Hodgkin's disease in patients with previous infectious mononucleosis

Kvåle, Gunnar; Høiby, E. Arne; Pedersen, E.M.

doi:10.1002/ijc.2910230502

Cited by 71 publications

(14 citation statements)

References 26 publications

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“…Epstein-Barr virus infections developing into mononucleosis have been associated with an increased risk of lymphoma (24,25). In the present cohort, a relatively high incidence of mononucleosis was reported (8.2%), which may indicate a high susceptibility to infections.…”

Section: Discussionmentioning

confidence: 40%

Cancer risk in Norwegian world class athletes

Robsahm

Hestvik

Veierød

et al. 2010

Cancer Causes Control

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Section: Discussionmentioning

confidence: 40%

Cancer risk in Norwegian world class athletes

Robsahm

Hestvik

Veierød

et al. 2010

Cancer Causes Control

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“…From reported associations of the lymphoma in this age group with small sibship size, low birth order, and other correlates of childhood socioeconomic affluence, it has been inferred that the postponement of common childhood infections may be accompanied by elevated HL risk in young adulthood (3)(4)(5)(6)(7)(8)(9)(10). Consistent with this, an increased risk of HL after infectious mononucleosis (IM), the characteristic clinical manifestation of primary Epstein-Barr virus (EBV) infection delayed to adolescence, has been reported in several studies (4,5,(11)(12)(13)(14)(15)(16)(17)(18). EBV has also been linked with HL by other lines of evidence.…”

Section: Introductionmentioning

confidence: 53%

Infectious Mononucleosis, Childhood Social Environment, and Risk of Hodgkin Lymphoma

Smedby²,

et al. 2007

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Infectious mononucleosis (IM) has been associated with an increased risk of Hodgkin lymphoma (HL), implicating a role for Epstein-Barr virus (EBV) in HL development. Although essential to the understanding of the association, it has remained uncertain if the relationship is restricted to the EBVpositive subset of HL. We collected information on mononucleosis history and childhood socioenvironmental characteristics in a population-based study of 586 patients with classic HL and 3,187 controls in Denmark and Sweden. Tumor EBV status was established for 499 cases by immunohistochemistry and in situ hybridization techniques. Odds ratios (OR) for the relationship between HL risk and mononucleosis and other risk factors were estimated by logistic regression for HL in younger (18-44 years) and older (45-74 years) adults, overall and by tumor EBV status. All analyses were adjusted for country-specific measures of maternal education and mononucleosis history. IM was associated with an increased risk of EBV-positive [OR, 3.23; 95% confidence interval (95% CI) 1.89-5.55] but not EBV-negative HL (OR, 1.35; 95% CI, 0.86-2.14). Risk of EBV-positive HL varied with time since IM and was particularly pronounced in younger adults (OR, 3.96; 95% CI,). IM-associated lymphomas occurred with a median of 2.9 years (1.8-4.9 years) after infection. The EBV specificity of the IM association was corroborated by a casecase comparison of IM history between younger adult EBVpositive and EBV-negative HL patients (OR IM EBV+ HL versus EBVÀ HL , 2.68; 95% CI, 1.40-5.12). We found further evidence that IM is associated only with EBV-positive HL. This finding is compatible with the notion that EBV-positive and EBV-negative HL may have different etiologies. [Cancer Res 2007;67(5):2382-8]

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“…3 Risk factors (small sibship size, high socioeconomic status, and growing up in a single-family dwelling) strongly suggest that it results from delayed exposure to a common childhood virus. 4,5 Epstein-Barr virus has been suggested as an etiologic agent on the basis of a higher frequency of past infectious mononucleosis in patients, 6,7 higher Epstein-Barr virus (EBV) titers in prospective serologic studies 8,9 and demonstration of the Epstein-Barr viral genome in some Hodgkin lymphoma tumors, (demonstrated more commonly in mixed cellularity tumors occurring in young children and the elderly than in nodular sclerosis tumors in young adults 10 ).Genetic factors also contribute to susceptibility. A 3-to 7-fold higher risk of childhood and young adult Hodgkin lymphoma is reported in siblings of case subjects.…”

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confidence: 99%

IL-6 levels and genotype are associated with risk of young adult Hodgkin lymphoma

Cozen

Gill

Ingles

et al. 2004

Blood

113

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Identical twins of young adult Hodgkin lymphoma case subjects are much more likely to develop the disease compared with fraternal twins of case subjects, suggesting a genetic determinant. Interleukin 6 (IL-6) levels are increased in patients with Hodgkin lymphoma and are correlated with a poor prognosis. We hypothesized that a heritable abnormality in IL-6 regulation may predispose to young adult Hodgkin lymphoma. We obtained blood specimens from 88 young adult Hodgkin lymphoma case subjects and their twins as well as from 87 matched control subjects. IL-6 was measured from unstimulated peripheral blood mononuclear cell (PBMC) supernatant with enzyme-linked immunosorbent assays (ELISAs) and compared by using analysis of covariance. Unaffected identical twins of case subjects (surrogate case subjects) had a 87.8% higher IL-6 level compared with matched control subjects (mean difference, ؉483.7 pg/mL, P ‫؍‬ .04). Analysis of the IL-6 174G>C promoter polymorphism genotypes showed that risk decreased with an increasing number of C alleles (P ‫؍‬ .01). The CC (low secreting) genotype was associated with a decreased risk of young adult Hodgkin lymphoma relative to the GG (high secreting) genotype (odds ratio [ IntroductionHodgkin lymphoma is characterized clinically by symptoms resembling those of a chronic infectious disease and pathologically by a rare neoplastic giant cell (Hodgkin or Reed-Sternberg cell) surrounded by a mixed inflammatory and benign small lymphocytic infiltrate that varies by histologic type. 1 In developed countries, the age-specific incidence curve is bimodal, 2 with a peak among young adults aged 15 to 34 years (young adult Hodgkin lymphoma), consisting mostly of the nodular sclerosis type, and a second peak among older adults (older than 50 years), consisting mainly of the mixed cellularity type. 3 Risk factors (small sibship size, high socioeconomic status, and growing up in a single-family dwelling) strongly suggest that it results from delayed exposure to a common childhood virus. 4,5 Epstein-Barr virus has been suggested as an etiologic agent on the basis of a higher frequency of past infectious mononucleosis in patients, 6,7 higher Epstein-Barr virus (EBV) titers in prospective serologic studies 8,9 and demonstration of the Epstein-Barr viral genome in some Hodgkin lymphoma tumors, (demonstrated more commonly in mixed cellularity tumors occurring in young children and the elderly than in nodular sclerosis tumors in young adults 10 ).Genetic factors also contribute to susceptibility. A 3-to 7-fold higher risk of childhood and young adult Hodgkin lymphoma is reported in siblings of case subjects. 11,12 We also reported that identical (monozygotic) twins of case subjects have a 100-fold higher risk of developing this lymphoma than that expected on the basis of population incidence, whereas no increased risk was observed among fraternal (dizygotic) twins of case subjects. 13 We hypothesized that an inherited immune phenotype was responsible for the development of young adult Hodgkin lymphoma,...

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Hodgkin's disease in patients with previous infectious mononucleosis

Cited by 71 publications

References 26 publications

Cancer risk in Norwegian world class athletes

Cancer risk in Norwegian world class athletes

Infectious Mononucleosis, Childhood Social Environment, and Risk of Hodgkin Lymphoma

IL-6 levels and genotype are associated with risk of young adult Hodgkin lymphoma

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