A blood cancer whose strongest inherited risk sits in the immune system's own HLA region — and whose most characteristic acquired feature, a translocation at BCL2, shares a gene with one of this page's five inherited variants.
Solid lines are connections this site curates. Dashed lines mean the two ends share a research paper — worth knowing, and not a claim that one explains the other.
Follicular lymphoma is the second most common type of non-Hodgkin lymphoma, a slow-growing cancer of B lymphocytes. This page holds 5 inherited (germline) variants from two studies, distinct from the acquired chromosomal changes that actually drive the cancer once it develops.
A 2010 study ran a three-stage genome-wide association study specifically targeting non-Hodgkin lymphoma subtypes, and found two follicular-lymphoma-associated variants at 6p21.32 — in the major histocompatibility complex (MHC/HLA) region — so tightly linked to each other (r² = 1.0) that they are effectively the same signal. This page's rs10484561, in HLA-DQB1, is that finding. It directly supports the idea that variation in the same immune machinery that presents antigens to T cells also shapes who develops this particular blood cancer.
A 2014 study by the same lead author, four times larger — 4,523 cases and 13,344 controls — deliberately searched outside the HLA region the 2010 study had already implicated, and found five new non-HLA risk loci. Two are on this page: rs4937362, near ETS1, and rs17749561, near BCL2. The BCL2 connection is worth stating plainly: the t(14;18) chromosomal translocation involving BCL2 is the single most characteristic acquired molecular feature of follicular lymphoma, found in the large majority of cases. This inherited common variant sits near that same gene — a different kind of change (inherited, weak, population-level) near the gene that an acquired, disease-defining chromosomal rearrangement directly disrupts.
The same 2014 study also went back into the HLA region itself and found it was not fully explained by the single 2010 signal: four linked HLA-DRβ1 amino acid positions, plus independent signals in HLA class I and class II, all carried their own separate associations with follicular lymphoma risk. This page's rs12195582 (HLA) and rs13254990 (near PVT1) are also from this study.
2025-11-18 · U.S. FDA, official approval summary (EPCORE FL-1 trial, NCT05409066, n=488)
FDA grants full approval to epcoritamab for relapsed follicular lymphoma
Verified directly against the FDA's own approval summary. On 18 Nov 2025 the FDA approved epcoritamab-bysp (Epkinly) with lenalidomide and rituximab for relapsed or refractory follicular lymphoma, and separately upgraded its 2024 accelerated approval as monotherapy (after 2+ prior therapies) to traditional approval. In the EPCORE FL-1 trial (488 patients), the combination cut the hazard of progression or death to 0.21 (95% CI 0.13-0.33) versus lenalidomide+rituximab alone -- median progression-free survival not reached versus 11.2 months, overall response 89% versus 74%. This is a treatment-regimen approval, not a new genetic finding -- unrelated to the inherited variants this page describes, which are population-level susceptibility factors, not treatment-selection markers.
Follicular lymphoma is diagnosed by lymph node biopsy and staging imaging, and its treatment is guided by the tumor's own acquired genetic changes (chiefly the BCL2 translocation) — not by the inherited variants on this page. None of the 5 germline variants here are used by any guideline to diagnose follicular lymphoma or select treatment.
The loci described above come from population-level genetic studies comparing thousands of people with follicular lymphoma to controls. They point at which biological systems (HLA-mediated immune surveillance, and pathways near ETS1 and BCL2) shape inherited susceptibility — they do not predict whether any one person will develop the disease, and they are a different question from the acquired BCL2 translocation an oncologist actually tests a tumor for.
What a 23andMe/AncestryDNA export or raw VCF can and can't tell you about Follicular Lymphoma comes down to these specific, well-studied positions — not a diagnosis.
The studies behind these variants recruited participants from different ancestries — a result found in one population doesn't always transfer to another. Based on 5 of 5 linked studies with a resolved discovery ancestry.
Databases, guidelines and references
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Follicular Lymphoma. MyGeneLog™. https://www.mygenelog.com/conditions/follicular-lymphoma
The second most common type of non-Hodgkin lymphoma, a slow-growing cancer of B lymphocytes.
Variation in the HLA region -- the same immune machinery that presents antigens to T cells. Multiple independent HLA signals are now known, first established by a 2010 study and expanded by a larger 2014 one.
Because both are real and distinct. The t(14;18) BCL2 translocation, acquired in the tumor, is the disease's single most characteristic molecular feature. Separately, this page holds an inherited common variant near the same BCL2 gene, carrying its own much weaker, population-level risk association -- a different kind of change near the same gene.
No. Follicular lymphoma is diagnosed by lymph node biopsy, and treatment is guided by the tumor's own acquired genetic changes. These are population-level findings from thousands of people, not a way to predict an individual case.
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