Obesity and Risk for Lymphoma: Possible Role of Leptin

Abstract

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.

Keywords: adipokines; leptin; lymphoma; obesity.

Figure 1

Overweight individuals could increase the risk of cancer, including lymphomas, through the accumulation of pro-inflammatory mediators and immunosuppressive cells within the tumor microenvironment. CCL—C–C motif chemokine ligand; IL—interleukin; TGF—tumor growth factor; TNF—tumor necrosis factor.

Figure 2

Leptin signaling pathways that could promote different types of lymphoma. ALCL—anaplastic large cell lymphoma; DLBCL—diffuse large B-cell lymphoma; FL—follicular lymphoma; HL—Hodgkin lymphoma; MCL—mantle cell lymphoma; NKTCL—natural killer/T-cell lymphoma; PTCL—peripheral T cell lymphoma; TCL—T-cell lymphoma.