leptin and Lymphoma

Obesity, which is considered a pandemic due to its high prevalence, is a risk factor for many types of cancers, including lymphoma, through a variety of mechanisms by promoting an inflammatory state. Specifically, over the last few decades, obesity has been suggested not only to increase the risk of lymphoma but also to be associated with poor clinical outcomes and worse responses to different treatments for those diseases. Within the extensive range of proinflammatory mediators that adipose tissue releases, leptin has been demonstrated to be a key adipokine due to its pleotropic effects in many physiological systems and diseases. In this sense, different studies have analyzed leptin levels and leptin/leptin receptor expressions as a probable bridge between obesity and lymphomas. Since both obesity and lymphomas are prevalent pathophysiological conditions worldwide and their incidences have increased over the last few years, here we review the possible role of leptin as a promising proinflammatory mediator promoting lymphomas.

Topics: Adipokines; Adipose Tissue; Humans; Leptin; Lymphoma; Obesity; Receptors, Leptin

Topics: Animals; Carcinogenesis; Cell Transformation, Neoplastic; Dogs; Exons; Humans; Leptin; Lymphoma; Mice; Obesity; Prostatic Neoplasms; Tumor Protein p73

Leptin has important effects on bone metabolism. Possible relationships between leptin and bone mineral density were evaluated in the survivors of the childhood leukemia and lymphoma. Twenty patients were included the study. Anthropometric parameters, growth hormone response to provocative test, serum calcium, phosphorus, alkaline phosphates, osteocalcin, leptin levels, urinary calcium and deoxyypyridinoline levels, and bone mineral density were obtained. Anthropometric parameters of patients were not significantly different from those of a control group. Growth hormone provocative test was abnormal in 3 patients who received cranial radiotherapy. The osteocalcin levels and bone mineral density of patients were significantly lower than in the control group (p=.001, p=.02). Nine patients were in the osteopenic and 7 were in the osteoporotic range. The leptin levels of patients were significantly lower (p=.01) than in the control group. Bone mineral density (BMD) was significantly correlated with leptin level, age, body mass index, and Tanner stage in simple correlation analysis. However, in multivariate analysis only age was significant (p<.000, r: .752). Markers of bone metabolism, BMD, and leptin levels were not related with the growth hormone status of patients and did not present a correlation with the cumulative doses of drugs. There are a few studies evaluating the relationship between BMD and leptin levels in childhood cancer. Although this study did not find any correlation between the leptin level and BMD, detailed studies of larger numbers of patients are necessary to evaluate causes of decreased leptin level and the possible role of leptin on osteopenia observed in survivors of childhood cancer.

Topics: Adolescent; Body Mass Index; Bone and Bones; Bone Density; Bone Diseases, Metabolic; Child; Disease-Free Survival; Female; Humans; Leptin; Leukemia; Lymphoma; Male; Minerals; Osteocalcin