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1.
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
2.
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
3.
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
4.
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
5.
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
6.
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
7.
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
8.
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
9.
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
10.
Luciane R. Cavalli Rebecca B. Riggins Antai Wang Robert Clarke Bassem R. Haddad 《Breast cancer research and treatment》2010,121(1):227-231
To date, many publications discussed the correlation between ERCC2 Asp312Asn polymorphism and breast cancer risk. However,
the results were not unanimous. In order to derive a more precise conclusion, a meta-analysis was performed in this study
by searching Medline, PubMed, and ISI Web of Knowledge databases. Finally, 17 studies including 12,019 cases and 10,747 controls
were collected for this meta-analysis. The strength of association between ERCC2 Asp312Asn polymorphism and breast cancer
risk was assessed by calculating crude ORs with 95% CIs. Overall, no significant associations between ERCC2 Asp312Asn polymorphism
and breast cancer susceptibility were found. In the stratified analysis by ethnicity, significant associations were observed
for Asn/Asn versus Asp/Asp (OR = 0.55; 95% CI 0.32–0.96) and Asn/Asn versus Asn/Asp + Asp/Asp (OR = 0.53; 95% CI 0.32–0.90)
in Asians. In the stratified analysis by study design, significant associations were found for Asn/Asn versus Asp/Asp (OR = 0.79;
95% CI 0.64–0.98) and Asn/Asn versus Asn/Asp + Asp/Asp (OR = 0.82; 95% CI 0.68–0.99) in population-based studies. In conclusion,
this meta-analysis provides an evidence that ERCC2 312Asn allele may have a protective effect for breast cancer development
in Asians. 相似文献
11.
Li-Xin Qiu Lei Yao Chen Mao Ke-Da Yu Ping Zhan Bo Chen Hui Yuan Jian Zhang Kai Xue Xi-Chun Hu 《Breast cancer research and treatment》2010,122(2):521-525
Published data on the association between cytochrome P-450 1A2 (CYP1A2)-164 A/C 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 CYP1A2-164 A/C polymorphism
and breast cancer risk. The pooled ORs were performed for co-dominant model (AC versus AA, CC versus AA), dominant model (CC + AC
versus AA), and recessive model (CC versus AA + AC), respectively. A total of 9 studies including 7,580 cases and 10,020 controls
were involved in this meta-analysis. Overall, no significantly elevated breast cancer risk was found in all genetic models
when all studies were pooled into the meta-analysis (AC versus AA: OR = 1.02, 95% CI = 0.92–1.13; CC versus AA: OR = 1.17,
95% CI = 0.83–1.64; dominant model: OR = 1.07, 95% CI = 0.93–1.23; and recessive model: OR = 1.13, 95% CI = 0.82–1.55). In
the subgroup analysis by ethnicity or source of controls, there was still no significant association detected in all genetic
models. In conclusion, upto date, there is still no enough evidence to indicate the association of CYP1A2-164 A/C polymorphism
and breast cancer development. 相似文献
12.
Yanlei Ma Jianjun Yang Zhihua Liu Peng Zhang Zhe Yang Yu Wang Huanlong Qin 《Breast cancer research and treatment》2011,125(1):201-205
Conflicting data have been published as to the possible association between polymorphism in codon 72 of the TP53 tumor suppressor gene and the risk of developing breast cancer. In order to address this question, we carried out a meta-analysis
of 21 studies of and this polymorphism and breast cancer risk, which collectively included 12,601 cases and 11,462 controls.
Studies were identified by searching the Medline, PubMed, Embase, and ISI Web of Knowledge databases. The strength of association
between the TP53 codon 72 polymorphism and breast cancer risk was assessed by calculating crude OR values with 95% CIs, with pooled OR values
calculated separately for three genetic inheritance models. We found no significant association between TP53 codon 72 polymorphism and breast cancer risk for either the codominant inheritance model (Pro/Arg vs. Pro/Pro: OR = 1.063,
95% CI = 0.967–1.169; Arg/Arg vs. Pro/Pro: OR = 1.245, 95% CI = 0.997–1.554), the dominant model (OR = 1.146, 95% CI = 0.979–1.340),
or the recessive model (OR = 1.179, 95% CI = 1.020–1.362). Stratified analysis by ethnicity and source of controls similarly
revealed no significant association for any of the genetic models. In summary, this meta-analysis provides strong evidence
that the TP53 codon 72 polymorphism is not associated with the risk of developing breast cancer. 相似文献
13.
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
14.
HER2 Ile655Val polymorphism contributes to breast cancer risk: evidence from 27 case–control studies
Proto-oncogene HER2 (also known as erbB-2 or neu) plays an important role in the carcinogenesis and the prognosis of breast
cancer. Many epidemiological studies have been conducted to explore the association between the HER2 Ile655Val polymorphism
and breast cancer risk. However, inconsistency existed in the results. Therefore, we performed a meta-analysis of 27 published
case–control studies including 11,504 cases and 12,538 controls. We assessed the strength of the association by crude odds
ratios (ORs) with 95% confidence intervals (CIs) and reached a result that HER2 Ile655Val polymorphism was associated with
an increased breast cancer risk in overall populations (for Ile/Val vs. Ile/Ile: OR = 1.05, 95% CI = 1.00–1.12, P = 0.07 for heterogeneity; for the dominant model Ile/Val + Val/Val vs. Ile/Ile: OR = 1.10, 95% CI = 1.01–1.20, P = 0.01 for heterogeneity). In subgroup analysis by ethnicity, we found a significant association among Africans (for Val/Val
vs. Ile/Ile: OR = 8.78, 95% CI = 1.94–39.72, P = 0.35 for heterogeneity; for the recessive model Val/Val vs. Ile/Val +Ile/Ile: OR = 8.60, 95% CI = 1.92–38.48, P = 0.31 for heterogeneity) and Asians (for Ile/Val vs. Ile/Ile: OR = 1.18, 95% CI = 1.01–1.39, P = 0.41 for heterogeneity; for the dominant model Val/Val + Ile/Val vs. Ile/Ile: OR = 1.18, 95% CI = 1.01–1.38, P = 0.27 for heterogeneity). In conclusion, our meta-analysis suggests that HER2 Ile 655Val polymorphism may contribute to
breast cancer risk. 相似文献
15.
Xiangyu Ma Chunhai Chen Hongyan Xiong Jin Fan Yafei Li Hui Lin Rufu Xu Guorong Huang Bin Xu 《Breast cancer research and treatment》2010,122(2):509-514
Breast cancer is the most common cancer in women worldwide, but its etiology is still unclear. It is believed that oxidative
stress plays an essential role in the development of breast cancer, while SOD2 is one of the primary enzymes that directly
convert potential harmful oxidizing species to harmless metabolites. The association of SOD2 Val16Ala polymorphism and breast
cancer risk has been widely reported, but results of previous studies were somewhat contradictory and underpowered. To overcome
the limitations of individual study and to understand the real situation, we conducted a systematic review and meta-analysis
toward the association between SOD2 Val16Ala polymorphism and breast cancer. Through retrieving MEDLINE, PubMed, Embase, and
Web of Science, a total of 17 studies with 9,710 cases and 11,041 controls were identified. The results showed that no significant
associations were found for the allele contrast (allele Ala vs. allele Val: OR = 1.020, 95% CI = 0.979–1.062), additive genetic
model (Ala/Ala vs. Val/Val: OR = 1.091, 95% CI = 0.969–1.229), dominant genetic model (Ala/Ala +Ala/Val vs. Val/Val: OR = 1.045,
95% CI = 0.961–1.136), and recessive genetic model (Ala/Ala vs. Val/Val +Ala/Val: OR = 1.027, 95% CI = 0.956–1.102). In the
stratified analysis by ethnicity and menopausal status, significant associations were also not detected in all genetic models.
Conclusively, this meta-analysis strongly suggests that SOD2 Val16Ala polymorphism is not associated with breast cancer susceptibility. 相似文献
16.
Chunbo Tang Zhanwei Wang Jinhua Yu Yunong Wu Zhijun Zhu Ning Chen 《Medical oncology (Northwood, London, England)》2011,28(4):1319-1324
CCND1 plays a critical role in cell cycle control and may contribute to head and neck cancer. We performed a meta-analysis
of eleven case–control studies that examined the association between CCND1 G870A polymorphism and head and neck cancer risk.
Overall, no significant association of this polymorphism with head and neck cancer was found (for AA vs. GG: OR = 0.96, 95%
CI = 0.59–1.58, P < 0.01 for heterogeneity; for GA vs. GG: OR = 1.00, 95% CI = 0.74–1.35, P < 0.01 for heterogeneity; for the dominant model GA/AA vs. GG: OR = 0.98, 95% CI = 0.69–1.39, P < 0.01 for heterogeneity; for the recessive model AA vs. GG/GA: OR = 0.94, 95% CI = 0.66–1.33, P < 0.01 for heterogeneity). In subgroup analysis by ethnicity, we also did not find any significant association in European
and Asians populations. All the results were not materially altered in any genetic model after the studies which did not fulfill
Hardy–Weinberg equilibrium were excluded. In conclusion, our meta-analysis strongly suggested that the CCND1 G870A polymorphism
is not associated with head and neck cancer risk. 相似文献
17.
Ju Won Seok Yoo Shin Choi SeMin Chong Gui Young Kwon Yun Jae Chung Beom Gyu Kim Sung Jun Park 《Breast cancer research and treatment》2010,122(2):453-457
In view of the essential role of Transforming Growth Factorβ1 (TGFB1) on both inhibiting the development of early benign breast
tumors as well as promoting tumor invasion, the association of TGFB1 L10P polymorphism and breast cancer risk has been widely
reported, but results of previous studies were somewhat contradictory and underpowered. To overcome the limitations of individual
study and to understand the real situation, we conducted a systematic review and meta-analysis towards the association between
TGFB1 L10P polymorphism and breast cancer. Through retrieving MEDLINE, PubMed, Embase, and Web of Science, a total of 16 studies
with 10,392 cases and 11,697 controls were identified. The results showed that significant association was found in the recessive
genetic model for Caucasian (OR = 1.152, 95% CI = 1.020–1.301). However, we did not find any associations in additive genetic
model (PP vs. LL for total: OR = 1.026, 95% CI = 0.940–1.121), allele contrast (L vs. P for total: OR = 1.004, 95% CI = 0.966–1.044),
and dominant genetic model (PP + LP vs. LL for total: OR = 1.001, 95% CI = 0.946–1.061). Conclusively, this meta-analysis
strongly suggests that TGFB1 L10P polymorphism may play a low penetrance role in breast cancer susceptibility in Caucasian.
Large well-designed epidemiological studies will be necessary to validate the risk identified in the current meta-analysis. 相似文献
18.
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
19.
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
20.
Zheng W Cong XF Cai WH Yang S Mao C Zou HW 《Breast cancer research and treatment》2011,128(3):811-815
Published data on the association between three polymorphisms (Lys939Gln, Ala499Val, and PAT±) of Xeroderma Pigmentosum group
C (XPC) 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 11 studies
including 5,090 cases and 5,214 controls were involved in this meta-analysis. For XPC Lys939Gln polymorphism, no obvious associations
were found for all genetic models when all studies were pooled into the meta-analysis (Lys/Gln vs. Lys/Lys: OR = 1.00, 95%
CI 0.92–1.10; Gln/Gln vs. Lys/Lys: OR = 0.96, 95% CI 0.84–1.09; dominant model: OR = 0.99, 95% CI 0.91–1.08; and recessive
model: OR = 0.97, 95% CI 0.86–1.09). In the subgroup analysis by ethnicity or study design, still no obvious associations
were found. For XPC Ala499Val polymorphism, also no obvious associations were found for all genetic models when all studies
were pooled into the meta-analysis (Val/Ala vs. Ala/Ala: OR = 0.91, 95% CI 0.79–1.05; Val/Val vs. Ala/Ala: OR = 1.07, 95%
CI 0.80–1.44; dominant model: OR = 0.93, 95% CI 0.81–1.06; and recessive model: OR = 1.11, 95% CI 0.84–1.48). For XPC PAT±
polymorphism, obvious associations were found for recessive model when all studies were pooled into the meta-analysis (OR = 1.41,
95% CI 1.05–1.89). In conclusion, this meta-analysis suggests that the XPC PAT± polymorphism allele may be a low-penetrant
risk factor for developing breast cancer. 相似文献