SynthesisHematological oncology2017
Candidate gene association studies and risk of Hodgkin lymphoma: a systematic review and meta-analysis.
Synthesis in Hematological oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Population based analysis of twenty year incidence trends of pediatric Hodgkin lymphoma in the United States.Scientific reports · 2025Article
- Integration of transcriptome-wide association study and gene-based association analysis identifies candidate genes for Hodgkin lymphoma.Journal of cancer research and clinical oncology · 2025Article
- The impact of autoimmune cytopenias on the clinical course and survival of Hodgkin lymphoma.International journal of hematology · 2021Article
- Article
- Article
- Computational Prediction of Probable Single Nucleotide Polymorphism-Cancer Relationships.Cancer informatics · 2020Article
- Overall survival of classical Hodgkins lymphoma in Saudi patients is affected by XPG repair gene polymorphism.Biomedical reports · 2019Article
- A Polymorphism Located Near PMAIP1/Noxa Gene Influences Susceptibility to Hodgkin Lymphoma Development in South IndiaAsian Pacific journal of cancer prevention : APJCP · 2017Article
- Evidence of Inbreeding in Hodgkin Lymphoma.PloS one · 2016Article
- Review
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3 authors.
Funding
Abstract
To evaluate the contribution of association studies of candidate polymorphisms to inherited predisposition to Hodgkin lymphoma (HL), we conducted a systematic review and meta-analysis of published case-control studies. Of the variants examined more than once in candidate gene association studies, we identified 21 studies that reported on 12 polymorphic variants in 10 genes. Data were also extracted from a published genome wide association study to allow analysis of an additional 47 variants in a further 30 genes. Promising associations were seen in nine of the variants (p < 0.05). Given that the estimated false positive report probabilities (FPRPs) for all associations are high (i.e. FPRP > 0.2), these findings should be interpreted with caution. While studies of candidate polymorphisms may be an attractive means of identifying risk factors for HL, future studies should employ sample sizes adequately powered to identify variants having only modest effects on HL risk. Furthermore, because of aetiological heterogeneity within HL, stratification of genotyping according to age, tumour Epstein-Barr virus status and histology is essential. Copyright © 2015 John Wiley & Sons, Ltd.
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