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1.
Li-Xin Qiu Lei Yao Hui Yuan Chen Mao Bo Chen Ping Zhan Kai Xue Jian Zhang Xi-Chun Hu 《Breast cancer research and treatment》2010,122(3):867-871
Published data on the association between insulin-like growth factor binding protein 3 (IGFBP3) A-202C polymorphism and breast
cancer risk are inconclusive. To derive a more precise estimation of the relationship, a meta-analysis was performed. Crude
ORs with 95% CIs were used to assess the strength of association between them. A total of 27 studies including 33,557 cases
and 45,254 controls were involved in this meta-analysis. Overall, significantly elevated breast cancer risk was associated
with IGFBP3 C allele when all studies were pooled into the meta-analysis (CC vs. AA: OR = 1.06, 95% CI = 1.02–1.11; dominant
model: OR = 1.04, 95% CI = 1.00–1.07). In the subgroup analysis by ethnicity, significantly increased risk was found for Caucasians
(AC vs. AA: OR = 1.04, 95% CI = 1.00–1.08; CC vs. AA: OR = 1.05, 95% CI = 1.01–1.10; dominant model: OR = 1.04, 95% CI = 1.00–1.08)
and Asians (CC vs. AA: OR = 1.35, 95% CI = 1.02–1.78; recessive model: OR = 1.38, 95% CI = 1.05–1.82). When stratified by
study design, statistically significantly elevated risk was found among population-based studies (CC vs. AA: OR = 1.06, 95%
CI = 1.01–1.11; dominant model: OR = 1.03, 95% CI = 1.00–1.07). In the subgroup analysis by menopausal status, no statistically
significantly increased risk was found among premenopausal or postmenopausal women. In conclusion, this meta-analysis suggests
that the IGFBP3 C allele is a low-penetrant risk factor for developing breast cancer. 相似文献
2.
Breast cancer is the most prevalent cancer in the world, which is a major public health challenge. To date, many publications
have evaluated the correlation between Cytochrome P450 1A1 (CYP1A1) T3801C polymorphism and breast cancer risk. However, the
results remain inconclusive. In order to derive a more precise estimation of the association, a meta-analysis was performed
in this study. By searching Medline, PubMed, and ISI Web of Knowledge databases, 23 studies including 10,520 cases and 14,567
controls were collected for CYP1A1 T3801C polymorphism. The strength of association between CYP1A1 T3801C polymorphism and
breast cancer risk was assessed by calculating crude ORs with 95% CIs. The pooled ORs were performed for codominant model,
dominant model, and recessive model, respectively. Overall, no significant associations between CYP1A1 T3801C polymorphism
and breast cancer susceptibility were found for TT versus CC (OR = 0.93; 95% CI: 0.72–1.19), TC versus CC (OR = 0.95; 95%
CI: 0.79–1.14), TT + TC versus CC (OR = 0.93; 95% CI: 0.75–1.15), and TT versus TC + CC (OR = 0.99; 95% CI: 0.87–1.13). In
the stratified analysis by ethnicity, menopausal status, and source of controls, no significant associations were detected
in all genetic models. In conclusion, this meta-analysis provides strong evidence that CYP1A1 T3801C polymorphism is not associated
with breast cancer risk. 相似文献
3.
Yonglan Zheng Jing Zhang Kisha Hope Qun Niu Dezheng Huo Olufunmilayo I. Olopade 《Breast cancer research and treatment》2010,124(3):857-861
Breast cancer is the most prevalent cancer worldwide. Many published articles have evaluated the association between the transforming
growth factor beta 1 (TGFB1) T29C polymorphism and breast cancer risk. However, the results remain inconclusive. In order
to derive a more precise estimation of the association, a meta-analysis was performed in this study. Odds ratios (ORs) and
95% confidence intervals (CIs) were used to assess the strength of the association. A total of 12 studies including 10,417
breast cancer cases and 11,455 controls were identified. Overall, no significant associations between the TGFB1 T29C polymorphism
and breast cancer risk were found for CC versus TT (OR = 1.00, 95% CI = 0.92–1.09), TC versus TT (OR = 0.98, 95% CI = 0.93–1.05),
CC/TC versus TT (OR = 0.99, 95% CI = 0.93–1.05), and CC versus TC/TT (OR = 1.00, 95% CI = 0.93–1.08). In the subgroup analysis
by ethnicity, source of controls, and menopausal status, there was still no significant association detected in all genetic
models. In conclusion, the present meta-analysis suggests that the TGFB1 T29C polymorphism is not a low-penetrant risk factor
for developing breast cancer. 相似文献
4.
The A2756G polymorphism in the methionine synthase (MTR) gene has been implicated in breast cancer risk. However, the published
findings are inconsistent. We therefore performed a meta-analysis to investigate this relationship. Eleven published case–control
studies, including 8,438 breast cancer cases and 10,515 controls were identified. Odds ratios (ORs) and 95% confidence intervals
(CIs) were used to assess the strength of the association. Overall, no significant associations between the MTR A2756G polymorphism
and breast cancer risk were found for GG versus AA (OR = 0.98, 95% CI: 0.84–1.15), AG versus AA (OR = 0.95, 95% CI: 0.89–1.01),
GG/AG versus AA (OR = 0.95, 95% CI = 0.89–1.01), and GG versus AG/AA (OR = 1.00, 95% CI: 0.86–1.17). However, in the stratified
analysis, significantly decreased breast cancer risks were found among Europeans (AG versus AA, OR = 0.90, 95% CI = 0.83–0.98;
GG/AG versus AA, OR = 0.90, 95% CI = 0.82–0.97) and studies with population-based controls (AG versus AA, OR = 0.93, 95% CI = 0.86–1.00;
GG/AG versus AA, OR = 0.93, 95% CI = 0.86–1.00). When stratifying by the menopausal status, no significant result was observed
in all genetic models. Taken together, the results suggest that the MTR A2756G polymorphism may contribute to susceptibility
to breast cancer among Europeans. 相似文献
5.
Lei Yao Fang Fang Qi Wu Zhen Yang Yang Zhong Long Yu 《Breast cancer research and treatment》2010,122(1):221-227
Breast cancer is one of the most common malignant tumors worldwide. To date, many articles have evaluated the association
between Cytochrome P450c17 (CYP17) T-34C polymorphism and breast cancer risk. However, the results remain inconclusive. In
order to derive a more precise estimation of the association, a meta-analysis was performed in this study. By searching Medline,
ISI Web of Knowledge, Cochrane, ScienceDirect, EBSCO, CNKI, and SinoMed databases, 43 studies including 26,008 cases and 32,806
controls were collected for CYP17 T-34C polymorphism. Crude ORs with 95% CIs were used to assess the strength of association
between CYP17 T-34C polymorphism and breast cancer risk. The pooled ORs were performed for codominant model, dominant model,
and recessive model, respectively. Overall, no significant associations between CYP17 T-34C polymorphism and breast cancer
susceptibility were found for TT versus CC (OR = 0.96; 95% CI: 0.89–1.05), TC versus CC (OR = 0.97; 95% CI: 0.89–1.06), TT + TC
versus CC (OR = 0.97; 95% CI: 0.89–1.05) and TT versus TC + CC (OR = 0.98; 95% CI: 0.93–1.03). In the stratified analysis
by ethnicity, menopausal status, and sources of controls, significant associations were still not detected in all genetic
models. In conclusion, this meta-analysis strongly suggests that CYP17 T-34C polymorphism is not associated with breast cancer
risk. 相似文献
6.
Haiming Sun Jing Bai Feng Chen Yan Jin Yang Yu Songbin Fu 《Breast cancer research and treatment》2011,125(1):175-179
Several studies have investigated the associations between AURKA T91A polymorphism and the susceptibility to breast cancer,
but the results have been inconclusive. To derive a more precise estimation of the relationship, a meta-analysis was performed.
A total of 11 case–control studies, including 14,361 cases and 17,780 controls, were selected. Crude odds ratios (ORs) with
95% confidence intervals (CIs) were used to assess the strength of association in the additive model, dominant model, and
recessive model. When all the studies were pooled into the meta-analysis, there was no evidence showing a significant association
between AURKA T91A polymorphism and breast cancer risk (for additive model, OR = 0.839, 95% CI = 0.678–1.038; for dominant
model: OR = 0.890, 95% CI = 0.757–1.074; and for recessive model: OR = 0.987, 95% CI = 0.963–1.012). In the subgroup analysis
by ethnicity, significantly decreased risks were found for Asians (additive model, OR = 0.857, 95% CI = 0.742–0.991). When
stratified by study design, no significant association was found between the polymorphism and breast cancer risk. In conclusion,
this meta-analysis indicates that the AURKA T91A polymorphism is not a risk factor for developing breast cancer. 相似文献
7.
Jian Zhang Li-Xin Qiu Zhong-Hua Wang Xiang-Hua Wu Xiao-Jian Liu Bi-Yun Wang Xi-Chun Hu 《Breast cancer research and treatment》2010,123(2):549-555
Published data on the association between MTHFR C677T polymorphism and breast cancer risk are inconclusive. To derive a more
precise estimation of the relationship, a meta-analysis was performed. Medline, PubMed, Embase, and Web of Science were searched.
Crude ORs with 95% CIs were used to assess the strength of association between the MTHFR C677T polymorphism and breast cancer
risk. The pooled ORs were performed with co-dominant model (CT vs. CC, TT vs. CC), dominant model (CT + TT vs. CC), and recessive
model (TT vs. CC + CT), respectively. A total of 37 studies including 15,260 cases and 20,411 controls were involved in this
meta-analysis. Overall, significantly elevated breast cancer risk was associated with TT variant genotype in homozygote comparison
and dominant genetic model when all studies were pooled into the meta-analysis (TT vs. CC: OR = 1.11, 95% CI = 1.01–1.23;
dominant model: OR = 1.04, 95% CI = 1.00–1.09). In the subgroup analysis by ethnicity, significantly increased risks were
found for TT allele carriers among Asians (TT vs. CC: OR = 1.18, 95% CI = 1.04–1.35; recessive model: OR = 1.15, 95% CI = 1.03–1.29).
When stratified by study design, statistically significantly elevated risk was found in hospital-based studies (TT vs. CC:
OR = 1.18, 95% CI = 1.02–1.38; recessive model: OR = 1.17, 95% CI = 1.05–1.29). In the subgroup analysis by menopausal status,
statistically significantly increased risk was found among postmenopausal women (CT vs. CC: OR = 1.12, 95% CI = 1.02–1.23;
dominant model: OR = 1.11, 95% CI = 1.01–1.22). In conclusion, this meta-analysis suggests that the MTHFR T allele is a low-penetrant
risk factor for developing breast cancer. 相似文献
8.
Yiyi Sun Zhihe Zang Xiaohong Xu Zhonglin Zhang Ling Zhong Wang Zan Yan Zhao Lin Sun 《Breast cancer research and treatment》2011,125(1):215-219
Epidemiological studies on the association between SULT1A1 codon 213 polymorphism and breast cancer risk are inconclusive.
In order to derive a more precise estimation of the association, a meta-analysis was conducted in this article. Sixteen studies
including 9,881 cases and 13,564 controls were collected for SULT1A1 codon 213 polymorphism by searching the databases of
Medline, PubMed, Embase, and ISI Web of Knowledge. The strength of association between SULT1A1 codon 213 polymorphism and
breast cancer susceptibility was assessed by calculating crude ORs with 95% CIs. When all the 21 studies were pooled into
the meta-analysis, there was no evidence for significant association between SULT1A1 codon 213 polymorphism and breast cancer
susceptibility (for Arg/Arg versus Arg/His: OR = 0.999, 95% CI = 0.941–1.061; for Arg/Arg versus His/His: OR = 1.121, 95%
CI = 1.013–1.242; for dominant model: OR = 1.128, 95% CI = 1.01–1.26; for recessive model: OR = 1.151, 95% CI = 0.950–1.394).
In the subgroup analysis by the source of controls, significant increased risk was found for hospital-based studies (for Arg/Arg
versus Arg/His: OR = 1.173, 95% CI = 1.000–1.376; for Arg/Arg versus His/His: OR = 1.600, 95% CI = 1.134–2.256; for dominant
model: OR = 1.269, 95% CI = 1.134–2.256; for recessive model: OR = 1.664, 95% CI = 1.070–2.588). In summary, the meta-analysis
suggests that SULT1A1 codon 213 polymorphism may be associated with the hospital-based studies. However, large number of samples
and representative hospital-based studies with homogeneous breast cancer patients and well-matched controls are warranted
to confirm this finding. 相似文献
9.
Fang Fang Lei Yao Xiao Jia Yu Lu Yu Qi Wu Long Yu 《Breast cancer research and treatment》2010,122(1):267-271
Tumor necrosis factor α (TNFα) is a pleiotropic cytokine which can regulate a wide variety of cellular responses. Low concentrations
of TNFα seem to increase tumor growth and progression. The −308 G/A polymorphism in TNFα has been implicated in breast cancer
risk but the published data remain inconclusive. In order to derive a more precise estimation of the relationship, a meta-analysis
was performed by searching PubMed, Web of Science, ScienceDirect, EBSCO, CNKI, and Chinese Biomedicine Database. 11 studies
including 10,184 cases and 12,911 controls were collected for TNFα −308 G/A polymorphism. Crude ORs with 95% CIs were used
to assess the strength of association between the TNFα −308 G/A polymorphism and breast cancer risk. The pooled ORs were performed
for codominant model (GG versus AA; GA versus AA), dominant model (GG + GA versus AA), recessive model (GG versus GA + AA),
and G allele versus A allele, respectively. Overall, significantly elevated breast cancer risk was found for recessive model
(OR = 1.10, 95% CI = 1.04–1.17) and for G allele versus A allele (OR = 1.08, 95% CI = 1.02–1.14). In the subgroup analysis
by ethnicity, significantly increased risks were also found among Caucasians for recessive model and for G allele versus A
allele (for recessive model: OR = 1.10, 95% CI = 1.04–1.17; for G allele versus A allele: OR = 1.09, 95% CI = 1.03–1.14).
However, no significant associations were found among Asians for all genetic models. In conclusion, this meta-analysis suggests
that the TNFα −308 G allele is a risk factor for developing breast cancer, especially for Caucasians. 相似文献
10.
BRCA2 N372H polymorphism and breast cancer susceptibility: a meta-analysis involving 44,903 subjects
Li-Xin Qiu Lei Yao Kai Xue Jian Zhang Chen Mao Bo Chen Ping Zhan Hui Yuan Xi-Chun Hu 《Breast cancer research and treatment》2010,123(2):487-490
Published data on the association between BRCA2 N372H polymorphism and breast cancer risk are inconclusive. To derive a more
precise estimation of the relationship, a meta-analysis was performed. Crude ORs with 95% CIs were used to assess the strength
of association between them. A total of 22 studies including 22,515 cases and 22,388 controls were involved in this meta-analysis.
Overall, no significant associations were found between BRCA2 N372H polymorphism and breast cancer risk when all studies pooled
into the meta-analysis (NH versus NN: OR = 1.01, 95% CI = 0.97–1.05; HH versus NN: OR = 1.05, 95% CI = 0.97–1.13; dominant
model: OR = 1.01, 95% CI = 0.98–1.05; and recessive model: OR = 1.05, 95% CI = 0.98–1.13). In the subgroup analysis by ethnicity,
still no significant associations were found for Caucasians, Asians, or Africans. When stratified by study design, statistically
significantly elevated risk was found for 372H allele based on population-based studies (HH versus NN: OR = 1.11, 95% CI = 1.01–1.21;
dominant model: OR = 1.05, 95% CI = 1.00–1.10; recessive model: OR = 1.09, 95% CI = 1.00–1.18). In conclusion, this meta-analysis
suggests that the BRCA2 372H allele may be a low-penetrant risk factor for developing breast cancer. However, large sample
and representative population-based studies with homogeneous breast cancer patients and well matched controls are warranted
to confirm this finding. 相似文献
11.
Breast cancer is one of the most common malignant tumors worldwide. Endothelial nitric oxide synthase (eNOS) plays a key role
in breast cancer development. The associations between the two eNOS polymorphisms (E298D rs1799983, −786T>C rs2070744) and
breast cancer risk are inconclusive. A meta-analysis was performed in this study. By searching Medline, ISI Web of Knowledge,
ScienceDirect, EBSCO, CNKI, and SinoMed database, six case–control studies were collected for the eNOS E298D polymorphism
(3,038 cases and 2,508 controls) and three case–control studies were eligible for the eNOS −786T>C polymorphism. Crude ORs
with 95% CIs were used to assess the strength of association between the two eNOS polymorphisms and breast cancer risk. The
pooled ORs were performed for codominant model, dominant model, and recessive model, respectively. Overall, significantly
decreased risk was observed for E298D (for EE vs. DD: OR = 0.74, 95% CI = 0.59–0.94; for ED vs. DD: OR = 0.78, 95% CI = 0.61–0.98;
for dominant model: OR = 0.77, 95% CI = 0.61–0.96) and −786T > C (for TT vs. CC: OR = 0.60, 95% CI = 0.42–0.86; for dominant
model: OR = 0.66, 95% CI = 0.47–0.94). In the subgroup analysis by ethnicity, significant decreased risks were found for E298D
(for EE vs. DD: OR = 0.75, 95% CI = 0.56–0.99) and −786T>C (for TT vs. CC: OR = 0.53, 95% CI = 0.35–0.81; for dominant model:
OR = 0.61, 95% CI = 0.41–0.91; for recessive model: OR = 0.70, 95% CI = 0.55–0.91) among Caucasians; significant decreased
risks were observed for E298D (for ED vs. DD: OR = 0.12, 95% CI = 0.02–0.96; for dominant model: OR = 0.13, 95% CI = 0.02–1.00)
among Asians. In conclusion, this meta-analysis suggests that both eNOS E298D and −786T>C polymorphisms are associated with
reduced breast cancer risk. 相似文献
12.
Lei Yao Fang Fang Qi Wu Yang Zhong Long Yu 《Breast cancer research and treatment》2010,122(1):237-242
Breast cancer is the most common cancer in women. To date, many publications have evaluated the association between Cytochrome
P450 1B1 (CYP1B1) Val432Leu polymorphism and breast cancer risk. However, the results remain inconclusive. In order to derive
a more precise estimation of the association, a meta-analysis was performed in this study. By searching Medline, Pubmed, and
ISI Web of Knowledge databases, 26 studies including 19,028 cases and 21,275 controls were collected for CYP1B1 Val432Leu
polymorphism. Crude ORs with 95% CIs were used to assess the strength of association between CYP1B1 Val432Leu polymorphism
and breast cancer risk. The pooled ORs were performed for codominant model, dominant model, and recessive model, respectively.
Overall, no significant associations between CYP1B1 Val432Leu polymorphism and breast cancer susceptibility were found for
Val/Val versus Leu/Leu (OR = 0.98; 95% CI: 0.90–1.06), Val/Leu versus Leu/Leu (OR = 1.01; 95% CI: 0.93–1.09), Val/Val + Val/Leu
versus Leu/Leu (OR = 1.00; 95% CI: 0.93–1.08) and Val/Val versus Val/Leu + Leu/Leu (OR = 0.96; 95% CI: 0.91–1.01). In the
stratified analysis by ethnicity, menopausal status and sources of controls, significant associations were still not observed
in all genetic models. In conclusion, this meta-analysis provides strong evidence that CYP1B1 Val432Leu polymorphism is not
associated with breast cancer risk. 相似文献
13.
Yanlei Ma Jianjun Yang Peng Zhang Zhihua Liu Zhe Yang Huanlong Qin 《Breast cancer research and treatment》2011,125(1):237-241
Epidemiological studies have investigated the association between HER2 codon 655 polymorphism and breast cancer susceptibility.
However, the results are still inconclusive. To obtain a more precise estimation of the relationship, this meta-analysis was
performed. A total of 22 studies including 9,209 cases and 10,132 controls were collected. The strength of association between
HER2 codon 655 polymorphism and breast cancer susceptibility was assessed by calculating crude ORs with 95% CIs. When all
the 22 studies were pooled into the meta-analysis, there was no evidence for significant association between HER2 codon 655
polymorphism and breast cancer susceptibility (for Val/Ile vs. Ile/Ile: OR = 1.069, 95% CI = 0.976–1.172; for Val/Val vs.
Ile/Ile: OR = 1.191, 95% CI = 0.922–1.538; for dominant model: OR = 1.093, 95% CI = 0.991–1.206; for recessive model: OR = 1.141,
95% CI = 0.902–1.444). In the subgroup analysis by the source of controls and ethnicity, no significant increased risk was
found in all genetic models. However, the current results indicated the modest association between the HER2 Ile655Val polymorphism
and Asian population (Val/Ile vs. Ile/Ile: OR = 1.207, CI = 1.006–1.450). In summary, the meta-analysis suggests that HER2
codon 655 polymorphism is not associated with the increased breast cancer risk. 相似文献
14.
Li-Xin Qiu Bo Chen Chen Mao Ping Zhan Hui Yuan Kai Xue Jin Li Xi-Chun Hu 《Breast cancer research and treatment》2009,118(3):599-603
Published data on the association between STK15 F31I polymorphism and breast cancer risk are inconclusive. In order to derive
a more precise estimation of the relationship, a meta-analysis was performed. Medline, PubMed, Embase, Web of Science, and
Chinese Biomedicine Database were searched. Crude ORs with 95% CIs were used to assess the strength of association between
the STK15 F31I polymorphism and breast cancer risk. The pooled ORs were performed for codominant model (FI vs. FF; II vs.
FF), dominant model (FI + II vs. FF), and recessive model (II vs. FI + FF), respectively. A total of 10 studies including
10,537 cases and 14,477 controls were involved in this meta-analysis. Overall, significantly elevated breast cancer risk was
associated with II variant genotype in homozygote comparison and recessive genetic model when all studies were pooled into
the meta-analysis (for II vs. FF: OR = 1.23, 95% CI = 1.10–1.37; for recessive model: OR = 1.21, 95% CI = 1.05–1.40). In the
subgroup analysis by ethnicity, significantly increased risks were found for II allele carriers among Caucasians (for II vs.
FF: OR = 1.24, 95% CI = 1.08–1.43; for recessive model: OR = 1.21, 95% CI = 1.00–1.45); significantly increased risks were
also found among Asians for II versus FF (OR = 1.21; 95% CI = 1.01–1.45). In conclusion, this meta-analysis suggests that
the STK15 31II allele is a low-penetrant risk factor for developing breast cancer. 相似文献
15.
Li-Xin Qiu Lei Yao Chen Mao Bo Chen Ping Zhan Hui Yuan Kai Xue Jian Zhang Xi-Chun Hu 《Breast cancer research and treatment》2010,123(2):543-547
Published data on the association between MnSOD Val16Ala polymorphism and breast cancer risk are inconclusive. To derive a
more precise estimation of the relationship, a meta-analysis was performed. Medline, PubMed, Embase, and Web of Science were
searched. Crude ORs with 95% CIs were used to assess the strength of association between the MnSOD Val16Ala polymorphism and
breast cancer risk. The pooled ORs were performed for co-dominant model (Val/Ala vs. Val/Val, Ala/Ala vs. Val/Val), dominant
model (Ala/Ala + Val/Ala vs. Val/Val), and recessive model (Ala/Ala vs. Val/Ala + Val/Val), respectively. A total of 32 studies
including 26,022 cases and 32,426 controls were involved in this meta-analysis. Overall, no significant associations were
found between MnSOD Val16Ala polymorphism and breast cancer risk when all studies pooled into the meta-analysis (Val/Ala vs.
Val/Val: OR = 1.022, 95% CI = 0.981–1.064; Ala/Ala vs. Val/Val: OR = 1.006, 95% CI = 0.934–1.083; dominant model: OR = 1.013,
95% CI = 0.962–1.066; and recessive model: OR = 0.985, 95% CI = 0.931–1.042). In the subgroup analysis by ethnicity or study
design, still no significant associations were found for all comparison models. In conclusion, this meta-analysis suggests
that the MnSOD Val16Ala polymorphism may be not associated with breast cancer development. However, large sample and representative
population-based studies with homogeneous breast cancer patients and well-matched controls are warranted to confirm this finding. 相似文献
16.
Li-Xin Qiu Lei Yao Chen Mao Bo Chen Ping Zhan Kai Xue Jian Zhang Hui Yuan Xi-Chun Hu 《Breast cancer research and treatment》2010,123(2):563-567
Published data on the association between TGFB1 L10P polymorphism and breast cancer risk are inconclusive. In order to derive
a more precise estimation of the relationship, a meta-analysis was performed. Crude ORs with 95% CIs were used to assess the
strength of association between them. A total of 30 studies including 20,401 cases and 27,416 controls were involved in this
meta-analysis. Overall, significantly elevated breast cancer risk was associated with TGFB1 10P allele when all studies were
pooled into the meta-analysis (LP vs. LL: OR = 1.046, 95% CI = 1.003–1.090; dominant model: OR = 1.052, 95% CI = 1.012–1.095).
In the subgroup analysis by ethnicity, statistically significantly elevated risk was found in Caucasians (dominant model:
OR = 1.045, 95% CI = 1.001–1.091). When stratified by study design, statistically significantly elevated risk was found based
on population-based studies (dominant model: OR = 1.076, 95% CI = 1.019–1.136). In conclusion, this meta-analysis suggests
that the TGFB1 10P allele may be a low-penetrant risk factor for developing breast cancer. However, large sample and representative
population-based studies with homogeneous breast cancer patients and well-matched controls are warranted to confirm this finding. 相似文献
17.
Studies investigating the association between cytochrome P450 1B1 (CYP1B1) Leu432Val (432 C/G, rs1056836) polymorphism and
colorectal cancer (CRC) risk report conflicting results. The aim of this study was to quantitatively summarize the evidence
for such a relationship. Two investigators independently searched the Medline, Embase, China National Knowledge Infrastructure,
and Chinese Biomedicine Databases. Summary odds ratios (ORs) and 95% confidence intervals (95% CIs) for CYP1B1 polymorphism
and CRC were calculated in a fixed-effects model and a random-effects model when appropriate. The pooled ORs were performed
for co-dominant model (GG vs. CC, GC vs. CC), dominant model (GG + GC vs. CC), and recessive model (GG vs. GC + CC). This
meta-analysis included ten case–control studies, which included 8,466 CRC cases and 9,301 controls. Overall, the variant genotypes
(GG and GC) of the 432 C/G were not associated with CRC risk when compared with the wild-type CC homozygote (GG vs. CC, OR = 1.01,
95% CI = 0.93–1.10; GC vs. CC, OR = 0.97, 95% CI = 0.90–1.04), without any between-study heterogeneity. Similarly, no associations
were found in the dominant and recessive models (dominant model, OR = 0.98, 95% CI = 0.92–1.05; recessive model, OR = 1.03,
95% CI = 0.96–1.11). Limiting the analysis to the studies within Hardy–Weinberg equilibrium, the results were persistent and
robust. When stratifying for country, matched control and source of controls, no evidence of significant association was observed
in any subgroup. No publication bias was found in the present study. No association is found between the CYP1B1 Leu432Val
polymorphism and risk of CRC among Caucasians. 相似文献
18.
Chen Mao Xi-Wen Wang Ben-Fu He Li-Xin Qiu Ru-Yan Liao Rong-Cheng Luo Qing Chen 《Breast cancer research and treatment》2010,122(1):259-265
Epidemiological studies have evaluated the association between CYP17 MspA1 polymorphism and breast cancer risk. However, the results remain conflicting rather than conclusive. To derive a more
precise estimation of the relationship, we performed this meta-analysis. Systematic searches of the PubMed and Medline databases
were performed. A total of 35 studies including 22,090 cases and 28,498 controls were identified. Genotype distributions of
CYP17 in the controls of all studies were in agreement with Hardy–Weinberg equilibrium (HWE) except for three studies. When all
35 studies were pooled into the meta-analysis, there was no evidence for significant association between CYP17 MspA1 polymorphism and breast cancer risk (for A1/A2 vs. A1/A1: OR = 1.00, 95% CI = 0.96–1.04; for A2/A2 vs. A1/A1: OR = 1.03,
95% CI = 0.97–1.08; for dominant model: OR = 1.01, 95% CI = 0.97–1.05; for recessive model: OR = 1.03, 95% CI = 0.98–1.08).
In the subgroup analyses by ethnicity, menopausal status and source of controls, no significant associations were found in
all genetic models. When sensitivity analyses were performed by excluding HWE-violating studies, all the results were not
materially altered. In summary, the meta-analysis strongly suggests that CYP17 MspA1 polymorphism is not associated with increased breast cancer risk. 相似文献
19.
Xiaowei Qi Xiangyu Ma Xinhua Yang Linjun Fan Yi Zhang Fan Zhang Li Chen Yan Zhou Jun Jiang 《Breast cancer research and treatment》2010,120(2):499-506
The association between methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and breast cancer risk has been widely
reported, but results were inconsistent and underpowered. To clarify the effects of MTHFR polymorphisms on the risk of breast
cancer, an updated meta-analysis of all available studies relating C677T and/or A1298C polymorphisms of MTHFR gene to the
risk of breast cancer was conducted. Eligible articles were identified by search of databases including MEDLINE, PubMed, Web
of Science, EMBASE and Chinese Biomedical Literature database (CBM) for the period up to January 2010. Finally, a total of
41 studies with 16,480 cases and 22,388 controls were included, all for C677T polymorphism and 20 with 12,170 cases and 15,865
controls for A1298C polymorphism. The pooled ORs were performed for the allele contrasts, additive genetic model, dominant
genetic model, and recessive genetic model, respectively. Subgroup analyses were also performed by ethnicity and menopausal
status. With respect to C677T polymorphism, significantly elevated breast cancer risk was found in overall analysis (T vs.
C: OR = 1.041, 95% CI = 1.009–1.073; TT vs. CC: OR = 1.132, 95% CI = 1.019–1.259; TT vs. CC + CT: OR = 1.119, 95% CI = 1.014–1.236);
in the subgroup analysis by ethnicity, significantly increased risk was found in East Asian population (T vs. C: OR = 1.121,
95% CI = 1.016–1.237; TT vs. CC: OR = 1.331, 95% CI = 1.073–1.650; TT vs. CC + CT: OR = 1.265, 95% CI = 1.058–1.513) but not
in Caucasian population; in the subgroup analysis by menopausal status, no statistically significant association was found.
With respect to A1298C polymorphism, no significant association with breast cancer risk was demonstrated in overall, ethnicity-
and menopausal status-based population. It can be concluded that potentially functional MTHFR C677T polymorphism may play
a low penetrance role in the development of breast cancer. 相似文献
20.
Xiangyu Ma Xiaowei Qi Chunhai Chen Hui Lin Hongyan Xiong Yafei Li Jun Jiang 《Breast cancer research and treatment》2010,122(2):495-501
The association of CYP19 gene polymorphisms with breast cancer has been widely reported, but results of previous studies were
somewhat contradictory and underpowered. In order to overcome the limitations of individual study and to understand the real
situation, we conducted a systematic review and meta-analysis including three CYP19 gene polymorphisms [R264C polymorphism,
CYP19_630 3-bp del/Ins polymorphism, and CYP19_681 (TTTA)n polymorphisms]. A total of 22 studies with 10,592 cases and 11,720 controls were identified, and the results showed that
R264C polymorphism was not associated with breast cancer risk in overall (T vs. C: OR = 1.061, 95% CI = 0.929–1.212) or race-based
populations (T vs. C for Asian: OR = 1.169, 95% CI = 1.002–1.363; for Caucasian: OR = 0.787, 95% CI = 0.597–1.037); meanwhile,
for Asian individuals, 3-bpDel/Ins polymorphism showed a significantly association with breast cancer susceptibility (for
allele Del vs. allele Ins: OR = 1.278, 95% CI = 1.066–1.532) while the carriers of allele (TTTA)12 can significantly decrease breast cancer risk (OR = 0.752, 95% CI = 0.603–0.939). Furthermore, the carriers of allele (TTTA)10 were significantly associated with breast cancer susceptibility (OR = 1.515, 95% CI = 1.115–2.058). It can be concluded that
potentially functional CYP19_630 3-bp del/Ins polymorphism and CYP19_681 (TTTA)n polymorphisms may play a low penetrance role in breast cancer susceptibility in an ethnicity-specific manner. 相似文献