Yuan-Ping Wang

Fujian Provincial Cancer Hospital, Min-hou, Fujian, China

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Publications (4)4.22 Total impact

  • Ping Tao · Hui Li · Qiong Wang · Lan-Qing Cao · Jia-Yuan Li · Fei Yang · Yuan-Ping Wang
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    ABSTRACT: To assess the association of smoked meat intake, SULT1A1 polymorphism as well as their combined effects with breast cancer risk. A total of 400 newly diagnosed breast cancer cases from a cancer hospital in Sichuan province and 400 healthy controls from participants of physical examination in a hospital in Chengdu city were recruited from May 2007 to July 2009. A valid questionnaire was designed to collect their demographic characteristics and breast cancer risk factors. Daily intake of foods was collected using semi-quantitative frequency questionnaire and then the daily intake of smoked meat was calculated and transformed to energy-adjusted smoked meat intake by the residual method. Gene sequencing was used to analyze SULT1A1 Arg213His genotypes. Multivariable conditional logistic regression was used to estimate adjusted odds ratios (ORs) and 95% confidence intervals (95%CIs). The energy-adjusted daily intake of smoked meat (Median (P(25), P(75))) was 8.65 (3.63, 18.44) g/d in cases and 4.44 (0.19, 8.71) g/d in controls. The frequency of SULT1A1 variant allele was 14.75% (59/400) among cases and 12.75% (51/400) among controls. High energy-adjusted daily intake of smoked meat (≥ 4.44 g/d) was significantly associated with breast cancer risk among premenopausal (OR = 2.31, 95%CI: 1.46 - 3.66) and postmenopausal subjects (OR = 3.13, 95%CI: 1.89 - 5.17). High energy-adjusted daily intake of smoked meat combined with carrying SULT1A1 variant allele elevated breast cancer risk among premenopausal (OR = 3.31, 95%CI: 1.66 - 6.62) and postmenopausal subjects (OR = 3.81, 95%CI: 1.79 - 8.10). High smoked meat intake contributes to high risk of breast cancer. SULT1A1 variant allele increases breast cancer risk among subjects who were exposed to high smoked meat intake.
    Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] 09/2012; 46(9):831-5.
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    ABSTRACT: CYP1A1, CYP1B1, and COMT are key enzymes involved in estrogen metabolism. Soy isoflavones, phytoestrogens found in soy foods, may modify the activity of these enzymes. A case-control study was conducted to assess the associations between soy isoflavone intake and the CYP1A1 Ile462Val, CYP1B1 Val432Leu, and COMT Val158Met polymorphisms and breast cancer, as well as their combined effects on breast cancer. A total of 400 newly diagnosed breast cancer cases and 400 healthy controls were recruited. Participants' daily intake of soy isoflavones (DISI [mg/day]) was calculated and transformed to energy-adjusted DISI by the residual method. Gene sequencing was used to analyze CYP1A1, CYP1B1, and COMT polymorphisms. Adjusted odds ratios (aORs) and 95% confidence intervals (95% CIs) were estimated by conditional logistic regression. A strong protective dose-dependent effect of energy-adjusted DISI on breast cancer was found in both pre- and postmenopausal women (P(trend) < 0.05). Among all women and in the postmenopausal subgroup, COMT Met/Met and CYP1B1 Leu/Leu susceptible genotype carriers had higher risk of breast cancer (aORs > 1, OR 95% CIs exclude 1). In premenopausal women, only carrying CYP1B1 Leu/Leu was associated with breast cancer risk (aOR = 2.05, 95% CI: 1.11-3.79). Carrying CYP1A1 Val/Val was related to breast cancer risk only among all women. A stratified analysis was performed at two levels of energy-adjusted DISI, with wildtype homozygous genotypes and low energy-adjusted DISI as the reference. In the high energy-adjusted DISI subgroup, carrying the CYP1B1 Leu/Leu genotype did not affect breast cancer risk in either all women or in the menopausal subgroups, compared with the reference. Overall, in Han Chinese women, carrying CYP1A1 Val/Val and COMT Met/Met appears to be associated with breast cancer risk, especially in postmenopausal women. CYP1B1 susceptible genotypes (Val/Leu or Leu/Leu) also contribute to increased breast cancer risk, regardless of menopausal status, but high soy isoflavone intake may reduce this risk.
    DNA and cell biology 03/2011; 30(8):585-95. DOI:10.1089/dna.2010.1195 · 2.06 Impact Factor
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    Qiong Wang · Yuan-Ping Wang · Jia-Yuan Li · Ping Yuan · Fei Yang · Hui Li
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    ABSTRACT: Genetic polymorphism Val158Met of catechol-O-methyltransferase (COMT) may contribute to estrogen-induced carcinogenesis of breast cancer. Soy isoflavones possesses chemical structure similar to endogenous estrogen and may promote the carcinogenesis of breast cancer. This study was to investigate the relationship between the polymorphism of COMT, soy isoflavones, and breast cancer in postmenopausal women. In total, 176 patients newly diagnosed histopathologically with breast cancer were recruited from May 2007 to July 2009, and 176 age-matched cancer-free women as controls were selected from a community-based physical check-up population at the same period. The food-frequency questionnaire was used to collect information on soy food intake. Allele-specific polymerase chain reaction (AS-PCR) was employed to analyze genetic polymorphism Val158Met of COMT. Adjusted odd ratios (aORs) and 95% confidence intervals (95% CI) were estimated by multivariable nonconditional logistic regression. The proportion of susceptible genotype (COMT-LL) in breast cancer patients was significantly higher than that in the controls. After adjusting selected risk factors, the aOR and 95% CI of COMT-LL were 3.14 (1.48-6.66) as compared with those of COMT-HH genotype. The intake of soy isoflavones had a negative correlation with breast cancer in a dose-dependent manner (Chi2 = 28.26, P < 0.001). The women with high intake of soy isoflavones (> or = 16.26 mg/d) and carrying susceptible genotype (COMT-LL), as compared with the women carrying the COMT-HH + COMT-HL genotypes and consuming low level of soy isoflavones (< 16.26 mg/d), had no significantly increased risk for breast cancer [ aOR (95% CI) = 1.66 (0.52-5.24)]. In postmenopausal women, carrying COMT-LL genotype may increase the risk for breast cancer, and soy isoflavones intake may protect them from breast cancer. But there may be no interaction between intake of soy isoflavones and COMT-LL genotype.
    Chinese journal of cancer 07/2010; 29(7):683-8. DOI:10.5732/cjc.009.10700 · 2.16 Impact Factor
  • Yuan-ping Wang · Hui Li · Jia-yuan Li · Ping Yuan · Fei Yang · Fang-ming Lei · Yi Pang · Jie Guo
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    ABSTRACT: To explore the relationship between the polymorphism of estrogen-biosynthesis genes (CYP17, CYP19, HSD17beta1) and risk of breast cancer. A matched case-control study was designed. From May 2007 to July 2008, 200 pairs of subjects with and without breast cancer were enrolled, who were matched by age and menstruation status. Demographical characteristics, dietary factors and reproductive factors were investigated by questionnaire. CYP17 locus 1931 (T-->C), CYP19 codon 264 (Arg-->Cys) and HSD17beta1 locus 1954 (A-->G) were identified by AS-PCR (allele-specific PCR). The gene-gene interaction were analyzed with the MDR model (multifactor dimensionality reduction). Based on the results of MDR model, an unconditional logistic regression model was simulated to estimate the ORs of interaction factors and other risk factors. The main effect of CYP17, CYP19 and HSD17beta1 susceptible genotypes were not correlated to breast cancer (OR approximately 1, P > 0.05). The positive interaction effect between CYP17 (T 1931C) and HSD17beta1 (A1954G) was discovered by MDR model with a statistically significant difference (Sign test, P = 0.05). The model's testing balance accuracy was 56.00%, and crossing validation consistency was 10/10. Multivariable unconditional logistic regression showed that after adjusting BMI, intake of estrogen, age of first birth, number of abortion and period of breast feeding, the interaction item of CYP17 (T1931C) and HSD17beta1 (A1954G) was strongly and positively correlated to breast cancer (OR = 2.52, 95%CI = 1.54 to 4.11). The estrogen-biosynthesis genes CYP17 (T1931C) and HSD17beta1 (A1954G) polymorphism may jointly increase the risk of breast cancer.
    Zhonghua zhong liu za zhi [Chinese journal of oncology] 12/2009; 31(12):899-903.