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1.  Dietary Pattern and Risk of Hodgkin Lymphoma in a Population-Based Case-Control Study 
American Journal of Epidemiology  2015;182(5):405-416.
Classic Hodgkin lymphoma (cHL) has few known modifiable risk factors, and the relationship between diet and cHL risk is unclear. We performed the first investigation of an association between dietary pattern and cHL risk in 435 cHL cases and 563 population-based controls from Massachusetts and Connecticut (1997–2000) who completed baseline diet questionnaires. We identified 4 major dietary patterns (“vegetable,” “high meat,” “fruit/low-fat dairy,” “desserts/sweets”) using principal components analysis. We computed multivariable odds ratios and 95% confidence intervals for associations of dietary pattern score (quartiles) with younger-adult (age <50 years), older-adult (age ≥50 years), and overall cHL risk. Secondary analyses examined associations by histological subtype and tumor Epstein-Barr virus (EBV) status. A diet high in desserts/sweets was associated with younger-adult (odds ratio(quartile 4 vs. quartile 1) = 1.60, 95% confidence interval: 1.05, 2.45; Ptrend = 0.008) and EBV-negative, younger-adult (odds ratio = 2.11, 95% confidence interval: 1.31, 3.41; Ptrend = 0.007) cHL risk. A high meat diet was associated with older-adult (odds ratio = 3.34, 95% confidence interval: 1.02, 10.91; Ptrend = 0.04) and EBV-negative, older-adult (odds ratio = 4.64, 95% confidence interval: 1.03, 20.86; Ptrend = 0.04) cHL risk. Other dietary patterns were not clearly associated with cHL. We report the first evidence for a role of dietary pattern in cHL etiology. Diets featuring high intake of meat or desserts and sweets may increase cHL risk.
PMCID: PMC4552267  PMID: 26182945
case-control study; diet; Hodgkin lymphoma; principal components analysis
2.  Serum IgA to Epstein-Barr virus Early Antigen-Diffuse identifies Hodgkin's Lymphoma 
Journal of medical virology  2013;86(9):1621-1628.
Hodgkin's lymphoma is associated with immune dysregulation. Immune impairment often results in aberrant immune responses and lytic reactivation of ubiquitous Herpesviruses such as Epstein-Barr virus (EBV) in mucosal tissues. Accordingly, the specificity of IgA to EBV early-lytic antigens, which are important for reactivation, was evaluated to determine Hodgkin's lymphoma-specific sero-reactive patterns. Sera from 42 previously described patients with Hodgkin's lymphoma were compared to sera from 17 patients with infectious mononucleosis (IM), another EBV-related condition that often presents in a similar manner; and to sera from 15 healthy EBV-seropositive subjects. Flow cytometry analysis demonstrated that like IM sera, most Hodgkin's lymphoma sera contained IgA that labeled cells expressing EBV early-lytic antigens whereas healthy EBV-seropositive sera did not. Further evaluation to distinguish Hodgkin's lymphoma from IM showed that IgA in most Hodgkin's lymphoma, irrespective of the presence of EBV in primary tumors, detected only modified forms of EBV lytic Early Antigen-Diffuse (EA-D) while IM sera detected the un-modified form as well, further supporting the presence of immune dysregulation in Hodgkin's lymphoma patients. This IgA pattern distinguished Hodgkin's lymphoma from IM sera with a sensitivity of 92.9%, specificity 100%, positive predictive value 100%, and negative predictive value 85%. Our findings lay the groundwork for additional scientific and clinical investigation, particularly into the potential for developing Hodgkin's lymphoma -associated diagnostic and prognostic biomarkers.
PMCID: PMC3969873  PMID: 24122847
Hodgkin's lymphoma; Epstein-Barr virus; immune dysregulation; biomarker; lytic antigens
3.  Antibody titers against EBNA1 and EBNA2 in relation to Hodgkin lymphoma and history of infectious mononucleosis 
A role for Epstein Barr virus (EBV) in Hodgkin lymphoma (HL) pathogenesis is supported by the detection of EBV genome in about one-third of HL cases, but is not well defined. We previously reported that an elevated pre-diagnosis antibody titer against EBV nuclear antigens (EBNA) was the strongest serologic predictor of subsequent HL. For the present analysis, we measured antibody levels against EBNA components EBNA1 and EBNA2 and computed their titer ratio (anti-EBNA1:2) in serum samples from HL cases and healthy siblings. We undertook this analysis to examine whether titer patterns atypical of well-resolved EBV infection, such as an anti-EBNA1:2 ratio ≤1.0, simply reflect history of infectious mononucleosis (IM), an HL risk factor, or independently predict HL risk. Participants were selected from a previous population-based case-control study according to their history of IM. We identified 55 EBV-seropositive persons with a history of IM (IM+; 33 HL cases, 22 siblings) and frequency-matched a comparison series of 173 IM history-negative, EBV-seropositive subjects on HL status, gender, age, and year of blood draw (IM−; 105 cases, 58 siblings). In multivariate logistic regression models, an anti-EBNA1:2 ratio ≤1.0 was significantly more prevalent in HL cases than siblings (odds ratio, 95% confidence interval=2.43, 1.05–5.65); similar associations were apparent within the IM+ and IM− groups. EBNA antibodies were not significantly associated with IM history in HL cases or siblings. These associations suggest that chronic or more severe EBV infection is a risk factor for HL, independent of IM history.
PMCID: PMC3899938  PMID: 21805472
Hodgkin lymphoma; Epstein-Barr virus; infectious mononucleosis; EBNA1; EBNA2
4.  Nutrients and Genetic Variation Involved in One-Carbon Metabolism and Hodgkin Lymphoma Risk: A Population-based Case-Control Study 
American Journal of Epidemiology  2011;174(7):816-827.
Nutritional and genetic determinants of the one-carbon metabolism pathway have been related to risk of malignant lymphomas, but little is known about their associations with Hodgkin lymphoma risk specifically. The authors examined nutrient intake (folate, vitamin B2, vitamin B6, vitamin B12, methionine) and multivitamin use among 497 Hodgkin lymphoma patients and 638 population-based controls (Massachusetts and Connecticut, 1997–2000), and genetic variation (MTHFR 677C>T, MTHFR 1298A>C, MTR 2756A>G, SHMT1 1420C>T, TYMS 1494del6) and gene-diet interactions in a subset. Unconditional logistic regression was used to calculate multivariable odds ratios and 95% confidence intervals. Hodgkin lymphoma risk was not associated with total nutrient intake or intake from food alone (excluding supplements). Multivitamin use (odds ratio (OR) = 1.46, 95% CI: 1.09, 1.96), total vitamin B6 (ORquartile 4 vs. 1 = 1.62) (Ptrend = 0.03), and total vitamin B12 (ORquartile 4 vs. 1 = 1.75) (Ptrend = 0.02) intakes were positively associated with risk of Epstein-Barr virus-negative, but not -positive, disease. The 5 genetic variants were not significantly associated with Hodgkin lymphoma risk; no significant gene-diet interactions were observed after Bonferroni correction. Study findings do not support a strong role for nutrients and genetic variation in the one-carbon metabolism pathway in susceptibility to Hodgkin lymphoma. Associations between diet and risk of Epstein-Barr virus-negative disease require confirmation in other populations.
PMCID: PMC3203380  PMID: 21810727
case-control studies; diet; folic acid; Hodgkin disease; vitamins
6.  Polymorphic variation in NFKB1 and other aspirin-related genes and risk of Hodgkin lymphoma 
We found that regular use of aspirin may reduce the risk of Hodgkin lymphoma (HL), a common cancer of adolescents and young adults in the US. To explore possible biological mechanisms underlying this association, we investigated whether polymorphic variation in genes involved in nuclear factor (NF)-κB activation and inhibition, other inflammatory pathways, and aspirin metabolism influences HL risk. Twenty single nucleotide polymorphisms (SNPs) in seven genes were genotyped in DNA from 473 classical HL cases and 373 controls enrolled between 1997 and 2000 in a population-based case-control study in the Boston, Massachusetts, metropolitan area and the state of Connecticut. We selected target genes and SNPs primarily using a candidate-SNP approach and estimated haplotypes using the expectation-maximization algorithm. We used multivariable logistic regression to estimate odds ratios (ORs) for associations with HL risk. HL risk was significantly associated with rs1585215 in NFKB1 (AG vs. AA: OR=2.1, 95% confidence interval [CI]=1.5–2.9; GG vs. AA: OR=3.5, 95% CI=2.2–5.7, Ptrend=1.7×10−8) and with NFKB1 haplotypes (Pglobal=6.0×10−21). Similar associations were apparent across categories of age, sex, tumor Epstein-Barr virus status, tumor histology, and regular aspirin use, although statistical power was limited for stratified analyses. Nominally significant associations with HL risk were detected for SNPs in NFKBIA and CYP2C9. HL risk was not associated with SNPs in IKKA/CHUK, PTGS2/COX2, UDP1A6, or LTC4S. In conclusion, genetic variation in the NF-κB pathway appears to influence risk of HL. Pooled studies are needed to detect any heterogeneity in the association with NF-κB across HL subgroups, including aspirin users and non-users.
PMCID: PMC2720066  PMID: 19223558
Hodgkin lymphoma; genetic polymorphism; nuclear factor kappa B; NFKB1 protein; aspirin; case-control

Results 1-6 (6)