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1.
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
2.
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
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.
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
5.
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
6.
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
7.
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
8.
Jian Zhang Li-Xin Qiu Shiang-Jiin Leaw Xi-Chun Hu Jian-Hua Chang 《Medical oncology (Northwood, London, England)》2011,28(3):655-660
To derive a more precise estimation of the relationship between the xeroderma pigmentosum group D (XPD) Asp312Asn polymorphism
and lung cancer risk, a meta-analysis was performed. PubMed, Medline, Embase, and Web of Science were searched. Crude ORs
with 95% CIs were used to assess the strength of association between the XPD Asp312Asn polymorphism and lung cancer risk.
The pooled ORs were performed with co-dominant model (Asp/Asn vs. Asp/Asp, Asn/Asn vs. Asp/Asp), dominant model (Asp/Asn + Asn/Asn
vs. Asp/Asp), and recessive model (Asn/Asn vs. Asp/Asp + Asp/Asn), respectively. A total of 18 studies including 7,552 cases
and 9,397 controls were involved in this meta-analysis. Overall, significantly elevated lung cancer risk was associated with
XPD Asn allele when all studies were pooled into the meta-analysis (Asn/Asn vs. Asp/Asp: OR = 1.158, 95% CI = 1.018–1.317;
recessive model: OR = 1.161, 95% CI = 1.029–1.311). In the subgroup analysis by ethnicity, significantly increased risks were
found for both Caucasians (Asn/Asn vs. Asp/Asp: OR = 1.164, 95% CI = 1.003–1.351; recessive model: OR = 1.169, 95% CI = 1.016–1.345)
and Asians (Asn/Asn vs. Asp/Asp: OR = 8.056, 95% CI = 2.420–26.817; recessive model: OR = 7.956, 95% CI = 2.391–26.477). When
stratified by study design, statistically significantly elevated risk was noted in hospital-based studies (Asn/Asn vs. Asp/Asp:
OR = 1.315, 95% CI = 1.110–1.558; recessive model: OR = 1.290, 95% CI = 1.099–1.513). In conclusion, this meta-analysis suggests
that the XPD Asn allele is a low-penetrant risk factor for developing lung cancer. 相似文献
9.
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
10.
Haiming Sun Jing Bai Feng Chen Yan Jin Yang Yu Lianhong Jin Songbin Fu 《Breast cancer research and treatment》2011,125(1):157-161
Several studies have investigated the associations between RAD51 G135C polymorphism and the susceptibility to breast cancer,
but results have been inconclusive. In order to derive a more precise estimation of the relationship, a meta-analysis was
performed. A total of 17 case control studies, including 12,153 cases and 10,245 controls, were selected. Overall, significant
decreased risk was found for the additive model (OR = 0.995, 95% CI = 0.991–0.998) and dominant model (OR = 0.994, 95% CI = 0.991–0.998).
In the subgroup analysis by ethnicity, statistically significantly decreased risk was found in Asians (additive model: OR = 0.977,
95% CI = 0.954–1.000 and dominant model: OR = 0.981, 95% CI = 0.963–1.000). In conclusion, this meta-analysis suggests that
the RAD51 G135C polymorphism is a low-penetrant risk factor for developing breast cancer. 相似文献
11.
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
12.
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
13.
Weiguang Yuan Lidan Xu Yuanxi Feng Yue Yang Wangyang Chen Jingwei Wang Da Pang Dianjun Li 《Breast cancer research and treatment》2010,122(3):835-842
It was reported that the functional polymorphism Ser326Cys in the human 8-oxoguanine DNA glycosylase gene was associated with
breast cancer risk; however, the published studies have inconsistent conclusions. To elucidate the effect of hOGG1 Ser326Cys
on the susceptibility to breast cancer, all available studies were collected in this meta-analysis. We extracted the data
from 10 case–control studies that were published in the PubMed database from 2003 to 2008 using the search phrases “human
8-oxoguanine DNA glycosylase, hOGG1, OGG1, OGG, polymorphism, genetic variation, and breast cancer.” This meta-analysis included
4,963 breast cancer cases and 4,776 control subjects. The results showed that individuals who carrying the hOGG1 326Cys allele
in the additive model did not have significantly increased risk of breast cancer compared with those carrying the 326Ser allele
(P = 0.47, OR = 1.02; 95% CI = 0.96–1.09); similarly, no significant association between the hOGG1 326Cys allele and breast
cancer risk was found either in the recessive genetic model (P = 0.34, OR = 1.06; 95% CI = 0.94–1.18) for Cys/Cys versus Ser/Cys + Ser/Ser, or dominant genetic model (P = 0.78, OR = 1.01; 95% CI = 0.93–1.11) for Cys/Cys + Ser/Cys versus Ser/Ser. In the stratified analysis, the meta-analysis
showed the association between hOGG1 326Cys allele in the additive model and breast cancer was significant in European subjects
(P = 0.04, OR = 0.71; 95% CI = 0.51–0.98), and dominant genetic model (P = 0.004, OR = 0.44; 95% CI = 0.25–0.77). However, the association was not significant between this polymorphism and different
menopausal status (premenopausal and postmenopausal) and the other ethnicities (Asians and Americans). The meta-analysis suggested
that the hOGG1 326Cys allele plays a significant protective effect to breast cancer in European women. 相似文献
14.
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
15.
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
16.
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
17.
Fang Fang Xiao-Jia Yu Lu Yu Lei Yao 《Medical oncology (Northwood, London, England)》2011,28(4):981-985
The murine double minute 2 (MDM2) gene encodes an important regulator which mainly functions as an E3 ligase. The role of the MDM2 protein in the P53 pathway
has been especially well-studied. In this study, our aim was to explore the relationship between MDM2 gene 309 T/G polymorphism and colorectal cancer risk. Performing both the overall meta-analysis and the subgroup meta-analysis
based on ethnicity and source of controls with a total of 7 eligible studies (2,543 cases and 2,115 controls in all), we detected
a significant colorectal cancer risk variation for TG versus GG (OR = 0.73, 95% CI = 0.62–0.86) in the overall analysis and
another significant colorectal cancer risk variation for TG versus GG (OR = 0.70, 95% CI = 0.59–0.83) in the population-based
controls’ subgroup as well. Moreover, in the subgroup analysis based on ethnicity, significant associations were observed
for all genetic models in Asians (OR = 0.51, 95% CI = 0.41–0.64 for TT versus GG; OR = 0.64, 95% CI = 0.53–0.78 for TG versus
GG; OR = 0.59, 95% CI = 0.49–0.71 for dominant model; OR = 0.69, 95% CI = 0.57–0.82 for recessive model), while in Caucasians
there was no obvious association. In summary, according to the results of our meta-analysis, the MDM2 309 G allele probably acts as a colorectal cancer risk factor, especially in Asians. 相似文献
18.
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
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.
Ke-Da Yu Ao-Xiang Chen Chen Yang Lei Fan A-Ji Huang Zhi-Ming Shao 《Breast cancer research and treatment》2012,131(1):27-31
The association between single-nucleotide polymorphisms (SNPs) in the interleukin-10 (IL-10) gene promoter and breast cancer
risk is still ambiguous. We here performed a meta-analysis based on the evidence currently available from the literature to
make a more precise estimation of the relationship between two genetic variants in the IL-10 gene promoter, −1082A > G (rs1800896)
and −592C > A (rs1800872), and breast cancer. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the
corresponding strengths of association under the codominant, dominant, and recessive models. A total of ten studies (4,181
cases and 4,384 controls) were eligible for meta-analysis. There were six studies with 3,032 cases and 3,190 controls for
rs1800872, and eight studies with 1,636 cases and 1,670 controls for rs1800896. Meta-analysis showed that neither of the two
polymorphisms had any association with increased breast cancer risk (for rs1800896: OR = 1.060, 95% CI = 0.785–1.432 in the
dominant model, and OR = 1.152, 95% CI = 0.958–1.386 in the recessive model; and for rs1800872: OR = 0.952, 95% CI = 0.859–1.056
in the dominant model, and OR = 0.892, 95% CI = 0.741–1.072 in the recessive model). The results did not change when the analyses
were restricted in Caucasians, or in the studies fulfilling Hardy–Weinberg equilibrium, or according to source of controls.
In outlier analysis, no individual study affected the overall OR dominantly, since omission of any single study made no material
huge difference. In conclusion, the present meta-analysis suggests a lack of association between the two SNPs (rs1800896 and
rs1800872) in the IL-10 gene promoter and breast cancer risk. Further studies, either with larger sample size or regarding
other SNPs/haplotypes within the IL-10 gene, are needed to clarify the role of IL-10 in breast carcinogenesis. 相似文献