Morbid Obesity and Thyroid Cancer Rate. A Review of Literature

Abstract

In the past three decades, several recent studies have analyzed the alarming increase of obesity worldwide, and it has been well established that the risk of many types of malignancies is increased in obese individuals; in the same period, thyroid cancer has become the fastest growing cancer of all malignancies. We investigated the current literature to underline the presence of a connection between excess body weight or Body Mass Index (BMI) and risk of thyroid cancer. Previous studies stated that the contraposition between adipocytes and adipose-resident immune cells enhances immune cell production of multiple pro-inflammatory factors with subsequent induction of hyperlipidemia and vascular injury; these factors are all associated with oxidative stress and cancer development and/or progression. Moreover, recent studies made clear the mitogenic and tumorigenic action of insulin, carried out through the stimulation of mitogen-activated protein kinase (MAPK) and phosphoinositide-3 kinase/AKT (PI3K/AKT) pathways, which is correlated to the hyperinsulinemia and hyperglycemia found in obese population. Our findings suggest that obesity and excess body weight are related to an increased risk of thyroid cancer and that the mechanisms that combine overweight with this cancer should be searched for in the adipokine pathways and chronic inflammation onset.

Keywords: adipokines; chronic inflammation; obesity; thyroid cancer.

Figure 1

Molecular Mechanisms supporting the relation between obesity and thyroid cancer onset. AMPK: 5’ AMP-activated protein kinase; MAPK: mitogen-activated protein kinase; PI3K: Phosphoinositide 3-kinases; mTOR: mammalian target of rapamycin; STAT3: Signal transducer and activator of transcription 3; AKT: serine/threonine kinase.