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1 e poorly differentiated phenotype in primary prostatic tumors.
2 es are likely to be highly effective against prostatic tumors.
3 ncer antigen 3 (PCA3) is highly expressed in prostatic tumors.
4 of caspase protein expression in the primary prostatic tumors analyzed.
5 n long-term regression of the injected human prostatic tumor and also of a distant uninjected tumor,
6 nin where it inhibits progression of primary prostatic tumor and also shows protective efficacy again
7 tected in the secretory epithelium of benign prostatic tumors and in primary and metastatic prostate
8 on of epithelial cells and stromal region in prostatic tumors, and (iii) detected in human blood.
9 stem was injected directly into prostates or prostatic tumors as a replication-incompetent adenovirus
10  by alteration in metabolic profile of TRAMP prostatic tumors as indicated by 6-fold (P = 0.016) incr
11 mmunohistochemistry analyses showed that the prostatic tumors as well as metastatic lesions expressed
12 tarvation-induced cell death using the human prostatic tumor cell line LNCap and NIH 3T3 fibroblasts,
13 hic tissue or in cultures of the LNCaP human prostatic tumor cell line.
14 vitro, differentiation of the LNCaP and PC3M prostatic tumor cell lines to a NE phenotype can be indu
15 tential was additionally demonstrated in rat prostatic tumor cell lines, and human cutaneous and uvea
16               We utilized androgen-dependent prostatic tumor cells to demonstrate that androgen exert
17 vivo occurs via induction of apoptosis among prostatic tumor cells.
18 uced in moderately and poorly differentiated prostatic tumors compared with well-differentiated prost
19  a potential mechanism underlying aggressive prostatic tumor development, which has been frequently o
20 es of prostate cancer using a model in which prostatic tumors established in nude mice from orthotopi
21 established adverse-effect profiles, against prostatic tumors for the treatment of advanced prostate
22 al stress fields in the prostate that impede prostatic tumor growth and limit its invasiveness.
23 ts suggest that neuroendocrine-like cells of prostatic tumors have the potential to enhance androgen-
24 ed development, proliferation, and growth of prostatic tumors in both TRAMP and LADY double TG mice.
25 D mice were first injected s.c. with a human prostatic tumor line, forming a skin tumor that produces
26 explanation for the existence of significant prostatic tumor mass despite a low-serum PSA.
27 h, and the formation of androgen-independent prostatic tumors may be because of misregulation of thes
28 he pattern of caspase-1 and -3 expression in prostatic tumors may have prognostic significance in dis
29                    Here we report that human prostatic tumors, neoplasias and certain pre-malignant l
30 hat p53 gene inactivation is rare in primary prostatic tumors, not essential to the development of pr
31 se studies suggest that benign and malignant prostatic tumors of mesenchymal origin may be distinguis
32 its downstream target genes were detected in prostatic tumors of the compound mice.
33 ect link between IFN-inducible molecules and prostatic tumor progression.
34 nces were observed in the mRNA expression in prostatic tumors relative to the normal gland for any of
35 bility may be an additional way of assessing prostatic tumor response to antiandrogen treatment.
36 data suggest that overexpression of SFRP1 by prostatic tumor stroma may account for the previously re
37 ount for the previously reported capacity of prostatic tumor stroma to provide a pro-proliferative pa
38 e adult prostate, and elevated expression in prostatic tumor stroma.
39                 Analysis of multiple primary prostatic tumor tissues as well as normal and tumor tiss
40 g permits differentiation of histopathologic prostatic tumor types.
41 ivo experiments, in mouse xenograft model of prostatic tumor, using EGCG-loaded NPs, with a model of
42 S: (a) has a potent antitumor effect against prostatic tumors via induction of apoptosis; and (b) inc
43 < or = .033), were inversely correlated with prostatic tumor volume (P =.037), and declined after pro