Background <p>The <i>CCAT2</i> gene is associated with carcinogenesis, but its effect on neuroblastoma, the most common extracranial tumor in children, remains unclear.</p> Methods <p>We conducted a case–control study involving 402 children with neuroblastoma and 473 children without neuroblastoma. TaqMan genotyping of two <i>CCAT2</i> polymorphisms (rs3843549 A &gt; G and rs6983267 T &gt; G) was conducted for all participants. Correlations were analyzed by calculating the odds ratio (OR) and 95% confidence interval (CI). Furthermore, we performed stratified analyses for both polymorphisms to evaluate their associations more comprehensively.</p> Results <p>We performed a statistical analysis employing three distinct genetic models to evaluate the rs3843549 A &gt; G polymorphism and the rs6983267 T &gt; G polymorphism. Moreover, we further investigated the potential protective polymorphisms (rs3843549 AG/GG and rs6983267 TG/GG) by stratified analysis. There was no significant association between <i>CCAT2</i> gene polymorphisms and neuroblastoma susceptibility.</p> Conclusion <p><i>CCAT2</i> gene polymorphisms (rs3843549 A &gt; G and rs6983267 T &gt; G) were not associated with susceptibility to neuroblastoma. However, the accuracy of this conclusion may be limited by various confounding factors. Future analyses would benefit from a more comprehensive approach that accounts for additional variables.</p>

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Associations of CCAT2 gene polymorphisms with neuroblastoma susceptibility in children from Jiangsu province

  • Shengyu Chen,
  • Zhuo Wang,
  • Chunlei Zhou,
  • Wenli Zhang,
  • Jiaming Chang,
  • Xinxin Zhang,
  • Jing He,
  • Peng Yi

摘要

Background

The CCAT2 gene is associated with carcinogenesis, but its effect on neuroblastoma, the most common extracranial tumor in children, remains unclear.

Methods

We conducted a case–control study involving 402 children with neuroblastoma and 473 children without neuroblastoma. TaqMan genotyping of two CCAT2 polymorphisms (rs3843549 A > G and rs6983267 T > G) was conducted for all participants. Correlations were analyzed by calculating the odds ratio (OR) and 95% confidence interval (CI). Furthermore, we performed stratified analyses for both polymorphisms to evaluate their associations more comprehensively.

Results

We performed a statistical analysis employing three distinct genetic models to evaluate the rs3843549 A > G polymorphism and the rs6983267 T > G polymorphism. Moreover, we further investigated the potential protective polymorphisms (rs3843549 AG/GG and rs6983267 TG/GG) by stratified analysis. There was no significant association between CCAT2 gene polymorphisms and neuroblastoma susceptibility.

Conclusion

CCAT2 gene polymorphisms (rs3843549 A > G and rs6983267 T > G) were not associated with susceptibility to neuroblastoma. However, the accuracy of this conclusion may be limited by various confounding factors. Future analyses would benefit from a more comprehensive approach that accounts for additional variables.