ライフサイエンスコーパス: prostatic tumor

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1 ncer antigen 3 (PCA3) is highly expressed in prostatic tumors.

2 e poorly differentiated phenotype in primary prostatic tumors.

3 es are likely to be highly effective against 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 es of prostate cancer using a model in which prostatic tumors established in nude mice from orthotopi

20 established adverse-effect profiles, against prostatic tumors for the treatment of advanced prostate

21 ts suggest that neuroendocrine-like cells of prostatic tumors have the potential to enhance androgen-

22 ed development, proliferation, and growth of prostatic tumors in both TRAMP and LADY double TG mice.

23 D mice were first injected s.c. with a human prostatic tumor line, forming a skin tumor that produces

24 explanation for the existence of significant prostatic tumor mass despite a low-serum PSA.

25 h, and the formation of androgen-independent prostatic tumors may be because of misregulation of thes

26 he pattern of caspase-1 and -3 expression in prostatic tumors may have prognostic significance in dis

27 Here we report that human prostatic tumors, neoplasias and certain pre-malignant l

28 hat p53 gene inactivation is rare in primary prostatic tumors, not essential to the development of pr

29 se studies suggest that benign and malignant prostatic tumors of mesenchymal origin may be distinguis

30 ect link between IFN-inducible molecules and prostatic tumor progression.

31 nces were observed in the mRNA expression in prostatic tumors relative to the normal gland for any of

32 bility may be an additional way of assessing prostatic tumor response to antiandrogen treatment.

33 data suggest that overexpression of SFRP1 by prostatic tumor stroma may account for the previously re

34 ount for the previously reported capacity of prostatic tumor stroma to provide a pro-proliferative pa

35 e adult prostate, and elevated expression in prostatic tumor stroma.

36 Analysis of multiple primary prostatic tumor tissues as well as normal and tumor tiss

37 g permits differentiation of histopathologic prostatic tumor types.

38 ivo experiments, in mouse xenograft model of prostatic tumor, using EGCG-loaded NPs, with a model of

39 S: (a) has a potent antitumor effect against prostatic tumors via induction of apoptosis; and (b) inc

40 < or = .033), were inversely correlated with prostatic tumor volume (P =.037), and declined after pro

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