Obesity is a serious risk factor for cancer development and progression, but is also associated with poor prognosis in many tumor types. Obesity causes changes in energy balance, insulin, insulin-like growth factor-1 leptin, adiponectin, steroid hormones and cytokine levels. Each of these factors has the potential to create an environment that supports the onset and progression of cancer. Although the relationship between obesity and cancer is still uncertain, the reduction of systemic, hormonal and inflammatory changes leads to significant clinical benefits. Although the relationship between obesity and cancer is quite complex, there are some pathophysiological mechanisms that explain this connection. Adipose tissue dysfunction caused by obesity affects the production of various adipokines and plays an important role in carcinogenesis. At the same time, obesity includes hormone and growth factors such as insulin, insulin-like growth factor-1 (IGF-1), insulin resistance and vascular endothelial growth factor (VEGF); changes in adipokines, such as increased sex hormones, leptin levels and decreased adinopectin levels, such as the mammalian target (mTOR) and 5-adenosine monophosphate-activated kinase (AMPK) of the phosphatidyl inositol 3-kinase (PI3K) / protein kinaseB (AKT) / rapamycin protein complex. It causes intracellular signaling pathways, macrophage infiltration, cytokines, nuclear factor-nükleerB (NF sitB) and inflammatory factors. In addition, obesity related molecules have been shown to induce tumor growth, tumor growth and metastasis. In this review, the effects of some of the molecules on the pathophysiological processes will be investigated.
Birincil Dil | Türkçe |
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Konular | Sağlık Kurumları Yönetimi |
Bölüm | Araştırma Makaleleri |
Yazarlar | |
Yayımlanma Tarihi | 1 Temmuz 2019 |
Yayımlandığı Sayı | Yıl 2019 Cilt: 1 Sayı: 2 |