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http://purl.uniprot.org/citations/20087644http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20087644http://www.w3.org/2000/01/rdf-schema#comment"

Background

Tumor necrosis factor (TNF) and interleukin 10 (IL10) are promising candidate susceptibility genes for non-Hodgkin lymphoma (NHL). Chromosomal translocation breakpoint genes are of interest, given their documented involvement in lymphoma progression.

Methods

We analyzed 11 polymorphisms in BCL2, CCND1, MYC, TNF, and IL10 in a large, population-based, Danish-Swedish case-control study including 2,449 NHL cases and 1,980 controls. Relative risk of NHL was computed as odds ratios (OR).

Results

There was no clear evidence of associations between variants in BCL2, CCND1, and MYC and risk of NHL overall or subtypes. TNF rs1800629 was associated with risk of NHL (OR 1.53, 95% confidence interval, CI, 1.06-2.19 for minor allele homozygosity), T-cell lymphoma (OR 2.54, CI 1.27-5.09) and mantle cell lymphoma (OR 2.84, CI 1.38-5.87). IL10 rs1800890 was associated with risk of diffuse large B-cell lymphoma (OR 1.41, CI 1.08-1.85 for minor allele homozygosity) and mantle cell lymphoma (OR 1.77, CI 1.04-3.00). We did not replicate a previously reported interaction with autoimmunity.

Conclusions

We found no support for a role of the studied variants in BCL2, CCND1, or MYC in risk of NHL or subtypes, but we provide further evidence of putative susceptibility loci in TNF and IL10 for specific NHL subtypes."xsd:string
http://purl.uniprot.org/citations/20087644http://purl.org/dc/terms/identifier"doi:10.1007/s10552-010-9504-y"xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/author"Hjalgrim H."xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/author"Chang E.T."xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/author"Melbye M."xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/author"Humphreys K."xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/author"Duvefelt K."xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/author"Porwit A."xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/author"Sorensen K.M."xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/author"Ekstrom Smedby K."xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/author"Eloranta S."xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/author"Fernberg P."xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/name"Cancer Causes Control"xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/pages"759-769"xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/title"Genetic variation in chromosomal translocation breakpoint and immune function genes and risk of non-Hodgkin lymphoma."xsd:string
http://purl.uniprot.org/citations/20087644http://purl.uniprot.org/core/volume"21"xsd:string
http://purl.uniprot.org/citations/20087644http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/20087644
http://purl.uniprot.org/citations/20087644http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/20087644
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