins OR 0.71 (0.42–1.20). Statin type (simvastatin vs atorvastatin) was not associated with pancreatic cancer risk. Conclusion Statin use at doses for managing hypercholesterolaemia, in a UK population, was not associated with the risk of exocrine pancreatic cancer. Statins (dpeaa)DE-He213 Pancreatic cancer (dpeaa)DE-He213 General practice research database (dpeaa)DE-He213 Hughes, Carmel M. verfasserin aut Cantwell, Marie M. verfasserin aut Murray, Liam J. verfasserin aut Enthalten in Cancer causes & control Dordrecht [u.a.] : Springer Science + Business Media B.V., 1990 21(2010), 12 vom: 10. Aug., Seite 2093-2100 (DE-627)306324288 (DE-600)1496544-6 1573-7225 nnns volume:21 year:2010 number:12 day:10 month:08 pages:2093-2100 https://dx.doi.org/10.1007/s10552-010-9628-0 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_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_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 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_2018 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_2943 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 21 2010 12 10 08 2093-2100
allfieldsSound	10.1007/s10552-010-9628-0 doi (DE-627)SPR011187484 (SPR)s10552-010-9628-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Bradley, Marie C. verfasserin aut Statins and pancreatic cancer risk: a nested case–control study 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Objective To investigate the relationship between statin use and pancreatic cancer risk. Methods A nested case–control study was conducted within the UK GPRD. Cases had a diagnosis of primary malignant neoplasia of the exocrine pancreas. Controls were matched with cases on general practice site, sex and year of birth. Exposure of interest was exposure to statins since entry into the GPRD until 1 year before the case diagnosis date. Conditional logistic regression analyses were used to generate ORs and 95% CI associated with statin use compared to non-use. Results A total of 1,141 pancreatic cancer cases and 7,954 controls were identified. Any use of a statin since entry into the GPRD (excluding the year prior to diagnosis) was not associated with the risk of pancreatic cancer OR 0.93 (95% CI, 0.76–1.14). Neither dose nor duration of statin use affected pancreatic cancer risk. When dose and duration of statin use combined were assessed, no evidence of reduced risk was seen for long-term users of high-dose statins OR 0.71 (0.42–1.20). Statin type (simvastatin vs atorvastatin) was not associated with pancreatic cancer risk. Conclusion Statin use at doses for managing hypercholesterolaemia, in a UK population, was not associated with the risk of exocrine pancreatic cancer. Statins (dpeaa)DE-He213 Pancreatic cancer (dpeaa)DE-He213 General practice research database (dpeaa)DE-He213 Hughes, Carmel M. verfasserin aut Cantwell, Marie M. verfasserin aut Murray, Liam J. verfasserin aut Enthalten in Cancer causes & control Dordrecht [u.a.] : Springer Science + Business Media B.V., 1990 21(2010), 12 vom: 10. Aug., Seite 2093-2100 (DE-627)306324288 (DE-600)1496544-6 1573-7225 nnns volume:21 year:2010 number:12 day:10 month:08 pages:2093-2100 https://dx.doi.org/10.1007/s10552-010-9628-0 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_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_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 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_2018 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_2943 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 21 2010 12 10 08 2093-2100
language	English
source	Enthalten in Cancer causes & control 21(2010), 12 vom: 10. Aug., Seite 2093-2100 volume:21 year:2010 number:12 day:10 month:08 pages:2093-2100
sourceStr	Enthalten in Cancer causes & control 21(2010), 12 vom: 10. Aug., Seite 2093-2100 volume:21 year:2010 number:12 day:10 month:08 pages:2093-2100
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Statins Pancreatic cancer General practice research database
dewey-raw	610
isfreeaccess_bool	false
container_title	Cancer causes & control
authorswithroles_txt_mv	Bradley, Marie C. @@aut@@ Hughes, Carmel M. @@aut@@ Cantwell, Marie M. @@aut@@ Murray, Liam J. @@aut@@
publishDateDaySort_date	2010-08-10T00:00:00Z
hierarchy_top_id	306324288
dewey-sort	3610
id	SPR011187484
language_de	englisch
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Methods A nested case–control study was conducted within the UK GPRD. Cases had a diagnosis of primary malignant neoplasia of the exocrine pancreas. Controls were matched with cases on general practice site, sex and year of birth. Exposure of interest was exposure to statins since entry into the GPRD until 1 year before the case diagnosis date. Conditional logistic regression analyses were used to generate ORs and 95% CI associated with statin use compared to non-use. Results A total of 1,141 pancreatic cancer cases and 7,954 controls were identified. Any use of a statin since entry into the GPRD (excluding the year prior to diagnosis) was not associated with the risk of pancreatic cancer OR 0.93 (95% CI, 0.76–1.14). Neither dose nor duration of statin use affected pancreatic cancer risk. When dose and duration of statin use combined were assessed, no evidence of reduced risk was seen for long-term users of high-dose statins OR 0.71 (0.42–1.20). Statin type (simvastatin vs atorvastatin) was not associated with pancreatic cancer risk. 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author	Bradley, Marie C.
spellingShingle	Bradley, Marie C. ddc 610 bkl 44.81 misc Statins misc Pancreatic cancer misc General practice research database Statins and pancreatic cancer risk: a nested case–control study
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topic_title	610 ASE 44.81 bkl Statins and pancreatic cancer risk: a nested case–control study Statins (dpeaa)DE-He213 Pancreatic cancer (dpeaa)DE-He213 General practice research database (dpeaa)DE-He213
topic	ddc 610 bkl 44.81 misc Statins misc Pancreatic cancer misc General practice research database
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title	Statins and pancreatic cancer risk: a nested case–control study
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title_full	Statins and pancreatic cancer risk: a nested case–control study
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journal	Cancer causes & control
journalStr	Cancer causes & control
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author_browse	Bradley, Marie C. Hughes, Carmel M. Cantwell, Marie M. Murray, Liam J.
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class	610 ASE 44.81 bkl
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title_sort	statins and pancreatic cancer risk: a nested case–control study
title_auth	Statins and pancreatic cancer risk: a nested case–control study
abstract	Objective To investigate the relationship between statin use and pancreatic cancer risk. Methods A nested case–control study was conducted within the UK GPRD. Cases had a diagnosis of primary malignant neoplasia of the exocrine pancreas. Controls were matched with cases on general practice site, sex and year of birth. Exposure of interest was exposure to statins since entry into the GPRD until 1 year before the case diagnosis date. Conditional logistic regression analyses were used to generate ORs and 95% CI associated with statin use compared to non-use. Results A total of 1,141 pancreatic cancer cases and 7,954 controls were identified. Any use of a statin since entry into the GPRD (excluding the year prior to diagnosis) was not associated with the risk of pancreatic cancer OR 0.93 (95% CI, 0.76–1.14). Neither dose nor duration of statin use affected pancreatic cancer risk. When dose and duration of statin use combined were assessed, no evidence of reduced risk was seen for long-term users of high-dose statins OR 0.71 (0.42–1.20). Statin type (simvastatin vs atorvastatin) was not associated with pancreatic cancer risk. Conclusion Statin use at doses for managing hypercholesterolaemia, in a UK population, was not associated with the risk of exocrine pancreatic cancer.
abstractGer	Objective To investigate the relationship between statin use and pancreatic cancer risk. Methods A nested case–control study was conducted within the UK GPRD. Cases had a diagnosis of primary malignant neoplasia of the exocrine pancreas. Controls were matched with cases on general practice site, sex and year of birth. Exposure of interest was exposure to statins since entry into the GPRD until 1 year before the case diagnosis date. Conditional logistic regression analyses were used to generate ORs and 95% CI associated with statin use compared to non-use. Results A total of 1,141 pancreatic cancer cases and 7,954 controls were identified. Any use of a statin since entry into the GPRD (excluding the year prior to diagnosis) was not associated with the risk of pancreatic cancer OR 0.93 (95% CI, 0.76–1.14). Neither dose nor duration of statin use affected pancreatic cancer risk. When dose and duration of statin use combined were assessed, no evidence of reduced risk was seen for long-term users of high-dose statins OR 0.71 (0.42–1.20). Statin type (simvastatin vs atorvastatin) was not associated with pancreatic cancer risk. Conclusion Statin use at doses for managing hypercholesterolaemia, in a UK population, was not associated with the risk of exocrine pancreatic cancer.
abstract_unstemmed	Objective To investigate the relationship between statin use and pancreatic cancer risk. Methods A nested case–control study was conducted within the UK GPRD. Cases had a diagnosis of primary malignant neoplasia of the exocrine pancreas. Controls were matched with cases on general practice site, sex and year of birth. Exposure of interest was exposure to statins since entry into the GPRD until 1 year before the case diagnosis date. Conditional logistic regression analyses were used to generate ORs and 95% CI associated with statin use compared to non-use. Results A total of 1,141 pancreatic cancer cases and 7,954 controls were identified. Any use of a statin since entry into the GPRD (excluding the year prior to diagnosis) was not associated with the risk of pancreatic cancer OR 0.93 (95% CI, 0.76–1.14). Neither dose nor duration of statin use affected pancreatic cancer risk. When dose and duration of statin use combined were assessed, no evidence of reduced risk was seen for long-term users of high-dose statins OR 0.71 (0.42–1.20). Statin type (simvastatin vs atorvastatin) was not associated with pancreatic cancer risk. Conclusion Statin use at doses for managing hypercholesterolaemia, in a UK population, was not associated with the risk of exocrine pancreatic cancer.
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container_issue	12
title_short	Statins and pancreatic cancer risk: a nested case–control study
url	https://dx.doi.org/10.1007/s10552-010-9628-0
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author2	Hughes, Carmel M. Cantwell, Marie M. Murray, Liam J.
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doi_str	10.1007/s10552-010-9628-0
up_date	2024-07-03T21:02:10.367Z
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Methods A nested case–control study was conducted within the UK GPRD. Cases had a diagnosis of primary malignant neoplasia of the exocrine pancreas. Controls were matched with cases on general practice site, sex and year of birth. Exposure of interest was exposure to statins since entry into the GPRD until 1 year before the case diagnosis date. Conditional logistic regression analyses were used to generate ORs and 95% CI associated with statin use compared to non-use. Results A total of 1,141 pancreatic cancer cases and 7,954 controls were identified. Any use of a statin since entry into the GPRD (excluding the year prior to diagnosis) was not associated with the risk of pancreatic cancer OR 0.93 (95% CI, 0.76–1.14). Neither dose nor duration of statin use affected pancreatic cancer risk. When dose and duration of statin use combined were assessed, no evidence of reduced risk was seen for long-term users of high-dose statins OR 0.71 (0.42–1.20). Statin type (simvastatin vs atorvastatin) was not associated with pancreatic cancer risk. 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Statins and pancreatic cancer risk: a nested case–control study

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