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Recently, it has been shown that prostate cancer specimens had higher levels of p66Shc than adjacent noncancerous cells [ 15].
It has been shown that prostate cancer is characterized by a decreased level of citrate and an increased level of (phospho choline[ 43].
Supporting this, it has been shown that prostate tumour cells show invasion in response to TGF-β and not non-tumourigenic cells [ 10].
It has been shown that prostate epithelial cells interact directly with the BME cells, initially via selectins and this interaction is then stabilised by integrin binding (Orr et al, 2000).
The role of lipid uptake is currently unclear but it is possible that the lipid may be utilised as an energy substrate to meet the needs of the accelerated cellular metabolism, known to be a feature of the metastasising malignant cell, and indeed it has been shown that prostate cancer cells interact with adipocytes.
It has been shown that prostate cancer patients undergoing external beam radiation therapy have a higher risk of secondary cancer than do surgically treated patients and patients treated with other forms of radiation (Neugut et al, 1997; Brenner, 2000, 2006; Baxter et al, 2005; Brenner and Hall, 2006; Moon et al, 2006).
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More recently, it has been shown that prostate-specific ablation of FAK in an SV40 T antigen mouse model resulted in the inability of prostate tumours to progress to the aggressive neuroendocrine phenotype [ 13].
It has been shown that increased prostate size is a risk factor for lower urinary tract symptom (LUTS) progression in men who currently have LUTS presumed due to benign prostatic hyperplasia (BPH).
Moreover, it has been shown that in prostate cancer specimens both the p66Shc protein level and the ERK/MAPK phoshorylation are elevated [ 17].
It has been shown that within prostate cancer cells, wild-type AR physically interacts with Nemo-like kinase (NLK) and that NLK is able to regulate the activity and transcription of AR in this context (Emami et al., 2009).
In accordance with our results, it has been shown that in prostate cancer patients, the aggressiveness of the histologic grade increased significantly as the percentage of free PSA/total PSA decreased (Li et al, 1999).
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Justyna Jupowicz-Kozak
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