AI Article Synopsis

  • - The XRCC3 gene, particularly the rs861539 (Thr241Met) polymorphism, has been frequently studied for its potential link to lung cancer risk, but results across various populations remain inconsistent.
  • - A systematic review and meta-analysis of 21 studies involving nearly 14,000 participants were conducted, finding no significant association between the XRCC3 Thr241Met variant and lung cancer risk across different genetic models and ethnic groups.
  • - The findings suggest no strong evidence supporting the connection between this specific gene variant and lung cancer risk; future research should explore gene-gene interactions for a better understanding of lung cancer susceptibility.

Article Abstract

Background: The X-ray repair cross-complementing group 3 (XRCC3) is a highly suspected candidate gene for cancer susceptibility, and a large amount studies have examined the association of the rs861539 in XRCC3 (Thr241Met) with lung cancer risk in various populations. However, the results remain inconclusive.

Methods: The electronic database of PubMed, Medline, Embase and CNKI (China National Knowledge Infrastructure) were searched for case-control studies published up to December 05, 2013. A systematic review and meta-analysis was performed to evaluate the relationship between XRCC3 Thr241Met polymorphism and lung cancer risk. Data were extracted and pooled odds ratio (OR) with its 95% confidence intervals (CI) were calculated.

Results: Total 21 studies, including 6880 lung cancer cases and 8329 controls, were available for meta-analysis. Overall, our results showed that the XRCC3 Thr241Met polymorphism was not associated with risk of lung cancer in all genetic contrast models (P>0.05). Stratified analyses by ethnicity (Asians, Caucasians and mixed population) showed similar results. Additionally, no evidence of publication bias was observed by using the funnel plot.

Conclusions: There is no clear evidence showing a significant correlation between XRCC3 Thr241Met polymorphism and lung cancer risk in total population and stratified analysis by ethnicity. However, studies assessing the gene-gene interactions should be considered to further estimate this gene variant in lung cancer risk.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bulcan.2015.02.003DOI Listing

Publication Analysis

Top Keywords

lung cancer
28
xrcc3 thr241met
20
cancer risk
20
thr241met polymorphism
12
cancer
8
polymorphism lung
8
lung
7
xrcc3
6
risk
6
thr241met
5

Similar Publications

Lung cancer is correlated with a high death rate, with approximately 1.8 million mortality cases reported worldwide in 2022. Despite development in the control of lung cancer, most cases are detected at higher stages with short survival rates.

View Article and Find Full Text PDF

MicroRNA abundance as a particular biomarker for precisely identifying cancer metastases has emerged in recent years. The expression levels of miRNA are analyzed to get insights into cancer tissue detection and subtypes. Similar to other cancer types, the miRNA shows high levels of target mRNA dysregulation in association with non-small cell lung carcinoma (NSCLC).

View Article and Find Full Text PDF

Novel Ru(II) Complexes as Type-I/-II Photosensitizers for Multimodal Hypoxia-Tolerant Chemo-Photodynamic/Immune Therapy.

Mol Pharm

January 2025

School of Pharmacy, Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong 226001, Jiangsu Province, China.

Photodynamic therapy (PDT) is increasingly regarded as an attractive approach for cancer treatment due to its advantages of low invasiveness, minimal side effects, and high efficiency. Here, two novel Ru(II) complexes , were designed and synthesized by coordinating phenanthroline and biquinoline ligands with Ru(II) center, and their chemo-photodynamic therapy and immunotherapy were explored. Both and exhibited significant phototoxicity against A549 and 4T1 tumor cells type-I/-II PDT.

View Article and Find Full Text PDF

Microenvironmental β-TrCP negates amino acid transport to trigger CD8 T cell exhaustion in human non-small cell lung cancer.

Cell Rep

January 2025

The Fourth Affiliated Hospital of Soochow University, Institutes of Biology and Medical Sciences, Suzhou Medical College of Soochow University, Soochow University, Suzhou, China; Jiangsu Key Laboratory of Infection and Immunity, Soochow University, Suzhou, China. Electronic address:

CD8 T cell exhaustion (Tex) has been widely acknowledged in human cancer, while the underlying mechanisms remain unclear. Here, we demonstrate that reduced amino acid (aa) metabolism and mTOR inactivation are accountable for Tex in human non-small cell lung cancer (NSCLC). NSCLC cells impede the T cell-intrinsic transcription of SLC7A5 and SLC38A1, disrupting aa transport and consequently leading to mTOR inactivation.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!