title: Racial/ethnic variation in EBV-positive classical Hodgkin lymphoma in California populations.
abstract: Epstein-Barr virus (EBV) is detected in the tumor cells of some but not all Hodgkin lymphoma (HL) patients, and evidence indicates that EBV-positive and -negative HL are distinct entities. Racial/ethnic variation in EBV-positive HL in international comparisons suggests etiologic roles for environmental and genetic factors, but these studies used clinical series and evaluated EBV presence by differing protocols. Therefore, we evaluated EBV presence in the tumors of a large (n = 1,032), racially and sociodemographically diverse series of California incident classical HL cases with uniform pathology re-review and EBV detection methods. Tumor EBV-positivity was associated with Hispanic and Asian/Pacific Islander (API) but not black race/ethnicity, irrespective of demographic and clinical factors. Complex race-specific associations were observed between EBV-positive HL and age, sex, histology, stage, neighborhood socioeconomic status (SES), and birth place. In Hispanics, EBV-positive HL was associated not only with young and older age, male sex, and mixed cellularity histology, but also with foreign birth and lower SES in females, suggesting immune function responses to correlates of early childhood experience and later environmental exposures, respectively, as well as of pregnancy. For APIs, a lack of association with birth place may reflect the higher SES of API than Hispanic immigrants. In blacks, EBV-positive HL was associated with later-stage disease, consistent with racial/ethnic variation in certain cytokine polymorphisms. The racial/ethnic variation in our findings suggests that EBV-positive HL results from an intricate interplay of early- and later-life environmental, hormonal, and genetic factors leading to depressed immune function and poorly controlled EBV infection.
authors.affiliation: Northern California Cancer Center, Fremont, CA 94538, USA. sglaser@nccc.org
authors.forename: Sally L
authors.initials: SL
authors.lastname: Glaser
authors.forename: Margaret L
authors.initials: ML
authors.lastname: Gulley
authors.forename: Christina A
authors.initials: CA
authors.lastname: Clarke
authors.forename: Theresa H
authors.initials: TH
authors.lastname: Keegan
authors.forename: Ellen T
authors.initials: ET
authors.lastname: Chang
authors.forename: Sarah J
authors.initials: SJ
authors.lastname: Shema
authors.forename: Fiona E
authors.initials: FE
authors.lastname: Craig
authors.forename: Joseph A
authors.initials: JA
authors.lastname: Digiuseppe
authors.forename: Ronald F
authors.initials: RF
authors.lastname: Dorfman
authors.forename: Risa B
authors.initials: RB
authors.lastname: Mann
authors.forename: Hoda
authors.initials: H
authors.lastname: Anton-Culver
authors.forename: Richard F
authors.initials: RF
authors.lastname: Ambinder
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002140:California / Q000453:epidemiology; D002648:Child; D002675:Child, Preschool; D005006:Ethnicity; D005260:Female; D014644:Genetic Variation; D004854:Herpesvirus 4, Human / Q000302:isolation & purification*; D006689:Hodgkin Disease / Q000208:ethnology* / Q000235:genetics* / Q000821:virology; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D008875:Middle Aged; D044469:Racial Groups