Non-Hodgkin's lymphoma, obesity and energy homeostasis polymorphisms

Abstract

A population-based case -control study of lymphomas in England collected height and weight details from 699 non-Hodgkin's lymphoma (NHL) cases and 914 controls. Obesity, defined as a body mass index (BMI) over 30 kg m À2 at five years before diagnosis,, was associated with an increased risk of NHL (OR ¼ 1.5, 95% CI 1.1 -2.1). The excess was most pronounced for diffuse large B-cell lymphoma (OR ¼ 1.9, 95% CI 1.3 -2.8). Genetic variants in the leptin (LEP 19G4A, LEP À2548G4A) and leptin receptor genes (LEPR 223Q4R), previously shown to modulate NHL risk, as well as a polymorphism in the energy regulatory gene adiponectin (APM1 276G4T), were investigated. Findings varied with leptin genotype, the risks being decreased with LEP 19AA (OR ¼ 0.7, 95% CI 0.5 -1.0) and increased with LEP À2548GA (OR ¼ 1.3, 95% CI 1.0 -1.7) and À2548AA (OR ¼ 1.4, 95% CI 1.0 -1.9), particularly for follicular lymphoma. These genetic findings, which were independent of BMI, were stronger for men than women.

Non‐Hodgkin lymphoma and obesity: A pooled analysis from the InterLymph Consortium

“…Of the seven studies in this subset, no effect of BMI on NHL risk was observed, and the lack of association with obesity was consistent across NHL subtypes, amongst men and women, and at age 45, 46-55, 56-65 and 66 years. Six of the case-control studies included in this pooled analysis have previously published data on NHL and obesity 3,8,11,14,23,24,50 and a further 12 are included here for the first time. Apart from case-control studies, adiposity has been investigated in cohorts where height and weight were measured 9,10,12,13,25-27 or selfreported, 5,15,20,21 and among persons with a hospital discharge for obesity.…”

“…6 Hitherto only a few individual case-control studies and two cohort studies have considered lymphoma subtypes, proposing an association with excess adiposity for DLBCL, but less so for FL and CLL/SLL. 8,11,14,15,21,22,24,50 A recent meta-analysis of published risk estimates suggested a slight increased risk of NHL, particularly DLBCL based upon data from both case-control and cohort studies. 51 The pooled analysis presented here has the advantage of being less susceptible to positive publication bias since it is based on all studies within the InterLymph consortium Odds ratios and 95% confidence intervals adjusted for study, sex, age and race were estimated using unconditional logistic regres-…”

The non-Hodgkin lymphomas: A review of the epidemiologic literature

“…Two studies also found that SNPs in the leptin and leptin receptor genes, which participate in regulation of body weight and energy homeostasis, were associated with NHL risk. 487,488 Several genetic association studies of biotransformation enzymes, which detoxify or activate xenobiotic substances, have not yielded consistent findings, although polymorphisms in some genes have variously been associated with NHL. [489][490][491][492][493] In general, single reports of genetic associations should be interpreted cautiously; rather, large genetic studies with standardized methods are needed for validation and synthesis of results.…”

The growing incidence of cancer: Role of lifestyle and screening detection (Review)

“…Indeed, because obesity by itself increases mortality, these studies do not prove that obesity per se is a factor involved in cancer mortality. However, in many studies, obesity was found to be associated with an increased incidence of several cancer types (50,51) with the exception of lymphoma (52) and childhood cancers (53). Consequently, aside from these cancers, a recent hypothesis is that the observed increase of incidence of several cancer types, such as breast, colon, liver or kidney cancers may be partially due to obesity (54).…”