Insulinlike Growth Factor Signaling Pathways

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There is growing interest in the role of growth factors in prostate cancer development as these proteins can play important roles in regulating cell proliferation in the prostate. Particular attention has been focused on IGF-I and its binding proteins as prospective studies of circulating levels of IGF-I have suggested that individuals with high levels, especially when combined with low levels of binding proteins, may be at high risk of prostate cancer.76,77 Moreover, IGF-I activity may be one mechanism by which multiple possible etiological pathways are joined, including vitamin D pathways and androgen signaling, as both vitamin D analogues and castration can upregulate IGF-I binding proteins.78,79 As described above, an important androgen-regulated gene, the PSA gene, encodes a protease that can cleave IGF-I from its binding protein, leading to increased IGF-1 bioavailability, thus offering another possible connection between etiological pathways.

Animal models are consistent with an etiolog-ical role of IGF signaling in prostate cancer. In rat prostates, IGF-I induces prostate growth but deficiency reduces cell proliferation.80 Prostate cancer progression in the transgenic adenocar-cinoma of the mouse prostate (TRAMP) model is associated with increased IGF-I expression.81 Administration of the 5a-reductase inhibitor fi-nasteride in animal models reduces IGF-I levels, suggesting a further tie between androgen and IGF signaling pathways in prostate cancer development.82 The genes encoding IGF-1 and its growth factors are polymorphic and may in

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Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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