SynthesisMedicine2025
Association between variants of gelatinases and lung carcinoma risk: A systematic review, meta-analysis, trial sequential analysis with prevalence and transcriptional predictions.
Synthesis in Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
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Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMatrix metalloproteinases (MMPs) are a group of genes that play a crucial role in cancer progression. In this study, we conducted a systematic review and meta-analysis to evaluate the association between gelatinase polymorphisms (specifically MMP2 and MMP9) and lung cancer (LC) susceptibility.
methodsA comprehensive search was conducted across 4 databases - PubMed, Scopus, Cochrane Library, and Web of Science - for relevant studies published up to June 20, 2024. RevMan 5.3 software was used to calculate effect sizes, including odds ratios and 95% confidence intervals, for the prevalence of MMP2 and MMP9 polymorphisms in LC patients and controls. Additionally, comprehensive meta-analysis version 3.0 was used to assess publication bias, perform meta-regression, and conduct sensitivity analyses. Trial sequential analysis (TSA) was performed using TSA software.
resultsThe meta-analysis included 22 articles comprising 28 studies. For the MMP2 - 1306 C/T polymorphism, the P-values were as follows: allelic model, .005; homozygous model, .03; heterozygous model, .002; dominant model, .003; and recessive model, .11. For the MMP2 - 735 C/T polymorphism, the P-values were: allelic model, .24; homozygous model, .003; heterozygous model, .53; dominant model, .97; and recessive model, .38. For the MMP9 - 1562 C/T polymorphism, the P-values were: allelic model, .97; homozygous model, .90; heterozygous model, .53; dominant model, .27; and recessive model, .80. For the MMP9 R279Q polymorphism, the P-values were: allelic model, .32; homozygous model, .07; heterozygous model, .39; dominant model, .33; and recessive model, .12.
conclusionsWhile our meta-analysis highlights a potential association between MMP2 polymorphisms and LC risk, the TSA indicates that further studies are needed to reach a definitive conclusion.
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