ライフサイエンスコーパス: prostatic carcinoma

1 g tissue to make a histological diagnosis of prostatic carcinoma.

2 monary metastases in experimental models for prostatic carcinoma.

3 n relation to its role in the development of prostatic carcinoma.

4 hyperplasia of the prostate and 16 cases of prostatic carcinoma.

5 ncers and 14 of 16 metastatic sites of human prostatic carcinoma.

6 is currently the tumour marker of choice for prostatic carcinoma.

7 wild-type AR expressed in hormone-dependent prostatic carcinomas.

8 trations may suppress cell growth of primary prostatic carcinomas.

9 n prostate differentiation and the growth of prostatic carcinomas.

10 i-class GST, are commonly hypermethylated in prostatic carcinomas.

11 al cells that is down-regulated or absent in prostatic carcinomas.

12 tal carcinomas, 9 endometrial cancers, and 3 prostatic carcinomas.

13 changes in matched PIN (48 foci), localized prostatic carcinoma (71 foci), and lymph node metastases

14 to define the role of IL-6 in the growth of prostatic carcinoma and benign prostatic hyperplasia (BP

15 2/neu are variably expressed or amplified in prostatic carcinoma and that such alteration may affect

16 three other histological origins, breast and prostatic carcinomas and osteogenic sarcoma, also demons

17 content of PC-3 cells (derived from p53 null prostatic carcinoma) and inhibits aneuploidy in these ce

18 e prostatic intraepithelial neoplasia (PIN), prostatic carcinoma, and metastases is not well-defined.

19 n the epithelial cells of high-grade PIN and prostatic carcinomas, and in cells of a perineural invas

20 was examined for evidence of inactivation in prostatic carcinomas, and results compared to those of a

21 rade prostatic intraepithelial neoplasia and prostatic carcinoma are consistent with recent evidence

22 model of advanced human androgen-independent prostatic carcinoma, as shown by the inhibition of prima

23 unction may contribute to the development of prostatic carcinomas, as well as other cancers.

24 study explores the mechanisms by which human prostatic carcinoma-associated fibroblasts (CAF) induce

25 rm tumors either by recombination with human prostatic carcinoma-associated fibroblasts (CAFs) or by

26 Human prostatic carcinoma-associated fibroblasts grown with in

27 sly shown that stromal cells associated with prostatic carcinoma can potentiate proliferation and red

28 liposomes) bound to the NRP-positive primary prostatic carcinoma cell line (PPC-1) but did not bind t

29 Treatment of human prostatic carcinoma cell line cultures with 5-azacytidin

30 The human prostatic carcinoma cell line LNCaP is sensitive to TNF-

31 a fourfold increase in the PSA mRNA level in prostatic carcinoma cell line LNCaP, in which the p53 pa

32 ponse of induction of apoptosis in the human prostatic carcinoma cell line LNCaP.

33 Here we show that the human prostatic carcinoma cell line PC3 was sensitive to TRAIL

34 a, is incorporated into cells from the human prostatic carcinoma cell line PPC-1, and shows no appare

35 of HUVEC mediated by medium conditioned by a prostatic carcinoma cell line.

36 vitro experiment was carried out using human prostatic carcinoma cell lines (LNCaP, which is androgen

37 te stromal (PrSt)] primary cell cultures and prostatic carcinoma cell lines (PC-3, LNCaP, and DU145).

38 s derivatives (I, II, VIII, and IX) in human prostatic carcinoma cell lines and found that Bis IX was

39 way is involved in Fas-mediated apoptosis in prostatic carcinoma cell lines and that, in addition to

40 athways leading to Fas-mediated apoptosis in prostatic carcinoma cell lines are intact, because apopt

41 Of six prostatic carcinoma cell lines examined (ALVA31, DU145,

42 gation induced apoptosis in two of six human prostatic carcinoma cell lines investigated, the apoptot

43 nverted the phenotype of Fas-resistant human prostatic carcinoma cell lines to Fas-sensitive and that

44 ification of the gene products that enable a prostatic carcinoma cell to metastasize should facilitat

45 These data show that C-FABP is increased in prostatic carcinoma cells and suppression of its express

46 tisense thymosin beta 15 constructs into rat prostatic carcinoma cells demonstrates that this molecul

47 de (VP-16) induced apoptosis in human DU-145 prostatic carcinoma cells in a time- and concentration-d

48 eads to suppression of the tumorigenicity of prostatic carcinoma cells in vivo and growth suppression

49 educed MMP-9 expression in metastatic murine prostatic carcinoma cells using a ribozyme.

50 The stimulatory effect of CM on prostatic carcinoma cells was significantly reduced by t

51 These data indicate that in prostatic carcinoma cells, a1 and a3 isoform populations

52 tubules and cytoskeletal proteins from human prostatic carcinoma cells, the incorporation of [14C]est

53 aling in androgen-sensitive and -insensitive prostatic carcinoma cells.

54 undergoing sex steroid ablation therapy for prostatic carcinoma, demonstrating an increase in circul

55 Human prostatic carcinoma DU-145 cells were exposed to glucose

56 icantly reduced the growth rate of the human prostatic carcinoma DU145 cells and inhibited their soft

57 m paired benign prostate tissue and adjacent prostatic carcinoma from three patients.

58 cal stage T1 or T2, Gleason score 2 to 7/10, prostatic carcinoma had outpatient, CT-based transperine

59 express functional GM-CSF receptors and that prostatic carcinomas have prominent GM-CSF receptor expr

60 Coincident with progression from prostatic carcinoma in situ to metastatic disease is an

61 The Dunning rat prostatic carcinoma is a model system where cell motilit

62 report demonstrates that the investigational prostatic carcinoma marker known as the prostate-specifi

63 expression of both subunits was observed in prostatic carcinomas metastatic to lymph node and bone.

64 In prostatic carcinoma, numeric chromosomal anomalies were

65 ificant antiproliferative effects on certain prostatic carcinoma (PC) cell lines, although the precis

66 indows of immunodeficient mice bearing human prostatic carcinoma (PC-3) in their flank.

67 For the 34 prostatic carcinomas, the C-FABP expression was remarkab

68 o the development of chemoresistant cells in prostatic carcinomas through the up-regulation of MRP-1.

69 Analysis of murine prostatic carcinoma tissues revealed the significant dec

70 d no clinical evidence of metastatic spread) prostatic carcinoma, treated by radiation.

71 sion of GKLF in tumor cells of colorectal or prostatic carcinomas was reduced or unaltered compared w

72 inactivation in the progression of clinical prostatic carcinomas, we assessed 67 tumors derived from

73 Libraries from mouse prostate and human prostatic carcinoma were constructed to test the PST (pe