Background

MTHFR 677C>T polymorphism is a genetic alteration in an enzyme involved in folate metabolism, but its effect on host susceptibility to cervical cancer is still uncertain. The aim of this study was to investigate the association between MTHFR 677C>T polymorphism and cervical cancer by performing a meta-analysis.

Methods

Pubmed, Embase, Web of Science, and the Chinese Biomedical Database (CBM) databases were searched for case–control studies investigating the association between MTHFR 677C>T polymorphism and cervical cancer. Odds ratios (OR) and 95% confidence intervals (95%CI) were used to assess this possible association.

Results

11 studies with a total of 1898 cervical cancer cases and 2678 controls were included. Meta-analyses of a total 11 studies showed no association between MTHFR 677C>T polymorphism and cervical cancer using all five genetic models (All P values > 0.05). However, subgroup analyses showed the odds of the homozygous TT genotype were much less in cervical cancer cases than in controls in Europeans, which implied an association between the homozygous TT genotype and cervical cancer in Europeans (For TT versus CC, fixed-effects OR = 0.65, 95%CI 0.45-0.93, P = 0.020, I2 = 0.0%). The odds for the homozygous TT genotype were greater in cervical cancer cases than in controls in East Asians, which also implied an association between the homozygous TT genotype and cervical cancer in East Asians (For TT versus CC, random-effects OR = 1.66, 95%CI 1.05-2.62, P = 0.029, I2 = 52.6%; For TT versus CT/CC, random-effects OR = 1.55, 95%CI 1.09-2.22, P = 0.016, I2 = 42.4%). Both subgroup analyses and meta-regression analyses suggested ethnicity was the major source of heterogeneity. Publication bias was not evident.

Conclusions

This meta-analysis supports an association between MTHFR 677C>T polymorphism and cervical cancer, and the effect of this association may be race specific. Further studies with large sample sizes and careful design are needed to identify this association more comprehensively.

Background

With an increasing incidence of congenital heart defects (CHDs) in recent years, genotype-phenotype correlation and array-based methods have contributed to the genome-wide analysis and understanding of genetic variations in the CHD population. Here, we report a copy number deletion of chromosomal 14q23.1 in a female fetus with complex congenital heart defects. This is the first description of DAAM1 gene deletion associated with congenital heart anomalies.

Case Presentation

Compared with the control population, one CHD fetus showed a unique copy number deletion of 14q23.1, a region that harbored DAAM1 and KIAA0666 genes.

Conclusions

Results suggest that the copy number deletion on chromosome 14q23.1 may be critical for cardiogenesis. However, the exact relationship and mechanism of how DAAM1 and KIAA0666 deletion contributes to the onset of CHD is yet to be determined.

CD105 is a well-known tumor metastasis marker and useful for early monitoring of metastasis and cancer relapse. It is important to generate rapid, reliable and precise analytical information regarding CD105 levels. To establish a simple, selective and sensitive detection method, we prepared an immunosensor with novel bioconjugates based on Pt nanoparticles, thionin acetate and antibodies. The proposed immunosensor displayed a broader linear response to CD105, with a working range of 1.3 to 200.0 ng/mL and a detection limit of 0.9 ng/mL under optimal conditions. Moreover, the studied immunosensor exhibited high sensitivity, fast analysis and adequate stability. The proposed methodology could readily be extended to other clinical- or environment-related biospecies.