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GWAS Study

Genetic variation near CXCL12 is associated with susceptibility to HIV-related non-Hodgkin lymphoma.

Thorball CW, Oudot-Mellakh T, Ehsan N et al.

32675224 PubMed ID
GWAS Study Type
2202 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

TC
Thorball CW
OT
Oudot-Mellakh T
EN
Ehsan N
HC
Hammer C
SF
Santoni FA
NJ
Niay J
CD
Costagliola D
GC
Goujard C
ML
Meyer L
WS
Wang SS
HS
Hussain SK
TI
Theodorou I
CM
Cavassini M
RA
Rauch A
BM
Battegay M
HM
Hoffmann M
SP
Schmid P
BE
Bernasconi E
GH
Günthard HF
MP
Mohammadi P
MP
McLaren PJ
RC
Rabkin CS
BC
Besson C
FJ
Fellay J
Chapter II

Abstract

Summary of the research findings

Human immunodeficiency virus (HIV) infection is associated with an increased risk of non-Hodgkin lymphoma (NHL). Even in the era of suppressive antiretroviral treatment, HIV-infected individuals remain at higher risk of developing NHL compared to the general population. To identify potential genetic risk loci, we performed case-control genome-wide association studies and a meta-analysis across three cohorts of HIV+ patients of European ancestry, including a total of 278 cases and 1924 matched controls. We observed a significant association with NHL susceptibility in the C-X-C motif chemokine ligand 12 (CXCL12) region on chromosome 10. A fine mapping analysis identified rs7919208 as the most likely causal variant (P = 4.77e-11), with the G>A polymorphism creating a new transcription factor binding site for BATF and JUND. These results suggest a modulatory role of CXCL12 regulation in the increased susceptibility to NHL observed in the HIV-infected population.

278 European ancestry cases, 1,924 European ancestry controls

Chapter III

Study Statistics

Key metrics and study information

2202
Total Participants
GWAS
Study Type
No
Replicated
European
Ancestry
U.S., France, Switzerland
Recruitment Country
Chapter IV

AI-Generated Summary

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