Risk of Hodgkin lymphoma according to immigration status and origin: a migrant cohort study of 2.3 million Jewish Israelis.

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Abstract

Hodgkin Lymphoma (HL), a common early adulthood malignancy, has a complex etiology. We conducted a migrant cohort study to assess immigration status and origin as predictors of HL in Israel, which has among the highest rates of HL worldwide. Nationwide data on 2,285,009 16-19-year-old Jewish adolescents, collected from 1967-2011, were linked to Israel's Cancer Registry to obtain the incidence of HL until 2012. Two thousand and ninety-three HL cases were detected during 47.0 million person-years of follow-up. Using multivariable-adjusted Cox proportional hazards modeling, risk was higher for Israeli-born compared to immigrants, similarly across origin groups (HR = 1.59; 95%CI 1.32-1.92 for the dominant nodular sclerosis subtype). Risk of HL was greater for more recent year of birth, higher BMI, taller stature, and apparently for women. These findings suggest that exposure to as yet unidentified elements of the Israeli environment increase the risk of nodular sclerosis HL, and should aid in directing research efforts.

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Developmental origins of health and disease: new insights.

Jamie Hanson, Peter D. Gluckman (2008)

Epidemiological and animal studies show that small changes in the developmental environment can induce phenotypic changes affecting an individual's responses to their later environment. These may alter the risk of chronic disease such as metabolic syndrome or cardiovascular disease. Recent research shows that animals exposed to such a mismatch between prenatal and postnatal environment develop obesity, reduced activity, leptin and insulin resistance, elevated blood pressure and vascular endothelial dysfunction. Epigenetic processes are involved in such effects, targeted to promoter regions of specific genes in specific tissues. Such fine control of gene expression suggests that the mechanisms have been retained through evolution through their adaptive advantage, rather than representing extreme effects of developmental disruption akin to teratogenesis. There may be adaptive advantage in a developmental cue inducing a phenotypic change in generations beyond the immediate pregnancy, and a range of data that support this concept. In animals, epigenetic effects such as DNA methylation can be passed to successive generations. Environmental toxins, including endocrine disruptors, may induce greater risk of chronic disease, even at low exposure levels, if they affect such normal developmental epigenetic processes. Appropriate interventions may have long-term multigenerational effects to reduce the risk of chronic disease.

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Characteristics of Hodgkin's lymphoma after infectious mononucleosis.

Anne Madsen, Henrik Hjalgrim, Nils Rosdahl … (2003)

Infectious mononucleosis-related Epstein-Barr virus (EBV) infection has been associated with an increased risk of Hodgkin's lymphoma in young adults. Whether the association is causal remains unclear. We compared the incidence rates of Hodgkin's lymphoma in two population-based Danish cohorts of patients who were tested for infectious mononucleosis: 17,045 with serologic evidence of having had acute EBV infection, and 24,614 with no such evidence. We combined the cohort of patients who had serologically verified infectious mononucleosis with a cohort of 21,510 Swedish patients with infectious mononucleosis (combined total, 38,555). Biopsy specimens of Hodgkin's lymphomas occurring during follow-up in this combined cohort were tested serologically for the presence of EBV. Using this information, we modeled the relative risk of EBV-negative and EBV-positive Hodgkin's lymphoma in different periods after the diagnosis of infectious mononucleosis and estimated the median incubation time for mononucleosis-related EBV-positive Hodgkin's lymphoma. Only serologically confirmed infectious mononucleosis was associated with a persistently increased risk of Hodgkin's lymphoma. Sixteen of 29 tumors (55 percent), obtained from patients with infectious mononucleosis, had evidence of EBV. There was no evidence of an increased risk of EBV-negative Hodgkin's lymphoma after infectious mononucleosis. In contrast, the risk of EBV-positive Hodgkin's lymphoma was significantly increased (relative risk, 4.0; 95 percent confidence interval, 3.4 to 4.5). The estimated median incubation time from mononucleosis to EBV-positive Hodgkin's lymphoma was 4.1 years (95 percent confidence interval, 1.8 to 8.3). A causal association between infectious mononucleosis-related EBV infection and the EBV-positive subgroup of Hodgkin's lymphomas is likely in young adults. Copyright 2003 Massachusetts Medical Society