One of the most curable cancers — and with a strong genetic component. Know your susceptibility profile.
helixXY analyzes variants in the HLA class II region, NPAT, REL, IL13, GATA3 and TNFAIP3, providing a personalized map of your immune predisposition to classical Hodgkin Lymphoma.
Hodgkin Lymphoma is a neoplasm of germinal center B cells, characterized by the presence of Reed-Sternberg cells — giant binucleated cells that evade the immune system by manipulating inflammatory signals to their benefit.
Unlike many cancers, Hodgkin Lymphoma has a strong familial aggregation — siblings have a 3–9× higher risk, identical twins up to 99× higher. This heritability primarily reflects variants in adaptive immune system genes (HLA, NF-κB, Th2 cytokines).
helixXY maps relevant germline variants at all major susceptibility loci, with interpretation based on international GWAS meta-analyses and data from over 40,000 patients.
The HLA class II region is the primary genetic determinant. Specific variants influence how the immune system presents viral antigens (especially EBV) — modulating risk over decades.
At localized stages (I–II), the cure rate exceeds 90%. Knowing your genetic risk allows heightened attention to early symptoms such as persistent lymphadenopathy.
Use your file from 23andMe, Genera, AncestryDNA, etc. Within 15 minutes of uploading, your complete report is ready — no new sample required.
helixXY analyzes variants at all moderate and high-significance loci identified by GWAS for classical Hodgkin Lymphoma.
The HLA class II region is the strongest locus associated with Hodgkin Lymphoma. Variants in HLA-DPB1 alter viral antigen presentation (especially Epstein-Barr) and modulate the adaptive immune response, making it the primary genetic determinant of susceptibility.
RNA processing gene located near ATM. The rs2155209 variant in NPAT increases the risk of EBV-positive Hodgkin Lymphoma in young adults. Plays a role in regulating histone expression during the cell cycle.
Component of the NF-κB pathway, amplified in Reed-Sternberg cells (the hallmark of Hodgkin Lymphoma). REL polymorphisms increase chronic inflammatory signaling and the survival of malignant cells.
Essential Th2 cytokine in the pathogenesis of classical Hodgkin Lymphoma. Reed-Sternberg cells depend on autocrine IL-13 for proliferation. The rs20541 (R130Q) variant elevates IL-13 production and disease risk.
Master transcription factor for Th2 differentiation. GATA3 variants modulate the characteristic tumor microenvironment of Hodgkin Lymphoma, with rich infiltration of T lymphocytes and eosinophils.
Negative regulator of the NF-κB pathway. Loss-of-function in TNFAIP3 leads to uncontrolled NF-κB activation in Reed-Sternberg cells. Both somatic and germline mutations are associated with classical Hodgkin Lymphoma.
Additional loci also analyzed: The complete report also includes polymorphisms in HLA-A, HLA-DRB1, IL18R1, CXCR5 and other genes involved in adaptive immune response and inflammatory signaling relevant to Hodgkin Lymphoma.
An interpreted, contextualized, and actionable report — not just a list of variants.
We identify HLA class I and II haplotypes that influence the immune response to Epstein-Barr Virus — the main environmental cofactor for Hodgkin Lymphoma.
We combine dozens of small-effect variants into a polygenic score (PRS) that stratifies your risk against the population, validated in cohorts of over 40,000 patients.
Each finding is explained with reference to the literature, comparative odds ratios, and contextualization against population incidence.
Recommendations based on NCCN and ESMO guidelines for clinical surveillance in carriers of increased genetic risk, with signs and symptoms to watch.
As new loci are discovered by GWAS and meta-analyses are published, your report is automatically revised — at no additional cost.
Your data is processed with AES-256 encryption in a zero-knowledge architecture. Full GDPR compliance.
For carriers of increased genetic risk, knowing the early symptoms is essential for early detection.
Especially in the neck, armpits, and groin. Painless, firm, and persistent for more than 2 weeks.
Persistent fever above 38°C (100.4°F) without identifiable infection — a classic B symptom.
Profuse sweating enough to soak clothes and sheets — another classic B symptom.
Unintentional loss of more than 10% of body weight over the past 6 months.
Itching without apparent skin cause, often persistent — can be a paraneoplastic symptom.
Tiredness disproportionate to effort, not relieved by rest, lasting for weeks.
Our analysis integrates international GWAS meta-analyses with over 40,000 patients, ClinVar variant classifications, and clinical guidelines from NCCN, ESMO, and the American Society of Hematology.
Clear, evidence-based answers about genetics and Hodgkin Lymphoma.
Important medical notice: The information provided by helixXY is for educational and informational purposes only. It does not constitute a diagnosis, clinical laboratory report, or substitute for medical consultation. The diagnosis of Hodgkin Lymphoma requires a lymph node biopsy with histopathological analysis performed by a hematologist or oncologist. Always consult a qualified professional for interpretation and guidance.
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