Alternative MDM2 splicing is highly associated with lung cancer.

2 promoter polymorphisms of MDM2 and evaluated their associations with risk of lung cancer

Genetic polymorphisms in cell cycle regulatory genes MDM2 and TP53 contribute to the risk of developing lung cancer.

Results indicate that the MDM2 G/G genotype of SNP309 is associated with lung cancer risk with an odds ratio of 1.62 (95% CI: 1.06-2.50).

When the p73 and MDM2 polymorphisms were combined, the risk of lung cancer increased in a dose-dependent manner as the number of variant alleles increased

findings suggest that the G/G genotype of the MDM2 polymorphism is associated with worse overall survival among early-stage non-small-cell lung cancer patients, particularly those with squamous cell histology

In lung cancer patients, p53 accumulation could be due to a decrease in full-length MDM2 isoform together with an increase of the 57-kDa MDM2 isoform that was unable to stimulate p53 degradation.

a strong gene-smoking interaction was observed between the MDM2 SNP309 and nonsmall cell lung cancer risk

In stage III non-small cell lung cancer, there was a significant association between TTF-1 and Mdm2

Our results indicate that the MDM2 SNP309 is not significantly associated with lung carcinogenesis but point towards gender-specific differences.

This meta-analysis suggests that the MDM2 309G allele is a low-penetrant risk factor for developing lung cancer in Asians.

meta-analysis supports the view that MDM2(mouse double minute 2 ) SNP309 gene is a low-penetrance susceptible gene in the development of lung cancer, and the relationship of MDM2 SNP309 and lung cancer is stronger for never smokers.

Lower MDM2 promoter containing the SNP309 GG genotype was associated with p53-null lung cancer.

MDM2 SNP309 TT rather than the GG genotype is associated with increased risk of lung cancer in a population of non-smoking Chinese women in Singapore

Single nucleotide polymorphisms in MDM2 gene is associated with non-small cell lung cancer.

Neither MDM2 SNP309 nor SNP285 was associated with lung cancer risk or survival.

MDM2 T309G polymorphism might be a risk factor for lung cancer among never-smokers

MDM2 SNP309 polymorphism is associated with an increased lung adenocarcinoma risk.

We reveal a new mechanism that FOXO3a transcriptionally represses DNMT3B expression and this regulation can be attenuated by MDM2 overexpression in human lung cancer model.

focuses on lung cancer stem cells, p53 mutations noted in these cells, and importance of MDM2 interactions

Findings argue against a major effect of SNP309 status on the risk for cancer of the breast, prostate, lung or colon. In contrast, a possible tissue speci fi c protective effect of SNP285C was found on cancer risk.

Mir-660 inhibits lung tumorigenesis by targeting MDM2-p53 interaction.

Selective inhibition of HDAC2 in lung tumor cell causes survivin downregulation through activation of p53, which is mediated by downregulation of Mdm2.

MDM2 polymorphism may be one of the important factors for the increased expression mdm2, which was associated with down-regulation of p53 and ultimately may contribute in the poor clinical outcome of the non-small cell lung cancer patients

highly reliable association of combined susceptible genotypes of polymorphic markers Arg72Pro and T309G of TP53 and MDM2 genes with non small cell lung cancer and both its subtypes.

MDM2 (RS769412) G>A Polymorphism in cigarette smokers is associated with lung cancer Risk.

Overexpression of microRNA125a3p effectively inhibits the cell growth and invasion of lung cancer cells by regulating the mouse double minute 2 homolog/p53 signaling pathway

MDM2 T309G polymorphism is associated with risk and prognosis of lung cancer. TT or T genotype may be associated with the reduced risk of lung cancer, especially in Asians (Meta-Analysis)

The MDM2 T/T genotype was predictive of poorer survival in a Japanese population of lung adenocarcinoma patients.

Results suggest that inhibition the expression of c-mdm2 proto-oncogene protein (MDM2) might be a potential target in non-small cell lung cancer (NSCLC) treatment.

Overexpression of MDM2 independently predicted a reduced risk of death in non-small cell lung carcinoma patients.

MDM2 promoter SNP55 (rs2870820) affects risk of colon cancer but not breast-, lung-, or prostate cancer.

WDR79 colocalized and interacted with USP7 in the nucleus of non-small cell lung cancer cells. This event, in turn, reduced the ubiquitination of Mdm2 and p53, thereby increasing the stability and extending the half-life of the two proteins.

Data indicate that murine double minute 2 protein (MDMX) expression may serve as an independent unfavorable prognostic factor for non-small cell lung cancer (NSCLC). patient outcome, which in turn may at least partly be due to the ability of the MDMX protein to regulate the proliferative capacity and chemosensitivity of NSCLC cells.

Results demonstrate that Mdm2 is extremely important in breast cancer metastases to the lung. Specifically, Mdm2 is important to promote cancer invasiveness via cell migration, angiogenesis, and intravasation.

Overexpression of miR-641 decreased the expression of MDM2 and increased the expression of p53 in lung cancer cells.

MDM2 rs937283 A > G variant is associated with lung and gastric cancer.

The meta-analysis provides convincing evidence that the MDM2 T309 G polymorphism may contribute to non-small cell lung cancer susceptibility, especially for Asians and women

The present data indicated that MDM2 SNP 285 G>C (rs117039649) reduces the chance of lung cancer development in Bangladeshi population. However, MDM2 SNP 354 A>G (rs769412) has no such association in the same population.

Stromal-MDM2 Promotes lung cancer Cell Invasion through tumor-Host Feedback Signaling.

Association of Murine Double Minute 2 Genotypes and lung cancer Risk.

Explored expression of MMP-9 and MDM2 in the oncogenesis of lung cancer in rats.

G protein-coupled receptor family C group 5 member A (GPRC5A) deficiency contributes to dysregulated proto-oncogene protein c-mdm2 (MDM2) via activated epidermal growth factor receptor (EGFR) signaling, which promotes lung tumor development.