AustralieFrV1, PascalFrancis, Corpus, bibRecord, 003703

The rs743572 common variant in the promoter of CYP17A1 is not associated with prostate cancer risk or circulating hormonal levels

Identifieur interne : 003703 ( PascalFrancis/Corpus ); précédent : 003702; suivant : 003704

The rs743572 common variant in the promoter of CYP17A1 is not associated with prostate cancer risk or circulating hormonal levels

Auteurs : Gianluca Severi ; Vanessa M. Hayes ; Andrea A. Tesoriero ; Melissa C. Southey ; Hoa N. Hoang ; Emma J. D. Padilla ; Howard A. Morris ; Dallas R. English ; Robert L. Sutherland ; Peter Boyle ; John L. Hopper ; Graham G. Giles

Source :

BJU international : (Papier) [ 1464-4096 ] ; 2008.

RBID : Pascal:08-0137997

Descripteurs français

Pascal (Inist)
- Cancer de la prostate, Variant, Variabilité génétique, Génotype, Promoteur, Facteur risque, Epidémiologie, Cytochrome P450, Contrôle, Hormone, Néphrologie, Urologie, Cytochrome P450c17α.

English descriptors

KwdEn :
- Check, Cytochrome P450, Epidemiology, Genetic variability, Genotype, Hormone, Nephrology, Promoter, Prostate cancer, Risk factor, Urology, Variant.

Abstract

OBJECTIVE To use a large population-based case-control study to test the association between the common genetic variant rs743572 (-34 T to C), prostate cancer risk and circulating levels of several hormones. SUBJECTS AND METHODS A previous meta-analysis concluded that reported associations between rs743572 in the promoter of CYP17A1 and prostate cancer risk might reflect publication bias, but a few recent studies reported associations with prostate cancer risk and data suggesting that rs743572 is functional. We genotyped 824 prostate cancer cases and 737 population-based controls, and applied unconditional logistic regression to estimate the association between rs743572 and prostate cancer risk. We also used linear regression of transformed testosterone, androstanediol glucuronide, dehydroepiandrosterone sulphate, androstenedione, sex hormone-binding globulin and oestradiol (circulating levels) measured for controls, to estimate the association between these levels and rs743572. The linear models were adjusted for age and laboratory batch. RESULTS Men with different genotypes had similar circulating levels of all the hormones measured (all P< 0.05). In the case-control comparison using unconditional unadjusted logistic regression, the odds ratios (95% confidence interval) for prostate cancer were 1.07 (0.87-1.32) and 0.94 (0.71-1.25) for the dominant and recessive models, respectively, and for the co-dominant model, 1.10 (0.88-1.36) and 0.99 (0.73-1.35) for carriers of one or two copies of the C allele, respectively. There was no evidence of heterogeneity in the odds ratios by tumour stage (all P> 0.3) and grade (all P> 0.3). CONCLUSION The results of the present study are consistent with the conclusions of the previous meta-analysis, and suggest that rs743572 has no role in the risk of prostate cancer for men of Caucasian origin.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`01`	`1`		`@1 SEVERI (Gianluca)`
A11	`02`	`1`		`@1 HAYES (Vanessa M.)`
A11	`03`	`1`		`@1 TESORIERO (Andrea A.)`
A11	`04`	`1`		`@1 SOUTHEY (Melissa C.)`
A11	`05`	`1`		`@1 HOANG (Hoa N.)`
A11	`06`	`1`		`@1 PADILLA (Emma J. D.)`
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A11	`08`	`1`		`@1 ENGLISH (Dallas R.)`
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C01	`01`		`ENG`	@0 OBJECTIVE To use a large population-based case-control study to test the association between the common genetic variant rs743572 (-34 T to C), prostate cancer risk and circulating levels of several hormones. SUBJECTS AND METHODS A previous meta-analysis concluded that reported associations between rs743572 in the promoter of CYP17A1 and prostate cancer risk might reflect publication bias, but a few recent studies reported associations with prostate cancer risk and data suggesting that rs743572 is functional. We genotyped 824 prostate cancer cases and 737 population-based controls, and applied unconditional logistic regression to estimate the association between rs743572 and prostate cancer risk. We also used linear regression of transformed testosterone, androstanediol glucuronide, dehydroepiandrosterone sulphate, androstenedione, sex hormone-binding globulin and oestradiol (circulating levels) measured for controls, to estimate the association between these levels and rs743572. The linear models were adjusted for age and laboratory batch. RESULTS Men with different genotypes had similar circulating levels of all the hormones measured (all P< 0.05). In the case-control comparison using unconditional unadjusted logistic regression, the odds ratios (95% confidence interval) for prostate cancer were 1.07 (0.87-1.32) and 0.94 (0.71-1.25) for the dominant and recessive models, respectively, and for the co-dominant model, 1.10 (0.88-1.36) and 0.99 (0.73-1.35) for carriers of one or two copies of the C allele, respectively. There was no evidence of heterogeneity in the odds ratios by tumour stage (all P> 0.3) and grade (all P> 0.3). CONCLUSION The results of the present study are consistent with the conclusions of the previous meta-analysis, and suggest that rs743572 has no role in the risk of prostate cancer for men of Caucasian origin.
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Format Inist (serveur)

NO :	PASCAL 08-0137997 INIST
ET :	The rs743572 common variant in the promoter of CYP17A1 is not associated with prostate cancer risk or circulating hormonal levels
AU :	SEVERI (Gianluca); HAYES (Vanessa M.); TESORIERO (Andrea A.); SOUTHEY (Melissa C.); HOANG (Hoa N.); PADILLA (Emma J. D.); MORRIS (Howard A.); ENGLISH (Dallas R.); SUTHERLAND (Robert L.); BOYLE (Peter); HOPPER (John L.); GILES (Graham G.)
AF :	Cancer Epidemiology Centre, The Cancer Council Victoria/Melbourne/Australie (1 aut., 5 aut., 8 aut., 12 aut.); Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, The University of Melbourne/Australie (1 aut., 8 aut., 11 aut., 12 aut.); Cancer Research Program, Garvan Institute of Medical Research, St Vincent's Hospital, Darlinghurst/Sydney/Australie (2 aut., 6 aut., 9 aut.); University of New South Wales/Sydney/Australie (2 aut., 9 aut.); Department of Pathology, The University of Melbourne/Australie (3 aut., 4 aut.); School of Population Health, The University of Melbourne/Australie (5 aut.); Hanson Institute/Adelaide/Australie (7 aut.); International Agency for Research on Cancer/Lyon/France (10 aut.)
DT :	Publication en série; Niveau analytique
SO :	BJU international : (Papier); ISSN 1464-4096; Royaume-Uni; Da. 2008; Vol. 101; No. 4; Pp. 492-496; Bibl. 74 ref.
LA :	Anglais
EA :	OBJECTIVE To use a large population-based case-control study to test the association between the common genetic variant rs743572 (-34 T to C), prostate cancer risk and circulating levels of several hormones. SUBJECTS AND METHODS A previous meta-analysis concluded that reported associations between rs743572 in the promoter of CYP17A1 and prostate cancer risk might reflect publication bias, but a few recent studies reported associations with prostate cancer risk and data suggesting that rs743572 is functional. We genotyped 824 prostate cancer cases and 737 population-based controls, and applied unconditional logistic regression to estimate the association between rs743572 and prostate cancer risk. We also used linear regression of transformed testosterone, androstanediol glucuronide, dehydroepiandrosterone sulphate, androstenedione, sex hormone-binding globulin and oestradiol (circulating levels) measured for controls, to estimate the association between these levels and rs743572. The linear models were adjusted for age and laboratory batch. RESULTS Men with different genotypes had similar circulating levels of all the hormones measured (all P< 0.05). In the case-control comparison using unconditional unadjusted logistic regression, the odds ratios (95% confidence interval) for prostate cancer were 1.07 (0.87-1.32) and 0.94 (0.71-1.25) for the dominant and recessive models, respectively, and for the co-dominant model, 1.10 (0.88-1.36) and 0.99 (0.73-1.35) for carriers of one or two copies of the C allele, respectively. There was no evidence of heterogeneity in the odds ratios by tumour stage (all P> 0.3) and grade (all P> 0.3). CONCLUSION The results of the present study are consistent with the conclusions of the previous meta-analysis, and suggest that rs743572 has no role in the risk of prostate cancer for men of Caucasian origin.
CC :	002B14D02; 002B20B02
FD :	Cancer de la prostate; Variant; Variabilité génétique; Génotype; Promoteur; Facteur risque; Epidémiologie; Cytochrome P450; Contrôle; Hormone; Néphrologie; Urologie; Cytochrome P450c17α
FG :	Pathologie de l'appareil génital mâle; Pathologie de l'appareil urinaire; Tumeur maligne; Cancer; Pathologie de la prostate; Enzyme
ED :	Prostate cancer; Variant; Genetic variability; Genotype; Promoter; Risk factor; Epidemiology; Cytochrome P450; Check; Hormone; Nephrology; Urology
EG :	Male genital diseases; Urinary system disease; Malignant tumor; Cancer; Prostate disease; Enzyme
SD :	Cáncer de la próstata; Variante; Variabilidad genética; Genotipo; Promotor; Factor riesgo; Epidemiología; Citocromo P450; Control; Hormona; Nefrología; Urología
LO :	INIST-1050.354000161898220170
ID :	08-0137997

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Pascal:08-0137997

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">The rs743572 common variant in the promoter of CYP17A1 is not associated with prostate cancer risk or circulating hormonal levels</title>
<author><name sortKey="Severi, Gianluca" sort="Severi, Gianluca" uniqKey="Severi G" first="Gianluca" last="Severi">Gianluca Severi</name>
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</author>
<author><name sortKey="Hayes, Vanessa M" sort="Hayes, Vanessa M" uniqKey="Hayes V" first="Vanessa M." last="Hayes">Vanessa M. Hayes</name>
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<s3>AUS</s3>
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<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
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<author><name sortKey="Southey, Melissa C" sort="Southey, Melissa C" uniqKey="Southey M" first="Melissa C." last="Southey">Melissa C. Southey</name>
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</affiliation>
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<author><name sortKey="Hoang, Hoa N" sort="Hoang, Hoa N" uniqKey="Hoang H" first="Hoa N." last="Hoang">Hoa N. Hoang</name>
<affiliation><inist:fA14 i1="01"><s1>Cancer Epidemiology Centre, The Cancer Council Victoria</s1>
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<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>12 aut.</sZ>
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<affiliation><inist:fA14 i1="06"><s1>School of Population Health, The University of Melbourne</s1>
<s3>AUS</s3>
<sZ>5 aut.</sZ>
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</affiliation>
</author>
<author><name sortKey="Padilla, Emma J D" sort="Padilla, Emma J D" uniqKey="Padilla E" first="Emma J. D." last="Padilla">Emma J. D. Padilla</name>
<affiliation><inist:fA14 i1="03"><s1>Cancer Research Program, Garvan Institute of Medical Research, St Vincent's Hospital, Darlinghurst</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
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<author><name sortKey="Morris, Howard A" sort="Morris, Howard A" uniqKey="Morris H" first="Howard A." last="Morris">Howard A. Morris</name>
<affiliation><inist:fA14 i1="07"><s1>Hanson Institute</s1>
<s2>Adelaide</s2>
<s3>AUS</s3>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="English, Dallas R" sort="English, Dallas R" uniqKey="English D" first="Dallas R." last="English">Dallas R. English</name>
<affiliation><inist:fA14 i1="01"><s1>Cancer Epidemiology Centre, The Cancer Council Victoria</s1>
<s2>Melbourne</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>12 aut.</sZ>
</inist:fA14>
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<affiliation><inist:fA14 i1="02"><s1>Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, The University of Melbourne</s1>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
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<author><name sortKey="Sutherland, Robert L" sort="Sutherland, Robert L" uniqKey="Sutherland R" first="Robert L." last="Sutherland">Robert L. Sutherland</name>
<affiliation><inist:fA14 i1="03"><s1>Cancer Research Program, Garvan Institute of Medical Research, St Vincent's Hospital, Darlinghurst</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="04"><s1>University of New South Wales</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>2 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
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<author><name sortKey="Boyle, Peter" sort="Boyle, Peter" uniqKey="Boyle P" first="Peter" last="Boyle">Peter Boyle</name>
<affiliation><inist:fA14 i1="08"><s1>International Agency for Research on Cancer</s1>
<s2>Lyon</s2>
<s3>FRA</s3>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Hopper, John L" sort="Hopper, John L" uniqKey="Hopper J" first="John L." last="Hopper">John L. Hopper</name>
<affiliation><inist:fA14 i1="02"><s1>Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, The University of Melbourne</s1>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
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<author><name sortKey="Giles, Graham G" sort="Giles, Graham G" uniqKey="Giles G" first="Graham G." last="Giles">Graham G. Giles</name>
<affiliation><inist:fA14 i1="01"><s1>Cancer Epidemiology Centre, The Cancer Council Victoria</s1>
<s2>Melbourne</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>12 aut.</sZ>
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<affiliation><inist:fA14 i1="02"><s1>Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, The University of Melbourne</s1>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
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<series><title level="j" type="main">BJU international : (Papier)</title>
<title level="j" type="abbreviated">BJU int. : (Print)</title>
<idno type="ISSN">1464-4096</idno>
<imprint><date when="2008">2008</date>
</imprint>
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<seriesStmt><title level="j" type="main">BJU international : (Papier)</title>
<title level="j" type="abbreviated">BJU int. : (Print)</title>
<idno type="ISSN">1464-4096</idno>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Check</term>
<term>Cytochrome P450</term>
<term>Epidemiology</term>
<term>Genetic variability</term>
<term>Genotype</term>
<term>Hormone</term>
<term>Nephrology</term>
<term>Promoter</term>
<term>Prostate cancer</term>
<term>Risk factor</term>
<term>Urology</term>
<term>Variant</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Cancer de la prostate</term>
<term>Variant</term>
<term>Variabilité génétique</term>
<term>Génotype</term>
<term>Promoteur</term>
<term>Facteur risque</term>
<term>Epidémiologie</term>
<term>Cytochrome P450</term>
<term>Contrôle</term>
<term>Hormone</term>
<term>Néphrologie</term>
<term>Urologie</term>
<term>Cytochrome P450c17α</term>
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<front><div type="abstract" xml:lang="en">OBJECTIVE To use a large population-based case-control study to test the association between the common genetic variant rs743572 (-34 T to C), prostate cancer risk and circulating levels of several hormones. SUBJECTS AND METHODS A previous meta-analysis concluded that reported associations between rs743572 in the promoter of CYP17A1 and prostate cancer risk might reflect publication bias, but a few recent studies reported associations with prostate cancer risk and data suggesting that rs743572 is functional. We genotyped 824 prostate cancer cases and 737 population-based controls, and applied unconditional logistic regression to estimate the association between rs743572 and prostate cancer risk. We also used linear regression of transformed testosterone, androstanediol glucuronide, dehydroepiandrosterone sulphate, androstenedione, sex hormone-binding globulin and oestradiol (circulating levels) measured for controls, to estimate the association between these levels and rs743572. The linear models were adjusted for age and laboratory batch. RESULTS Men with different genotypes had similar circulating levels of all the hormones measured (all P< 0.05). In the case-control comparison using unconditional unadjusted logistic regression, the odds ratios (95% confidence interval) for prostate cancer were 1.07 (0.87-1.32) and 0.94 (0.71-1.25) for the dominant and recessive models, respectively, and for the co-dominant model, 1.10 (0.88-1.36) and 0.99 (0.73-1.35) for carriers of one or two copies of the C allele, respectively. There was no evidence of heterogeneity in the odds ratios by tumour stage (all P> 0.3) and grade (all P> 0.3). CONCLUSION The results of the present study are consistent with the conclusions of the previous meta-analysis, and suggest that rs743572 has no role in the risk of prostate cancer for men of Caucasian origin.</div>
</front>
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<fA05><s2>101</s2>
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<fA08 i1="01" i2="1" l="ENG"><s1>The rs743572 common variant in the promoter of CYP17A1 is not associated with prostate cancer risk or circulating hormonal levels</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>SEVERI (Gianluca)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>HAYES (Vanessa M.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>TESORIERO (Andrea A.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>SOUTHEY (Melissa C.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>HOANG (Hoa N.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>PADILLA (Emma J. D.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>MORRIS (Howard A.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>ENGLISH (Dallas R.)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>SUTHERLAND (Robert L.)</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>BOYLE (Peter)</s1>
</fA11>
<fA11 i1="11" i2="1"><s1>HOPPER (John L.)</s1>
</fA11>
<fA11 i1="12" i2="1"><s1>GILES (Graham G.)</s1>
</fA11>
<fA14 i1="01"><s1>Cancer Epidemiology Centre, The Cancer Council Victoria</s1>
<s2>Melbourne</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, The University of Melbourne</s1>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Cancer Research Program, Garvan Institute of Medical Research, St Vincent's Hospital, Darlinghurst</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>University of New South Wales</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>2 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Pathology, The University of Melbourne</s1>
<s3>AUS</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>School of Population Health, The University of Melbourne</s1>
<s3>AUS</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Hanson Institute</s1>
<s2>Adelaide</s2>
<s3>AUS</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>International Agency for Research on Cancer</s1>
<s2>Lyon</s2>
<s3>FRA</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA20><s1>492-496</s1>
</fA20>
<fA21><s1>2008</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
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<fA43 i1="01"><s1>INIST</s1>
<s2>1050</s2>
<s5>354000161898220170</s5>
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<fA44><s0>0000</s0>
<s1>© 2008 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>74 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>08-0137997</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>BJU international : (Papier)</s0>
</fA64>
<fA66 i1="01"><s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>OBJECTIVE To use a large population-based case-control study to test the association between the common genetic variant rs743572 (-34 T to C), prostate cancer risk and circulating levels of several hormones. SUBJECTS AND METHODS A previous meta-analysis concluded that reported associations between rs743572 in the promoter of CYP17A1 and prostate cancer risk might reflect publication bias, but a few recent studies reported associations with prostate cancer risk and data suggesting that rs743572 is functional. We genotyped 824 prostate cancer cases and 737 population-based controls, and applied unconditional logistic regression to estimate the association between rs743572 and prostate cancer risk. We also used linear regression of transformed testosterone, androstanediol glucuronide, dehydroepiandrosterone sulphate, androstenedione, sex hormone-binding globulin and oestradiol (circulating levels) measured for controls, to estimate the association between these levels and rs743572. The linear models were adjusted for age and laboratory batch. RESULTS Men with different genotypes had similar circulating levels of all the hormones measured (all P< 0.05). In the case-control comparison using unconditional unadjusted logistic regression, the odds ratios (95% confidence interval) for prostate cancer were 1.07 (0.87-1.32) and 0.94 (0.71-1.25) for the dominant and recessive models, respectively, and for the co-dominant model, 1.10 (0.88-1.36) and 0.99 (0.73-1.35) for carriers of one or two copies of the C allele, respectively. There was no evidence of heterogeneity in the odds ratios by tumour stage (all P> 0.3) and grade (all P> 0.3). CONCLUSION The results of the present study are consistent with the conclusions of the previous meta-analysis, and suggest that rs743572 has no role in the risk of prostate cancer for men of Caucasian origin.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B14D02</s0>
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<fC02 i1="02" i2="X"><s0>002B20B02</s0>
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<s5>01</s5>
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<s5>01</s5>
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<fC03 i1="01" i2="X" l="SPA"><s0>Cáncer de la próstata</s0>
<s2>NM</s2>
<s5>01</s5>
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<fC03 i1="02" i2="X" l="FRE"><s0>Variant</s0>
<s5>02</s5>
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<s5>03</s5>
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<s5>03</s5>
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<fC03 i1="03" i2="X" l="SPA"><s0>Variabilidad genética</s0>
<s5>03</s5>
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<s5>05</s5>
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<s5>06</s5>
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<s5>08</s5>
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<s5>08</s5>
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<s5>08</s5>
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<s5>09</s5>
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<s5>09</s5>
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<fC03 i1="08" i2="X" l="FRE"><s0>Cytochrome P450</s0>
<s5>11</s5>
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<fC03 i1="08" i2="X" l="ENG"><s0>Cytochrome P450</s0>
<s5>11</s5>
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<fC03 i1="08" i2="X" l="SPA"><s0>Citocromo P450</s0>
<s5>11</s5>
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<s5>17</s5>
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<s5>18</s5>
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<s5>18</s5>
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<s5>18</s5>
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<s5>19</s5>
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<s5>19</s5>
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<s5>19</s5>
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<s4>INC</s4>
<s5>86</s5>
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<s5>37</s5>
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<s5>37</s5>
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<s5>37</s5>
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<s2>NM</s2>
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<fC07 i1="04" i2="X" l="SPA"><s0>Cáncer</s0>
<s2>NM</s2>
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<fC07 i1="05" i2="X" l="FRE"><s0>Pathologie de la prostate</s0>
<s5>40</s5>
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<s5>40</s5>
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<s5>40</s5>
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<ET>The rs743572 common variant in the promoter of CYP17A1 is not associated with prostate cancer risk or circulating hormonal levels</ET>
<AU>SEVERI (Gianluca); HAYES (Vanessa M.); TESORIERO (Andrea A.); SOUTHEY (Melissa C.); HOANG (Hoa N.); PADILLA (Emma J. D.); MORRIS (Howard A.); ENGLISH (Dallas R.); SUTHERLAND (Robert L.); BOYLE (Peter); HOPPER (John L.); GILES (Graham G.)</AU>
<AF>Cancer Epidemiology Centre, The Cancer Council Victoria/Melbourne/Australie (1 aut., 5 aut., 8 aut., 12 aut.); Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, The University of Melbourne/Australie (1 aut., 8 aut., 11 aut., 12 aut.); Cancer Research Program, Garvan Institute of Medical Research, St Vincent's Hospital, Darlinghurst/Sydney/Australie (2 aut., 6 aut., 9 aut.); University of New South Wales/Sydney/Australie (2 aut., 9 aut.); Department of Pathology, The University of Melbourne/Australie (3 aut., 4 aut.); School of Population Health, The University of Melbourne/Australie (5 aut.); Hanson Institute/Adelaide/Australie (7 aut.); International Agency for Research on Cancer/Lyon/France (10 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>BJU international : (Papier); ISSN 1464-4096; Royaume-Uni; Da. 2008; Vol. 101; No. 4; Pp. 492-496; Bibl. 74 ref.</SO>
<LA>Anglais</LA>
<EA>OBJECTIVE To use a large population-based case-control study to test the association between the common genetic variant rs743572 (-34 T to C), prostate cancer risk and circulating levels of several hormones. SUBJECTS AND METHODS A previous meta-analysis concluded that reported associations between rs743572 in the promoter of CYP17A1 and prostate cancer risk might reflect publication bias, but a few recent studies reported associations with prostate cancer risk and data suggesting that rs743572 is functional. We genotyped 824 prostate cancer cases and 737 population-based controls, and applied unconditional logistic regression to estimate the association between rs743572 and prostate cancer risk. We also used linear regression of transformed testosterone, androstanediol glucuronide, dehydroepiandrosterone sulphate, androstenedione, sex hormone-binding globulin and oestradiol (circulating levels) measured for controls, to estimate the association between these levels and rs743572. The linear models were adjusted for age and laboratory batch. RESULTS Men with different genotypes had similar circulating levels of all the hormones measured (all P< 0.05). In the case-control comparison using unconditional unadjusted logistic regression, the odds ratios (95% confidence interval) for prostate cancer were 1.07 (0.87-1.32) and 0.94 (0.71-1.25) for the dominant and recessive models, respectively, and for the co-dominant model, 1.10 (0.88-1.36) and 0.99 (0.73-1.35) for carriers of one or two copies of the C allele, respectively. There was no evidence of heterogeneity in the odds ratios by tumour stage (all P> 0.3) and grade (all P> 0.3). CONCLUSION The results of the present study are consistent with the conclusions of the previous meta-analysis, and suggest that rs743572 has no role in the risk of prostate cancer for men of Caucasian origin.</EA>
<CC>002B14D02; 002B20B02</CC>
<FD>Cancer de la prostate; Variant; Variabilité génétique; Génotype; Promoteur; Facteur risque; Epidémiologie; Cytochrome P450; Contrôle; Hormone; Néphrologie; Urologie; Cytochrome P450c17α</FD>
<FG>Pathologie de l'appareil génital mâle; Pathologie de l'appareil urinaire; Tumeur maligne; Cancer; Pathologie de la prostate; Enzyme</FG>
<ED>Prostate cancer; Variant; Genetic variability; Genotype; Promoter; Risk factor; Epidemiology; Cytochrome P450; Check; Hormone; Nephrology; Urology</ED>
<EG>Male genital diseases; Urinary system disease; Malignant tumor; Cancer; Prostate disease; Enzyme</EG>
<SD>Cáncer de la próstata; Variante; Variabilidad genética; Genotipo; Promotor; Factor riesgo; Epidemiología; Citocromo P450; Control; Hormona; Nefrología; Urología</SD>
<LO>INIST-1050.354000161898220170</LO>
<ID>08-0137997</ID>
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The rs743572 common variant in the promoter of CYP17A1 is not associated with prostate cancer risk or circulating hormonal levels

The rs743572 common variant in the promoter of CYP17A1 is not associated with prostate cancer risk or circulating hormonal levels

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