Metastasis prostate cancer

In malignant prostate epithelial cells, auto- and paracrine release of ET-1 is a critical factor in ETA receptor-mediated proliferation [5]. In addition, the ET-1/ETa receptor axis has emerged as a potential target in prostate cancer bone metastasis... 

Ultrasensitive assays for PSA contribute to the earlier detection of prostate cancer relapse and (or) residual disease in prostatectomized patients as well as the more timely evaluation of response to current therapies. PSA determinations can be useful in detecting metastatic or persistent disease in patients following surgical or medical treatment of prostate cancer. Persistent elevation of PSA following treatment, or an increase in the pretreatment PSA concentrations, is indicative of recurrent or residual disease. Hence, PSA is widely accepted as an aid in the management of prostate cancer patients, and serum levels are most useful when sequential values are obtained and monitored over time. After complete removal of the prostate gland (radical prostatectomy), PSA levels should become very low or undetectable. A rise of the serum PSA level in prostatectomy patients indicates residual prostate tissue, recurrence, or metastasis of the disease (13, 16, 24, 36). 

Saleem M, Adhami VM, Ahmad N, Gupta S, Mukhtar H. 2005. Prognostic significance of metastasis-associated protein S100A4 (Mtsl) in prostate cancer progression and chemoprevention regimens in an autochthonous mouse model. Clin Cancer Res 11 147-153. 

Cameron et al. (1989) reported that flax oil prevented tumor formation in mice whereas mice on the corn oil and safflower oil diets had the greatest number of tumors. A diet consisting of 10% flax oil was sufficient to reduce tumor growth and metastasis in mice compared with corn or fish oil diets (Fritsche and Johnston, 1990). Although flaxseed and flaxseed oil and lig-nans have been shown to be beneficial, additional studies are needed to identify the mechanisms by which flaxseed or its components function to reduce prostate cancer. 

Jenkins D.E., Yu S.-F., Hornig Y.S., Purchio T., Contag P.R. (2003) In vivo monitoring of tumor relapse and metastasis using bioluminescent PC-3 M-luc-C6 cells in murine models of human prostate cancer. Clin Exp Metastasis20, 745-756. 

MS-based mass profiling combined with multivariate analysis identified platelet factor 4, a chemokine with prothrombolytic and antiangiogenic activities, as a diagnostically predictive protein in depleted serum of prostate cancer patients [99]. SELDI-TOF-MS was applied to the discovery of serum markers of bone metastasis in prostate cancer. Unique isoforms of serum amyloid A were identified in these patients. Machine-learning algorithms were used to identify these patients with a sensitivity and specificity of 89% [100],... 

Another factor that may be beneficial is physical activity, since it affects the immune function and antioxidant defenses, transit time of digestion, hormones, and body fat, and it improves energy balance. Therefore, it may have a protective effect on prostate cancer and it may even slow progression and metastasis (G14, H8, K7, 02, 03). In a 9-year follow-up study performed by Hartman et al., the relative risk for physical exercise in prostate cancer was compared with sedentary workers and found to be 0.6 (Cl = 0.4-1.0), 0.8 (Cl = 0.5-1.3), and 1.2 (Cl = 0.7-2.0) for occupational workers, walker/lifters, and heavy laborers, respectively. Except for heavy laborers, an inverse association was observed (RR = 0.7, Cl = 0.5-0.9) compared to men who were sedentary at work and leisure (H8). However, other studies indicate a positive association between vigorous exercise and prostate cancer Cl), and therefore further study is necessary to provide an activity optimum. Frequency, duration, intensity, type of exercise, and the period during a man s lifetime when exercise may be beneficial, must be investigated (02, 03). 

W4. Ware, J. L., Growth factor network disruption in prostate cancer progression. Cancer Metastasis Rev. 17,443 147 (1999). 

W7. Wikstrom, P., Stattin, P., Franck-Lissbrandt, I., Damber, J. E., and Bergh, A., Transforming growth factor beta 1 is associated with angiogenesis, metastasis, and poor outcome in prostate cancer. Prostate 37, 19-29 (1998). 

Gleave, M., Hsieh, J. T., von Eschenbach, A. C. and Chung, L. W. (1992). Prostate and bone fibroblasts induce human prostate cancer growth in vivo implications for bidirectional tumor-stromal cell interaction in prostate carcinoma growth and metastasis. J. Urol. 147, 1151-1159. 

Hall, S. J. and Thompson, T. C. (1997). Spontaneous but not experimental metastatic activities differentiate primary tumor-derived vs metastasis-derived mouse prostate cancer cell lines. Clin. Exptl. Metastasis 15, 630-638. 

Perez-Stable, C., Altman, N. H., Mehta, P. R, Deftos, L. J. and Roos, B. A. (1997). Prostate cancer progression, metastasis, and gene expression in transgenic mice. Cancer Res. 57, 900-906. 

Rabbani, S. A., Gladu, J., Harakidas, R, Jamison, B. and Goltzman, D. (1999). Over-production of parathyroid hormone-related peptide results in increased osteolytic skeletal metastasis by prostate cancer cells in vivo. Inti. J. Cancer 80, 257-264. 

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