SynthesisOncotarget2017
Role of CD152 genetic polymorphisms in the susceptibility to breast cancer.
Synthesis in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Correlation betweenJournal of dentistry (Shiraz, Iran) · 2025Article
- Immune Checkpoint Molecules-Inherited Variations as Markers for Cancer Risk.Frontiers in immunology · 2020Review
- Association between CTLA-4 + 49A > G and - 318C > T single-nucleotide polymorphisms and susceptibility to thyroid neoplasm.Endocrine · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe polymorphisms in cluster of differentiation 152 (CD152) gene have been reported to be associated with breast cancer (BC), but relevant findings were far from conclusive. Therefore, we carried out this meta-analysis to combine those results for a clearer perspective on this issue.
resultsIn our meta-analysis, a total of 8 eligible publications of 19 case-control studies were selected, which totally contained 7,442 BC cases and 7,376 normal controls. Among the five polymorphisms of CD152 gene, +49 G/A, -1661 A/G and -318 C/T significantly increased the risk of BC under corresponding genetic comparisons; while CT60 G/A polymorphism was negatively related to the cancer susceptibility. In addition, -1772 T/C polymorphism of CD152 gene was not associated with the development of BC. MATERIALS AND
methodsOnline databases and other sources were searched for published studies on the relationship between BC susceptibility and CD152 polymorphisms (+49 G/A, -1661 A/G, -1722 T/C, -318 C/T and CT60 G/A). The strength of association was evaluated with pooled odds ratios (ORs) and their corresponding 95% confidence intervals (95% CIs). Heterogeneity evaluation was conducted via Q test. Sensitivity analysis was used to detect the stability of our results. Begg's funnel plot and Egger's test were applied to investigate publication bias among selected studies.
conclusionsThe polymorphisms +49 G/A, -1661 A/G and -318 C/T may elevate the susceptibility to BC, but the polymorphism CT60 G/A may offer protection against the cancer.
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Registered trials
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