Exposure to childhood infections and risk of Epstein-Barr virus-defined Hodgkin's lymphoma in women

Sally L. Glaser, Theresa H Keegan, Christina A. Clarke, Muoi Trinh, Ronald F. Dorfman, Risa B. Mann, Joseph A. DiGiuseppe, Richard F. Ambinder

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

The role of Epstein-Barr virus (EBV) in Hodgkin's lymphoma (HL) etiology remains unresolved as EBV is detected in only some HL tumors and few studies have tried to reconcile its presence with factors suggesting viral etiology (e.g., childhood social class, infection history). In a population-based case-control study of San Francisco Bay area women, we analyzed interview data by tumor EBV status. Among 211 young adult cases, EBV-positive HL (11%) was associated with a single vs. shared bedroom at age 11 (OR = 4.0, 95% CI 1.1-14.4); risk was decreased for common childhood infections (OR = 0.3, 95% CI 0.1-1.0), including measles before age 10, but not with prior infectious mononucleosis (IM), which is delayed EBV infection. No study factors affected risk of young adult EBV-negative HL. Among 57 older adult cases, EBV-positive HL (23%) was unrelated to study factors; EBV-negative HL was associated with a single bedroom at age 11 (OR = 3.6, 95% CI 1.5-9.1) and IM in family members (OR = 3.1, 95% CI 1.1-9.0). Thus, delayed exposure to infection may increase risk of EBV-positive HL in young adults, but risk patterns differ in younger and older women for both EBV-positive and -negative HL. Late EBV infection does not appear relevant to risk, suggesting that other pathogens impact HL etiology in affluent female populations. Inconsistency of findings with prior studies may reflect failure of study risk factors to proxy meaningful exposures, risk differences by gender, or selection or misclassification bias. Null findings for EBV-negative HL indicate that etiologic models should be reconsidered for this common form.

Original languageEnglish (US)
Pages (from-to)599-605
Number of pages7
JournalInternational Journal of Cancer
Volume115
Issue number4
DOIs
StatePublished - Jul 1 2005
Externally publishedYes

Fingerprint

Epstein-Barr Virus Infections
Human Herpesvirus 4
Hodgkin Disease
Young Adult
Infectious Mononucleosis
Infection
Oncogenic Viruses
San Francisco
Measles
Proxy
Social Class
Population
Case-Control Studies
Interviews

Keywords

  • Epstein-Barr virus
  • Etiology
  • Hodgkin's lymphoma
  • Infectious mononucleosis
  • Risk factor

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Glaser, S. L., Keegan, T. H., Clarke, C. A., Trinh, M., Dorfman, R. F., Mann, R. B., ... Ambinder, R. F. (2005). Exposure to childhood infections and risk of Epstein-Barr virus-defined Hodgkin's lymphoma in women. International Journal of Cancer, 115(4), 599-605. https://doi.org/10.1002/ijc.20787

Exposure to childhood infections and risk of Epstein-Barr virus-defined Hodgkin's lymphoma in women. / Glaser, Sally L.; Keegan, Theresa H; Clarke, Christina A.; Trinh, Muoi; Dorfman, Ronald F.; Mann, Risa B.; DiGiuseppe, Joseph A.; Ambinder, Richard F.

In: International Journal of Cancer, Vol. 115, No. 4, 01.07.2005, p. 599-605.

Research output: Contribution to journalArticle

Glaser, SL, Keegan, TH, Clarke, CA, Trinh, M, Dorfman, RF, Mann, RB, DiGiuseppe, JA & Ambinder, RF 2005, 'Exposure to childhood infections and risk of Epstein-Barr virus-defined Hodgkin's lymphoma in women', International Journal of Cancer, vol. 115, no. 4, pp. 599-605. https://doi.org/10.1002/ijc.20787
Glaser, Sally L. ; Keegan, Theresa H ; Clarke, Christina A. ; Trinh, Muoi ; Dorfman, Ronald F. ; Mann, Risa B. ; DiGiuseppe, Joseph A. ; Ambinder, Richard F. / Exposure to childhood infections and risk of Epstein-Barr virus-defined Hodgkin's lymphoma in women. In: International Journal of Cancer. 2005 ; Vol. 115, No. 4. pp. 599-605.
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abstract = "The role of Epstein-Barr virus (EBV) in Hodgkin's lymphoma (HL) etiology remains unresolved as EBV is detected in only some HL tumors and few studies have tried to reconcile its presence with factors suggesting viral etiology (e.g., childhood social class, infection history). In a population-based case-control study of San Francisco Bay area women, we analyzed interview data by tumor EBV status. Among 211 young adult cases, EBV-positive HL (11{\%}) was associated with a single vs. shared bedroom at age 11 (OR = 4.0, 95{\%} CI 1.1-14.4); risk was decreased for common childhood infections (OR = 0.3, 95{\%} CI 0.1-1.0), including measles before age 10, but not with prior infectious mononucleosis (IM), which is delayed EBV infection. No study factors affected risk of young adult EBV-negative HL. Among 57 older adult cases, EBV-positive HL (23{\%}) was unrelated to study factors; EBV-negative HL was associated with a single bedroom at age 11 (OR = 3.6, 95{\%} CI 1.5-9.1) and IM in family members (OR = 3.1, 95{\%} CI 1.1-9.0). Thus, delayed exposure to infection may increase risk of EBV-positive HL in young adults, but risk patterns differ in younger and older women for both EBV-positive and -negative HL. Late EBV infection does not appear relevant to risk, suggesting that other pathogens impact HL etiology in affluent female populations. Inconsistency of findings with prior studies may reflect failure of study risk factors to proxy meaningful exposures, risk differences by gender, or selection or misclassification bias. Null findings for EBV-negative HL indicate that etiologic models should be reconsidered for this common form.",
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