Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Common variants in genes that mediate immunity and risk of multiple myeloma.

Authors: Brown, EE  Lan, Q  Zheng, T  Zhang, Y  Wang, SS  Hoar-Zahm, S  Chanock, SJ  Rothman, N  Baris, D 
Citation: Brown EE, etal., Int J Cancer. 2007 Jun 15;120(12):2715-22.
Pubmed: (View Article at PubMed) PMID:17315188
DOI: Full-text: DOI:10.1002/ijc.22618

Multiple myeloma (MM) is a B-cell malignancy characterized by aberrant immune function. Using genomic DNA extracted from 127 MM cases aged 21-84 years and 545 population-based controls, we examined the risk of MM associated with 82 common variants in 45 genes that mediate immunity among women of European American descent. Genotyping was determined using validated and optimized TaqMan assays. We estimated haplotype frequencies from unphased genotype data for 20 of these genes using the expectation-maximization progressive insertion algorithm. Compared with controls, MM risk was positively associated with homozygotes of single loci, IL4R (-28120T, rs2107356) and FCGR2A (-120G, rs1801274) (OR = 1.91, 95% CI 1.08-3.38 and 1.95, 95% CI 1.06-3.60, respectively). For genes in which linkage disequilibrium was observed between multiple loci, MM risk was positively associated with the haplotype block covering part of the LTA*TNF complex (LTA -82C/-90G *TNF -1036C/-487G/-417G, OR = 1.63, 95% CI 1.02-2.16) compared with the most frequently occurring haplotype observed among controls (LTA -82A/-90A *TNF -1036C/-487G/-417G). Our findings provide preliminary evidence that common genetic variants in specific immune-mediated pathways could influence the risk of MM.

Annotation

Disease Annotations
Objects Annotated

Additional Information

 
CRRD Object Information
CRRD ID: 11040938
Created: 2016-03-17
Species: All species
Last Modified: 2016-03-17
Status: ACTIVE



NHLBI Logo

RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.