Epidemiological link between obesity, type 2 diabetes mellitus and cancer

Figure 2 The pathophysiological mechanisms linking the hyperinsulinaemia in the tumour microenvironment to cancer with the associated intracellular signalling. IL-1β: Interleukin-1β; IL-6: Interleukin-6; TNF-α: Tumour necrosis factor-α; IR-A: Insulin receptor-A; IR-B: Insulin receptor-B; IGF-1: Insulin-like growth factor-1; IGF-2: Insulin-like growth factor-2; IGF-1R: Insulin-like growth factor-1 receptor; IR-A IGF1-R: Hybrid receptor of IR-A and IGF-1R; IR-B IGF1-R: Hybrid receptor of IR-B and IGF-1R; IGFBP: Insulin-like growth factor binding protein; ER-α: Oestrogen receptor-α; mER: membrane oestrogen receptor; Ob-R: Leptin-receptor; PI3K: Phosphatidyl-inositol-3-kinase; AKT: Protein kinase B; mTORC1: Mechanistic target of rapamycin complex 1 (Mammalian target of rapamycin complex 1); RAS: Rat sarcoma; RAF: Rapidly accelerated fibrosarcoma; MAPK: Mitogen activated protein kinase; ERK: Extracellular-regulated kinase; JAK2: Janus kinase-2; STAT3: Signal transducer and activator of transcription-3; VEGF: Vascular endothelial growth factor.