MDM2 SNP309 polymorphism contributes to endometrial cancer susceptibility: evidence from a meta-analysis

Peng, Qiliu; Mo, Cuiju; Qin, Aiping; Lao, Xianjun; Chen, Zhiping; Sui, Jingzhe; Wu, Junrong; Zhai, Limin; Yang, Shan; Qin, Xue; Li, Shan

doi:10.1186/1756-9966-32-85

Cited by 18 publications

(19 citation statements)

References 36 publications

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“…35 In addition, there are several studies showing the effects of MDM2 alteration on endometrial cancer. 36,37 Goumenou et al reported higher MDM2 expression in tissue samples of endometriomas. 38 Also, the relation between MDM2 expression and leiomyosarcomas have been reported.…”

Section: Discussionmentioning

confidence: 99%

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Age‐dependent association of MDM2 promoter polymorphisms and uterine leiomyoma in South‐East Iran: A preliminary report

Salimi

Hajizadeh

Khodamian

et al. 2014

J of Obstet and Gynaecol

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Section: Discussionmentioning

confidence: 99%

“…They reported that MDM2 overexpression may play a role in development of the subset of leiomyomas and leiomyosarcomas which have different patterns of molecular alterations with separate biologic entities . In addition, there are several studies showing the effects of MDM2 alteration on endometrial cancer . Goumenou et al .…”

Section: Discussionmentioning

confidence: 99%

Age‐dependent association of MDM2 promoter polymorphisms and uterine leiomyoma in South‐East Iran: A preliminary report

Salimi

Hajizadeh

Khodamian

et al. 2014

J of Obstet and Gynaecol

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“…PCOS is one Reproductive outcomes and individual repair capacity of the most common endocrine abnormalities in women of reproductive age and may be a serious risk factor for infertility, as it may interfere with ovulation patterns or altogether preclude ovulation. The variant (G) allele of the MDM2 SNP309 polymorphism (rs2279744) is known to be associated with higher levels of MDM2, resulting, in turn, in lower levels of p53 and, respectively, decreased p53-dependent suppression of cell proliferation [75], which may explain its association with increased risk for endometrial cancer [76]. The association with increased risk for PCOS was identified for the wildtype (T) MDM2 allele [74].…”

Section: Role Of Individual Repair Capacity In the Constitution Of Thmentioning

confidence: 99%

Reproductive outcomes in pregnant women aged 35 or older: the role of individual repair capacity

Petkova¹,

Dimitrova²,

Zhelev³

et al. 2015

Biodiscovery

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Abbreviations: 8-OH-dG -8-hydroxydeoxyguanosine, AMA -advanced maternal age, AR -assisted reproduction, BER -base excision repair, CDC -US Centre for disease prevention and control, DIC -disseminated intravascular coagulation, DS -Down syndrome, HELLP -haemolysis/elevated liver enzymes/low platelets, ICSI -intracytoplasmic sperm injection, IRC -individual repair capacity, IUGR -intrauterine growth restriction, IUI -intrauterine insemination, IVF -in vitro fertilisation, LIF -leukaemia inhibitory factor, NER -nucleotide excision repair, PCOS -polycystic ovary syndrome, PIH -pregnancy-induced hypertension, ROS -reactive oxygen species, TTD -trichothiodystrophy, w.g. -weeks of gestation, WHO -World Health Organisation, XP -xeroderma pigmentosum. AbstractAt present, childbirth is being progressively postponed until later age. Women aged 35 or older may have to wait longer to conceive than younger women and are more likely to be referred to fertility evaluations, but in a significant proportion a spontaneous conception would be achieved in the timeframe typical of younger women. Pregnancies where mothers are ≥ 35 are associated with more risks for pregnancy loss, chromosomal disease, pregnancy-associated complications, prematurity and low birthweight. These concerns, however, are not uncommon in younger women as well. This puts forward the question whether advanced age per se is the underlying cause for the increased risk for adverse outcomes in older pregnant women, or whether there might be other factors that account for it but do not radically worsen the prospects for favourable outcomes. The individual risks associated with childbirth late in life may stem from maternal genetic background rather than being a simple function of age. There is plenty of preliminary evidence that individual capacity for identification and repair of DNA damage may constitute a major factor in female fertility and fecundity. Subtle deficiencies in the repair capacity may have little to no importance in younger pregnant women but may make a significant difference in older women. The outcomes of pregnancies in women >35 are largely dependent on the prepregnancy health status and the quality of antenatal care, and may not be dramatically different from outcomes in younger women.

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“…If this data set had been included in the meta-analysis, it would weigh approximately 50 % and, therefore, would have had a major impact on the output, both in the overall assessments and even more so in the subgroup of Caucasians. Notably, our data set, in addition to being published in our original article [2], was also included in a previous meta-analysis assessing the impact of SNP309 on endometrial cancer risk [3].…”

Section: Dear Editormentioning

confidence: 99%

MDM2 SNP309 and risk of endometrial cancer

Knappskog

Lønning

2014

Tumor Biol.

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Dear Editor,We read with interest the paper "Common variant on MDM2 contributes to endometrial cancer susceptibility: evidence based on 7 studies" by Zhao et al. in Tumor Biology [1].In this paper, the authors assess the impact of the MDM2 promoter SNP309 (rs2279744) on risk of endometrial cancer by performing a meta-analysis of seven original articles (eight independent case-control designed studies). Based on their findings, the authors conclude that the SNP309G-allele is associated with an increased risk of endometrial cancer, both in an allele contrast model and in a recessive model. Further, the authors find this to be true both among Caucasians and Asians. Most original articles assessing the impact SNP309 on risk of endometrial cancer have so far been small, and it is therefore highly appropriate to perform meta-analyses in order to elucidate the potential role of this MDM2 variant. While the data presented by Zhao et al. are interesting, we would like to make some additional comments.In their meta-analysis, Zhao et al. included seven original articles, with a total number of 1,278 cases and 2,189 controls, omitting our study from 2012, which is the largest study on SNP309 in endometrial cancer to date [2]. In our study, we included 910 Caucasians diagnosed with endometrial cancer and 2,465 controls. If this data set had been included in the meta-analysis, it would weigh approximately 50 % and, therefore, would have had a major impact on the output, both in the overall assessments and even more so in the subgroup of Caucasians. Notably, our data set, in addition to being published in our original article [2], was also included in a previous meta-analysis assessing the impact of SNP309 on endometrial cancer risk [3].We would also like to point out that any study of MDM2 SNP309 in Caucasians has a potential confounding factor that needs to be taken into account/discussed. This relates to a second MDM2 promoter SNP, SNP285G>C (rs117039649). SNP285 is in complete linkage disequilibrium with SNP309. The variant C-allele of SNP285 is present on about 12 % of the SNP309G-alleles in North Western Caucasian populations but absent in East Asian and African populations [4][5][6]. Importantly, SNP285C has an antagonistic effect against SNP309G: in vitro studies have shown the SNP309G-allele to elongate a binding site for the transcription factor Sp1 and thereby increase MDM2 transcription [4,7], while the SNP285C-allele reduces Sp1 binding and transcription [4,8]. In line with the in vitro findings, case-control studies have shown SNP285C to significantly reduce the risk of ovarian, breast, and endometrial cancer [2,4]. Notably, censoring individuals harboring SNP285C from the analyses has been shown to increase the odds ratios related to SNP309G, for endometrial as well as for ovarian cancer [2,4]. Thus, any study assessing the impact of SNP309 on cancer risk among Caucasians may probably benefit from correcting for SNP285-status in the cohorts.Taken together, the data presented by Zhao et al. are interesting and g...

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MDM2 SNP309 polymorphism contributes to endometrial cancer susceptibility: evidence from a meta-analysis

Cited by 18 publications

References 36 publications

Age‐dependent association of MDM2 promoter polymorphisms and uterine leiomyoma in South‐East Iran: A preliminary report

Age‐dependent association of MDM2 promoter polymorphisms and uterine leiomyoma in South‐East Iran: A preliminary report

Reproductive outcomes in pregnant women aged 35 or older: the role of individual repair capacity

MDM2 SNP309 and risk of endometrial cancer

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