Essay On Prostate Cancer

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The Insulin and Insulin-like Growth Factor Network in Prostate Cancer
Introduction
Prostate cancer is the most common type of diagnosed cancer among men. According to the American Cancer Society, about 200,000 new cases will be diagnosed and 29,000 men will die from prostate cancer in 20141. Local prostate cancers can be cured with surgery and or radiotherapy. Metastatic diseases, however, have fewer treatment options, especially for patients with castrate-resistant prostate disease2.
The androgens testosterone and DHT are the primary growth factors responsible for the development and growth of the prostate. Other non-androgenic growth factors, such as insulin-like growth factors (IGF) and insulin, are also involved and have been implicated with the progression of prostate cancer2. IGF is a strong mitogen in both normal and cancerous cells, promoting cell cycle progression and DNA synthesis. Insulin carries out its classic metabolic actions in the prostate, while also initiating proliferation and anti-apoptotic effects.
IGF is secreted from the liver after Growth Hormone (GH) stimulation from the pituitary, commonly referred to as the IGF/GH axis. The IGF system consists of two ligands, IGF-1 and IGF-2, and two cell surface receptors IGF1R and IGF2R. IGFs bind to the IGF1R receptor, which is heterotetrameric with two alpha-ligand binding subunits and two transmembrane beta-subunits. Binding of IGF induces auto-phosphorylation of the beta subunits and activation of the protein-tyrosine kinase. IGFs also interact with six high affinity IGF-binding proteins (IGFBP) that modulate IGF activity by inhibition or activation. Upon phosphorylation multiple pathways may become activated, including the MAPK and PI3K pathways, as well a...

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The IGF axis is a complex system implicated in the pathogenesis of prostate cancer, yet the entire mechanism has not been clearly defined. Although IGF-1 and its receptor IGF1R are considered to be oncogenic in prostate cancer, the pathways involved have not been helpful in terms of its therapeutic potential. Here three different studies demonstrated novel pathways and molecules associated with IGF signaling in prostate cancer. Prostate cancerous and noncancerous cells respond to IGF stimulation in very different manners, inducing proliferation and differentiation respectively. This illustrates a clear difference in IGF signaling and potential avenues for targeted therapies. Since IGFs are necessary growth factors in various tissues, utilizing the different signaling response in normal and cancerous cells may be of use.

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