Repeat polymorphisms in estrogen metabolism genes and prostate cancer risk: Results from the Prostate Cancer Prevention Trial

Li Tang, Song Yao, Cathee Till, Phyllis J. Goodman, Catherine M. Tangen, Yue Wu, Alan R. Kristal, Elizabeth A. Platz, Marian L. Neuhouser, Frank Z. Stanczyk, Juergen K V Reichardt, Regina M. Santella, Ann Hsing, Ashraful Hoque, Scott M. Lippman, Ian M. Thompson, Christine B. Ambrosone

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Original languageEnglish
Pages (from-to)1500-1506
Number of pages7
JournalCarcinogenesis
Volume32
Issue number10
DOIs
StatePublished - Oct 2011

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Prostatic Neoplasms
Estrogens
Finasteride
Genes
Genotype
Odds Ratio
Placebos
Confidence Intervals
Hormones
Chemoprevention
Logistic Models
Steroids
Therapeutics
Serum

ASJC Scopus subject areas

  • Cancer Research

Cite this

Tang, L., Yao, S., Till, C., Goodman, P. J., Tangen, C. M., Wu, Y., ... Ambrosone, C. B. (2011). Repeat polymorphisms in estrogen metabolism genes and prostate cancer risk: Results from the Prostate Cancer Prevention Trial. Carcinogenesis, 32(10), 1500-1506. https://doi.org/10.1093/carcin/bgr139

Repeat polymorphisms in estrogen metabolism genes and prostate cancer risk : Results from the Prostate Cancer Prevention Trial. / Tang, Li; Yao, Song; Till, Cathee; Goodman, Phyllis J.; Tangen, Catherine M.; Wu, Yue; Kristal, Alan R.; Platz, Elizabeth A.; Neuhouser, Marian L.; Stanczyk, Frank Z.; Reichardt, Juergen K V; Santella, Regina M.; Hsing, Ann; Hoque, Ashraful; Lippman, Scott M.; Thompson, Ian M.; Ambrosone, Christine B.

In: Carcinogenesis, Vol. 32, No. 10, 10.2011, p. 1500-1506.

Research output: Contribution to journalArticle

Tang, L, Yao, S, Till, C, Goodman, PJ, Tangen, CM, Wu, Y, Kristal, AR, Platz, EA, Neuhouser, ML, Stanczyk, FZ, Reichardt, JKV, Santella, RM, Hsing, A, Hoque, A, Lippman, SM, Thompson, IM & Ambrosone, CB 2011, 'Repeat polymorphisms in estrogen metabolism genes and prostate cancer risk: Results from the Prostate Cancer Prevention Trial', Carcinogenesis, vol. 32, no. 10, pp. 1500-1506. https://doi.org/10.1093/carcin/bgr139
Tang, Li ; Yao, Song ; Till, Cathee ; Goodman, Phyllis J. ; Tangen, Catherine M. ; Wu, Yue ; Kristal, Alan R. ; Platz, Elizabeth A. ; Neuhouser, Marian L. ; Stanczyk, Frank Z. ; Reichardt, Juergen K V ; Santella, Regina M. ; Hsing, Ann ; Hoque, Ashraful ; Lippman, Scott M. ; Thompson, Ian M. ; Ambrosone, Christine B. / Repeat polymorphisms in estrogen metabolism genes and prostate cancer risk : Results from the Prostate Cancer Prevention Trial. In: Carcinogenesis. 2011 ; Vol. 32, No. 10. pp. 1500-1506.
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title = "Repeat polymorphisms in estrogen metabolism genes and prostate cancer risk: Results from the Prostate Cancer Prevention Trial",
abstract = "The etiology of prostate cancer remains elusive, although steroid hormones probably play a role. Considering the carcinogenic potential of estrogen metabolites as well as altered intraprostatic estrogen biosynthesis during the development of prostate cancer, we investigated associations between repeat polymorphisms of three key estrogen-related genes (CYP11A1, CYP19A1, UGT1A1) and risk of prostate cancer in the Prostate Cancer Prevention Trial (PCPT), designed to test finasteride versus placebo as a chemoprevention agent. Using data and specimens from 1154 cases and 1351 controls who were frequency matched on age, family history of prostate cancer and PCPT treatment arm, we used logistic regression to estimate odds ratios (ORs) and 95{\%} confidence intervals (95{\%} CIs) separately in the placebo and finasteride arms. Among men in the placebo arm, CYP19A1 7/8 genotype carriers had a significantly higher risk of prostate cancer compared with those with the 7/7 genotype (OR = 1.70, 95{\%} CI = 1.16-2.5), regardless of Gleason grade. This genotype was also associated with elevated serum estrogen levels. For the (TA) n repeat polymorphism in UGT1A1, the heterozygous short (<7 repeats)/long (≥7 repeats) genotype was significantly associated with the risk of low-grade prostate cancer (OR = 1.34, 95{\%} CI = 1.05-1.70) compared with the short/short genotype. No significant association was found with CYP11A1. These associations were not observed among men in the finasteride arm. The results indicate that repeat polymorphisms in genes involved in estrogen biosynthesis and metabolism may influence risk of prostate cancer but that their effects may be modified by factors altering hormone metabolism, such as finasteride treatment.",
author = "Li Tang and Song Yao and Cathee Till and Goodman, {Phyllis J.} and Tangen, {Catherine M.} and Yue Wu and Kristal, {Alan R.} and Platz, {Elizabeth A.} and Neuhouser, {Marian L.} and Stanczyk, {Frank Z.} and Reichardt, {Juergen K V} and Santella, {Regina M.} and Ann Hsing and Ashraful Hoque and Lippman, {Scott M.} and Thompson, {Ian M.} and Ambrosone, {Christine B.}",
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T1 - Repeat polymorphisms in estrogen metabolism genes and prostate cancer risk

T2 - Results from the Prostate Cancer Prevention Trial

AU - Tang, Li

AU - Yao, Song

AU - Till, Cathee

AU - Goodman, Phyllis J.

AU - Tangen, Catherine M.

AU - Wu, Yue

AU - Kristal, Alan R.

AU - Platz, Elizabeth A.

AU - Neuhouser, Marian L.

AU - Stanczyk, Frank Z.

AU - Reichardt, Juergen K V

AU - Santella, Regina M.

AU - Hsing, Ann

AU - Hoque, Ashraful

AU - Lippman, Scott M.

AU - Thompson, Ian M.

AU - Ambrosone, Christine B.

PY - 2011/10

Y1 - 2011/10

N2 - The etiology of prostate cancer remains elusive, although steroid hormones probably play a role. Considering the carcinogenic potential of estrogen metabolites as well as altered intraprostatic estrogen biosynthesis during the development of prostate cancer, we investigated associations between repeat polymorphisms of three key estrogen-related genes (CYP11A1, CYP19A1, UGT1A1) and risk of prostate cancer in the Prostate Cancer Prevention Trial (PCPT), designed to test finasteride versus placebo as a chemoprevention agent. Using data and specimens from 1154 cases and 1351 controls who were frequency matched on age, family history of prostate cancer and PCPT treatment arm, we used logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs) separately in the placebo and finasteride arms. Among men in the placebo arm, CYP19A1 7/8 genotype carriers had a significantly higher risk of prostate cancer compared with those with the 7/7 genotype (OR = 1.70, 95% CI = 1.16-2.5), regardless of Gleason grade. This genotype was also associated with elevated serum estrogen levels. For the (TA) n repeat polymorphism in UGT1A1, the heterozygous short (<7 repeats)/long (≥7 repeats) genotype was significantly associated with the risk of low-grade prostate cancer (OR = 1.34, 95% CI = 1.05-1.70) compared with the short/short genotype. No significant association was found with CYP11A1. These associations were not observed among men in the finasteride arm. The results indicate that repeat polymorphisms in genes involved in estrogen biosynthesis and metabolism may influence risk of prostate cancer but that their effects may be modified by factors altering hormone metabolism, such as finasteride treatment.

AB - The etiology of prostate cancer remains elusive, although steroid hormones probably play a role. Considering the carcinogenic potential of estrogen metabolites as well as altered intraprostatic estrogen biosynthesis during the development of prostate cancer, we investigated associations between repeat polymorphisms of three key estrogen-related genes (CYP11A1, CYP19A1, UGT1A1) and risk of prostate cancer in the Prostate Cancer Prevention Trial (PCPT), designed to test finasteride versus placebo as a chemoprevention agent. Using data and specimens from 1154 cases and 1351 controls who were frequency matched on age, family history of prostate cancer and PCPT treatment arm, we used logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs) separately in the placebo and finasteride arms. Among men in the placebo arm, CYP19A1 7/8 genotype carriers had a significantly higher risk of prostate cancer compared with those with the 7/7 genotype (OR = 1.70, 95% CI = 1.16-2.5), regardless of Gleason grade. This genotype was also associated with elevated serum estrogen levels. For the (TA) n repeat polymorphism in UGT1A1, the heterozygous short (<7 repeats)/long (≥7 repeats) genotype was significantly associated with the risk of low-grade prostate cancer (OR = 1.34, 95% CI = 1.05-1.70) compared with the short/short genotype. No significant association was found with CYP11A1. These associations were not observed among men in the finasteride arm. The results indicate that repeat polymorphisms in genes involved in estrogen biosynthesis and metabolism may influence risk of prostate cancer but that their effects may be modified by factors altering hormone metabolism, such as finasteride treatment.

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