Prostatic adenocarcinoma

Canene-Adams, K., B. L. Lindshield, S. Wang et al. 2007. Combinations of tomato and broccoli enhance antitumor activity in dunning r3327-h prostate adenocarcinomas. Cancer Res 67(2) 836-843. 

Prostate adenocarcinomas Prostate specific antigen (PSA) (25) Prostatic acid phosphatase (PAP)... 

Tables 8 and 9 show how some of the previously mentioned antibodies can distinguish between metastatic adenocarcinomas of unknown primaries in females and males, respectively. The panels are similar except for ERP (estrogen receptor protein), GCDFP-15, and S-100, which are used in females for their specificity for gynecologic tumors and PSA (prostatic specific antigen), used in males for its specificity for prostatic adenocarcinoma. These antibodies cannot absolutely distinguish among the tumor sources listed. However, they can guide pathologists and clinicians on which organs need to be further examined to determine the primary source of a metastatic tumor.

Mokhtari MJ, Motamed N, Shokrgozar MA. (2008) Evaluation of silibinin on the viability, migration and adhesion of the human prostate adenocarcinoma (PC-3) cell line. Cell Biol Int 32 888-892. 

Kim TG Hwi KK, Hung CS. (2005) Morphological and biochemical changes of andrographolide induced cell death in human prostatic adenocarcinoma PC-3 cells. In Vivo 19 551-557. 

Premenopausal use There is no indication for premenopausal use of raloxifene. Hepatic function impairment Raloxifene was studied, as a single dose, in Child-Pugh class A patients with cirrhosis and serum total bilirubin ranging from 0.6 to 2 mg/dL. Plasma raloxifene concentrations were approximately 2.5 times higher than in controls and correlated with total bilirubin concentrations. Safety and efficacy have not been evaluated further in patients with severe hepatic insufficiency. Carcinogenesis In long term carcinogenicity studies in animals there was an increased incidence of ovarian tumors, testicular interstitial cell tumors, and prostatic adenocarcinomas. 

Gupta S, Srivastava M, Ahmad N, et al. Over-expression of cyclooxygenase-2 in human prostate adenocarcinoma. Prostate 2000 42 73-78. 

Detection/staging/ follow-up of prostate adenocarcinoma Prevention of blood clots... 

Bjermer, and R. Henriksson. Effects of tobacco smoke on tumor growth and radiation response of dunning R3327 prostate adenocarcinoma in rats. Prostate 2000 42(4) 253-259. 

Fast neutrons were the first nonconventional radiation used in cancer therapy. Fast neutrons (a high-LET radiation) were introduced for the following radiobiological reasons (1) a reduction of the OER with increasing LET (2) a reduction in the difference in radiosensitivity related to the position of the cells in the mitotic cycle (3) and less repair and thus less clinical relevance of the different repair mechanisms. The best and clinically proven indications for fast neutrons are salivary gland tumors, locally advanced prostatic adenocarcinomas, and slowly growing, well-differentiated sarcomas. 

Salivary gland tumors and locally extended prostatic adenocarcinoma were proven to be an indication for fast neutrons. 

Prostatic Adenocarcinoma. For prostatic adenocarcinomas, their typical slow growth rate and low cycling fraction provide a logical radiobiological rationale for exploring neutrons (high LET) in the treatment of this disease. 

Figure 11 Clinical loco-regional control in patients treated with mixed (neutron/photon) beams or photons only (RTOG randomized trial) for locally extended prostatic adenocarcinoma. (From Ref. 34.)...

The third approach is the introduction of another type of radiation quality high-LET radiation. Clinical experience with neutrons has demonstrated that high-LET radiations are superior to low-LET radiations for some tumor types or sites. Fast neutrons were indeed the first high-LET radiations to be applied clinically (see Sec. 4.1). Although in the first studies they were applied in suboptimal conditions from a technical or dose distributions point of view, their advantage for some types of tumors is well established, particularly for slowly growing, well-differentiated tumors. Randomized trials have indeed shown their superiority over conventional photons for salivary gland tumors and prostatic adenocarcinomas. 

Myers, R. B., Srivasta, S., and Grizzle, W. E. 1995. Lewis Y antigen as detected by the monoclonal antibody BR96 is expressed strongly in prostatic adenocarcinoma. J. Urol. 753 1572-1574. 

Prostate Cancer 41,42, 45,44, 46,411 Progressive loss of annexins with increased histological stage. (Smitherman et al., 2004) Lehnigk et al., 2005) Annexin 1 expression reduced in prostatic adenocarcinoma and high-grade prostatic intraepithelial neoplasia (Kang et al., 2002 Patton et al., 2005) (Xin et al., 2003)... 

Patton, K.T., Chen, H.M., Joseph, L., and X.J. Yang, 2005, Decreased annexin I expression in prostatic adenocarcinoma and in high-grade prostatic intraepithelial neoplasia. Histopathology. 47(6) 597-601. 

McConkey, D. J., Lin, Y., Nutt, L. K., Ozel, H. Z. and Newman, R. A., 2000, Cardiac glycosides stimulate Ca2+ increases and apoptosis in androgen-independent, metastatic human prostate adenocarcinoma cells. Cancer Res 60, 3807-12. 

Byland, A., Zhang, J.X., Bergh, A., Damber, J.E., Widmark, A., Johansson, A., Adlercreutz, H., Aman, P., Shepherd, M J., and Hallmans, G. 2000. Rrye bran and soy protein delay growth and increase apoptosis of human LNCaP prostate adenocarcinoma in nude mice. Prostate 42, 304-314. 

M. Hussain. 2000. Phase II study of dolas-tatin-10 in patients with hormone-refractory metastatic prostate adenocarcinoma. Clin. Cancer Res. 6 4205-4208. 

Macdonald, J.M., Kurkanewicz, J., Dahiya, R., Espanol, M.T., Chang, L.-H., Goldberg, B., James, T.L., Narayan, P. (1993). Effect of glucose and confluency on phosphorus metabolites of perfused human prostatic adenocarcinoma cells as determined by 31P MRS. Magn. Reson. Med. 29, 244-248. 

N10. Noble, R. L., The development of prostatic adenocarcinoma in Nb rats following prolonged sex hormone administration. Cancer Res. 37, 1929-1933 (1977). 

D5. Damber, J. E., Landstrom, M., Bergh, A., and Tomic, R., The effects of castration, testosterone and oestrogen on epithelial and stromal growth and morphology of the Dunning (R3327H) prostatic adenocarcinoma. Scand. J. Urol. Nephrol. Suppl. 110, 145-148 (1988). 

D19. Dionne, C. A., Camoratto, A. M., Jani, J. P., Emerson, E., Neff, N., etal., Cell cycle-independent death of prostate adenocarcinoma is induced by the trk tyrosine kinase inhibitor CEP-751 (KT6587). Clin. Cancer Res. 4,1887-1898 (1998). 

E8. Esquenet, M., Swinnen, J. V., Heyns, W. and Verhoeven, G., LNCaP prostatic adenocarcinoma cells derived from low and high passage numbers display divergent responses not only to androgens but also to retinoids. J. Steroid Biochem. Mol. Biol. 62, 391—399 (1996). 

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