Progesterone receptor variation and risk of ovarian cancer is limited to the invasive endometrioid subtype: results from the Ovarian Cancer Association Consortium pooled analysis

C.L. Pearce; A.H. Wu; S.A. Gayther; A.E. Bale; P.A. Beck; J. Beesley; S. Chanock; D.W. Cramer; R. DiCioccio; R. Edwards; Z.S. Fredericksen; M. Garcia-Closas; E.L. Goode; A.C. Green; L.C. Hartmann; S.K. Kjaer; J. Lissowska; V. McGuire; F. Modugno; K. Moysich; R.B. Ness; S.J. Ramus; H.A. Risch; T.A. Sellers; H. Song; D.O. Stram; K.L. Terry; P.M. Webb; D.C. Whiteman; A.S. Whittemore; W. Zheng; P.D. Pharoah; G. Chenevix-Trench; M.C. Pike; J. Schildkraut; A. Berchuck; Estrid Vilma Solyom Høgdall

Progesterone receptor variation and risk of ovarian cancer is limited to the invasive endometrioid subtype: results from the Ovarian Cancer Association Consortium pooled analysis

C.L. Pearce, A.H. Wu, S.A. Gayther, A.E. Bale, P.A. Beck, J. Beesley, S. Chanock, D.W. Cramer, R. DiCioccio, R. Edwards, Z.S. Fredericksen, M. Garcia-Closas, E.L. Goode, A.C. Green, L.C. Hartmann, S.K. Kjaer, J. Lissowska, V. McGuire, F. Modugno, K. MoysichR.B. Ness, S.J. Ramus, H.A. Risch, T.A. Sellers, H. Song, D.O. Stram, K.L. Terry, P.M. Webb, D.C. Whiteman, A.S. Whittemore, W. Zheng, P.D. Pharoah, G. Chenevix-Trench, M.C. Pike, J. Schildkraut, A. Berchuck, Estrid Vilma Solyom Høgdall

44 Citationer (Scopus)

Abstract

There is evidence that progesterone plays a role in the aetiology of invasive epithelial ovarian cancer. Therefore, genes involved in pathways that regulate progesterone may be candidates for susceptibility to this disease. Previous studies have suggested that genetic variants in the progesterone receptor gene (PGR) may be associated with ovarian cancer risk, although results have been inconsistent. We have established an international consortium to pool resources and data from many ovarian cancer case-control studies in an effort to identify variants that influence risk. In this study, three PGR single nucleotide polymorphisms (SNPs), for which previous data have suggested they affect ovarian cancer risk, were examined. These were +331 C/T (rs10895068), PROGINS (rs1042838), and a 3' variant (rs608995). A total of 4788 ovarian cancer cases and 7614 controls from 12 case-control studies were included in this analysis. Unconditional logistic regression was used to model the association between each SNP and ovarian cancer risk and two-sided P-values are reported. Overall, risk of ovarian cancer was not associated with any of the three variants studied. However, in histopathological subtype analyses, we found a statistically significant association between risk of endometrioid ovarian cancer and the PROGINS allele (n=651, OR=1.17, 95% CI=1.01-1.36, P=0.036). We also observed borderline evidence of an association between risk of endometrioid ovarian cancer and the +331C/T variant (n=725 cases; OR=0.80, 95% CI 0.62-1.04, P=0.100). These data suggest that while these three variants in the PGR are not associated with ovarian cancer overall, the PROGINS variant may play a modest role in risk of endometrioid ovarian cancer
Udgivelsesdato: 2008/1/29

Originalsprog	Dansk
Tidsskrift	British Journal of Cancer
Vol/bind	98
Udgave nummer	2
Sider (fra-til)	282-288
Antal sider	6
ISSN	0007-0920
Status	Udgivet - 2008

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Citationsformater

Pearce, C. L., Wu, A. H., Gayther, S. A., Bale, A. E., Beck, P. A., Beesley, J., Chanock, S., Cramer, D. W., DiCioccio, R., Edwards, R., Fredericksen, Z. S., Garcia-Closas, M., Goode, E. L., Green, A. C., Hartmann, L. C., Kjaer, S. K., Lissowska, J., McGuire, V., Modugno, F., ... Høgdall, E. V. S. (2008). Progesterone receptor variation and risk of ovarian cancer is limited to the invasive endometrioid subtype: results from the Ovarian Cancer Association Consortium pooled analysis. British Journal of Cancer, 98(2), 282-288.

Progesterone receptor variation and risk of ovarian cancer is limited to the invasive endometrioid subtype: results from the Ovarian Cancer Association Consortium pooled analysis. / Pearce, C.L.; Wu, A.H.; Gayther, S.A. et al.

I: British Journal of Cancer, Bind 98, Nr. 2, 2008, s. 282-288.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

Pearce, CL, Wu, AH, Gayther, SA, Bale, AE, Beck, PA, Beesley, J, Chanock, S, Cramer, DW, DiCioccio, R, Edwards, R, Fredericksen, ZS, Garcia-Closas, M, Goode, EL, Green, AC, Hartmann, LC, Kjaer, SK, Lissowska, J, McGuire, V, Modugno, F, Moysich, K, Ness, RB, Ramus, SJ, Risch, HA, Sellers, TA, Song, H, Stram, DO, Terry, KL, Webb, PM, Whiteman, DC, Whittemore, AS, Zheng, W, Pharoah, PD, Chenevix-Trench, G, Pike, MC, Schildkraut, J, Berchuck, A & Høgdall, EVS 2008, 'Progesterone receptor variation and risk of ovarian cancer is limited to the invasive endometrioid subtype: results from the Ovarian Cancer Association Consortium pooled analysis', British Journal of Cancer, bind 98, nr. 2, s. 282-288.

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title = "Progesterone receptor variation and risk of ovarian cancer is limited to the invasive endometrioid subtype: results from the Ovarian Cancer Association Consortium pooled analysis",

abstract = "There is evidence that progesterone plays a role in the aetiology of invasive epithelial ovarian cancer. Therefore, genes involved in pathways that regulate progesterone may be candidates for susceptibility to this disease. Previous studies have suggested that genetic variants in the progesterone receptor gene (PGR) may be associated with ovarian cancer risk, although results have been inconsistent. We have established an international consortium to pool resources and data from many ovarian cancer case-control studies in an effort to identify variants that influence risk. In this study, three PGR single nucleotide polymorphisms (SNPs), for which previous data have suggested they affect ovarian cancer risk, were examined. These were +331 C/T (rs10895068), PROGINS (rs1042838), and a 3' variant (rs608995). A total of 4788 ovarian cancer cases and 7614 controls from 12 case-control studies were included in this analysis. Unconditional logistic regression was used to model the association between each SNP and ovarian cancer risk and two-sided P-values are reported. Overall, risk of ovarian cancer was not associated with any of the three variants studied. However, in histopathological subtype analyses, we found a statistically significant association between risk of endometrioid ovarian cancer and the PROGINS allele (n=651, OR=1.17, 95% CI=1.01-1.36, P=0.036). We also observed borderline evidence of an association between risk of endometrioid ovarian cancer and the +331C/T variant (n=725 cases; OR=0.80, 95% CI 0.62-1.04, P=0.100). These data suggest that while these three variants in the PGR are not associated with ovarian cancer overall, the PROGINS variant may play a modest role in risk of endometrioid ovarian cancer Udgivelsesdato: 2008/1/29",

author = "C.L. Pearce and A.H. Wu and S.A. Gayther and A.E. Bale and P.A. Beck and J. Beesley and S. Chanock and D.W. Cramer and R. DiCioccio and R. Edwards and Z.S. Fredericksen and M. Garcia-Closas and E.L. Goode and A.C. Green and L.C. Hartmann and S.K. Kjaer and J. Lissowska and V. McGuire and F. Modugno and K. Moysich and R.B. Ness and S.J. Ramus and H.A. Risch and T.A. Sellers and H. Song and D.O. Stram and K.L. Terry and P.M. Webb and D.C. Whiteman and A.S. Whittemore and W. Zheng and P.D. Pharoah and G. Chenevix-Trench and M.C. Pike and J. Schildkraut and A. Berchuck and H{\o}gdall, {Estrid Vilma Solyom}",

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T1 - Progesterone receptor variation and risk of ovarian cancer is limited to the invasive endometrioid subtype: results from the Ovarian Cancer Association Consortium pooled analysis

AU - Pearce, C.L.

AU - Wu, A.H.

AU - Gayther, S.A.

AU - Bale, A.E.

AU - Beck, P.A.

AU - Beesley, J.

AU - Chanock, S.

AU - Cramer, D.W.

AU - DiCioccio, R.

AU - Edwards, R.

AU - Fredericksen, Z.S.

AU - Garcia-Closas, M.

AU - Goode, E.L.

AU - Green, A.C.

AU - Hartmann, L.C.

AU - Kjaer, S.K.

AU - Lissowska, J.

AU - McGuire, V.

AU - Modugno, F.

AU - Moysich, K.

AU - Ness, R.B.

AU - Ramus, S.J.

AU - Risch, H.A.

AU - Sellers, T.A.

AU - Song, H.

AU - Stram, D.O.

AU - Terry, K.L.

AU - Webb, P.M.

AU - Whiteman, D.C.

AU - Whittemore, A.S.

AU - Zheng, W.

AU - Pharoah, P.D.

AU - Chenevix-Trench, G.

AU - Pike, M.C.

AU - Schildkraut, J.

AU - Berchuck, A.

AU - Høgdall, Estrid Vilma Solyom

N1 - IS - 0007-0920 (Print)LA - engPT - Journal ArticlePT - Meta-AnalysisPT - Research Support, N.I.H., ExtramuralPT - Research Support, N.I.H., IntramuralPT - Research Support, Non-U.S. Gov'tPT - Research Support, U.S. Gov't, Non-P.H.SRN - 0 (Receptors, Progesterone)SB - IM

PY - 2008

Y1 - 2008

N2 - There is evidence that progesterone plays a role in the aetiology of invasive epithelial ovarian cancer. Therefore, genes involved in pathways that regulate progesterone may be candidates for susceptibility to this disease. Previous studies have suggested that genetic variants in the progesterone receptor gene (PGR) may be associated with ovarian cancer risk, although results have been inconsistent. We have established an international consortium to pool resources and data from many ovarian cancer case-control studies in an effort to identify variants that influence risk. In this study, three PGR single nucleotide polymorphisms (SNPs), for which previous data have suggested they affect ovarian cancer risk, were examined. These were +331 C/T (rs10895068), PROGINS (rs1042838), and a 3' variant (rs608995). A total of 4788 ovarian cancer cases and 7614 controls from 12 case-control studies were included in this analysis. Unconditional logistic regression was used to model the association between each SNP and ovarian cancer risk and two-sided P-values are reported. Overall, risk of ovarian cancer was not associated with any of the three variants studied. However, in histopathological subtype analyses, we found a statistically significant association between risk of endometrioid ovarian cancer and the PROGINS allele (n=651, OR=1.17, 95% CI=1.01-1.36, P=0.036). We also observed borderline evidence of an association between risk of endometrioid ovarian cancer and the +331C/T variant (n=725 cases; OR=0.80, 95% CI 0.62-1.04, P=0.100). These data suggest that while these three variants in the PGR are not associated with ovarian cancer overall, the PROGINS variant may play a modest role in risk of endometrioid ovarian cancer Udgivelsesdato: 2008/1/29

AB - There is evidence that progesterone plays a role in the aetiology of invasive epithelial ovarian cancer. Therefore, genes involved in pathways that regulate progesterone may be candidates for susceptibility to this disease. Previous studies have suggested that genetic variants in the progesterone receptor gene (PGR) may be associated with ovarian cancer risk, although results have been inconsistent. We have established an international consortium to pool resources and data from many ovarian cancer case-control studies in an effort to identify variants that influence risk. In this study, three PGR single nucleotide polymorphisms (SNPs), for which previous data have suggested they affect ovarian cancer risk, were examined. These were +331 C/T (rs10895068), PROGINS (rs1042838), and a 3' variant (rs608995). A total of 4788 ovarian cancer cases and 7614 controls from 12 case-control studies were included in this analysis. Unconditional logistic regression was used to model the association between each SNP and ovarian cancer risk and two-sided P-values are reported. Overall, risk of ovarian cancer was not associated with any of the three variants studied. However, in histopathological subtype analyses, we found a statistically significant association between risk of endometrioid ovarian cancer and the PROGINS allele (n=651, OR=1.17, 95% CI=1.01-1.36, P=0.036). We also observed borderline evidence of an association between risk of endometrioid ovarian cancer and the +331C/T variant (n=725 cases; OR=0.80, 95% CI 0.62-1.04, P=0.100). These data suggest that while these three variants in the PGR are not associated with ovarian cancer overall, the PROGINS variant may play a modest role in risk of endometrioid ovarian cancer Udgivelsesdato: 2008/1/29

M3 - Tidsskriftartikel

SN - 0007-0920

VL - 98

SP - 282

EP - 288

JO - The British journal of cancer. Supplement

JF - The British journal of cancer. Supplement

IS - 2

ER -