Risk factors for Hodgkin’s disease by Epstein-Barr virus (EBV) status: prior infection by EBV and other agents

Alexander, FE; Jarrett, Ruth F.; Lawrence, Dana J.; Armstrong, Alona; Freeland, June; Gokhale, David; Kane, Eleanor; Taylor, G. Malcolm; Wright, D H; Cartwright, R. A.

doi:10.1054/bjoc.1999.1049

Cited by 117 publications

(101 citation statements)

References 13 publications

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“…Sleckman et al 11 found no association with education, income, childhood housing, sibship size or birth order when comparing 16 EBV-positive to 67 EBV-negative U.S. patients aged 15-55 with early-stage HL. Findings from the latter 2 studies do not support a delayed-exposure mechanism but also may not be directly comparable to ours as both used hospital-based patients, one was limited to early-stage disease 11 and neither stratified findings in women by age; 11,12 our differences with the findings of Alexander et al 13 for EBV-negative HL may be due in part to the much narrower age range of their subjects. Contradicting the delayed-exposure hypothesis in our data for young adults are the risk of EBV-positive HL with lower birth order and the lack of association with self-reported IM, a clinically evident expression of infection delayed past childhood.…”

Section: Discussioncontrasting

confidence: 80%

“…The inconsistencies of our findings with the delayed-exposure etiologic model for HL and with other published findings [11][12][13][14][15] have several possible explanations. (i) The proportion of HL tumors that are EBV-positive has been shown to vary markedly with the composition of the patient population.…”

Section: Discussioncontrasting

confidence: 50%

“…3 While the delayedexposure model was not anticipated to apply only to EBV-positive HL, such a restriction could occur if the immunologic challenge of common childhood infections occurring in adolescence and young adulthood led to poorer control of latent EBV infection and subsequent development of EBV-positive tumors, as postulated for various EBV-related malignancies. 30 Alexander et al 13 also found that having at least 2 childhood infections lowered risk of EBVpositive HL in subjects aged 16-24 but noted similar associations for EBV-negative HL. Flavell et al 12 reported no association of material deprivation scores (a community-level index) for 21 English EBV-positive compared to 78 EBV-negative patients but higher deprivation scores (indicating lower rather than higher socioeconomic status) predicting EBV-positive HL among females.…”

Section: Discussionmentioning

confidence: 88%

“…13 Among the 4 studies considering prior IM and risk of EBV-positive HL, one found no association 11 and 3 found a strong increase in risk. [13][14][15] To help resolve inconsistencies in the epidemiologic data regarding childhood infection and risk of EBV-defined HL, we analyzed interview information and tumor EBV status from a population-based case-control study of HL in Greater San Francisco Bay area women. Our purpose in these analyses was to evaluate whether determinants of childhood exposure to other children and self-reported history of several common infections (including IM) predicted development of EBV-positive or EBV-negative HL.…”

mentioning

confidence: 97%

“…12 A case-control study reported a protective effect of having had at least 2 common childhood infections for both EBV-positive and EBV-negative HL. 13 Among the 4 studies considering prior IM and risk of EBV-positive HL, one found no association 11 and 3 found a strong increase in risk. [13][14][15] To help resolve inconsistencies in the epidemiologic data regarding childhood infection and risk of EBV-defined HL, we analyzed interview information and tumor EBV status from a population-based case-control study of HL in Greater San Francisco Bay area women.…”

mentioning

confidence: 97%

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

Glaser

Keegan

Clarke

et al. 2005

Intl Journal of Cancer

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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 ¼ 4.0, 95% CI 1.1-14.4); risk was decreased for common childhood infections (OR ¼ 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 ¼ 3.6, 95% CI 1.5-9.1) and IM in family members (OR ¼ 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. ' 2005 Wiley-Liss, Inc.Key words: Hodgkin's lymphoma; Epstein-Barr virus; etiology; risk factor; infectious mononucleosis Infections have long been suspected in the etiology of HL, particularly for young adult cases. Initial clues came from its heterogeneous clinical behavior and histologic appearance, which suggest both a chronic infection and a malignancy. 1,2 Subsequently, epidemiologic studies showed that young adult HL cases tended to have childhood characteristics such as early birth order and small family size that are consistent with delayed exposure to other children, suggesting that timing of childhood infections was etiologically important. 3,4 EBV, a ubiquitous herpesvirus, was of early interest as a possible causative infectious agent because HL patients were more likely than controls to report prior IM (the clinical manifestation of primary infection with EBV delayed until adolescence) and to have elevated antibody titers to EBV before as well as after HL diagnosis. 5,6 Involvement by EBV was further supported when molecular studies identified EBV genes and gene products within malignant cells of affected HL tumors and in a form suggesting that infection preceded malignant transformation. 7 Nevertheless, the role of EBV in HL etiology remains unresolved as present methods detect evidence of EBV in the tumor cells of only a proportion of HL patients, and this evidence is least common in young adul...

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Section: Discussioncontrasting

confidence: 80%

Section: Discussioncontrasting

confidence: 50%

Section: Discussionmentioning

confidence: 88%

mentioning

confidence: 97%

mentioning

confidence: 97%

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

Glaser

Keegan

Clarke

et al. 2005

Intl Journal of Cancer

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Classical Hodgkin's lymphoma arising in different host's conditions: Pathobiology parameters, therapeutic options, and outcome

et al. 2011

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Epidemiologic and molecular findings suggest that classical Hodgkin's lymphoma (CHL) is not a single disease but consists of more than one entity and may occur in different clinical settings. This review analyzes similarities and disparities among CHL entities arising in different host's conditions with respect to pathobiology parameters, therapeutic options, and outcome. For the purpose of this analysis, CHL entities have been subdivided according to the immune status of the host. In nonimmunosuppressed hosts, according to the age, CHL include pediatric, adult, and elderly forms, whereas, in immunosuppressed hosts, according to the type of immunosuppression, CHL include human immunodeficiency virus (HIV)-associated, iatrogenic, and post-transplant types. CHL entities in different settings are similar in morphology of neoplastic cells, expression of activation markers, and aberrations/activation of NFKB, JAK/STAT, and P13K/AKT pathways, but differ in the association with Epstein-Barr virus (EBV) infection, persistent B-cell phenotype, and cellular background composition. Large B-cell lymphomas resembling CHL may also be observed in the same clinical settings. These lesions, however, do not fulfill the diagnostic criteria of CHL and clinically display a very aggressive behavior. In this article, current treatment options for the CHL entities, especially for elderly CHL and HIV-associated CHL, are specifically reviewed. ABVD remains the gold standard both in nonimmunosuppressed or immunosuppressed hosts even if there are several data suggesting a possible improvement in outcome using the aggressive BEACOPP regimen in advanced stages. Refractory CHL, a clinical condition that may occur throughout the entire spectrum of CHL, is discussed separately. Am. J. Hematol. 86:170-179, 2011. V

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Hodgkin lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Ansell

2011

American J Hematol

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Disease overview: Hodgkin lymphoma (HL) is an uncommon B‐cell lymphoid malignancy affecting 8,500 new patients annually and representing ∼11% of all lymphomas in the United States. Diagnosis: HL is composed of two distinct disease entities; the more commonly diagnosed classical HL and the rare nodular lymphocyte predominant HL. Nodular sclerosis, mixed cellularity, lymphocyte depletion, and lymphocyte‐rich HL are subgroups under the designation of classical HL. Risk stratification: An accurate assessment of the stage of disease in patients with HL is critical for the selection of the appropriate therapy. Prognostic models that identify patients at low or high risk for recurrence are used to optimize therapy for patients with limited or advanced stage disease. Risk‐adapted therapy: Initial therapy for HL patients is based on the histology of the disease, the anatomical stage, and the presence of poor prognostic features. Patients with early stage disease are treated with combined modality strategies using abbreviated courses of combination chemotherapy followed by involved‐field radiation therapy, while those with advanced stage disease receive a longer course of chemotherapy often without radiation therapy. Management of relapsed/refractory disease: High‐dose chemotherapy (HDCT) followed by an autologous stem‐cell transplant (ASCT) is the standard of care for most patients who relapse following initial therapy. For patients who fail HDCT with ASCT, palliative chemotherapy, nonmyeloablative allogeneic transplant, or participation in a clinical trial should be considered. Am. J. Hematol. 86:852–858, 2011. © 2011 Wiley‐Liss, Inc.

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Risk factors for Hodgkin’s disease by Epstein-Barr virus (EBV) status: prior infection by EBV and other agents

Cited by 117 publications

References 13 publications

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

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

Classical Hodgkin's lymphoma arising in different host's conditions: Pathobiology parameters, therapeutic options, and outcome

Hodgkin lymphoma: 2011 update on diagnosis, risk‐stratification, and management

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