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1 on is altered in the carcinogenesis of human prostatic cancer.
2  and an immunocompetent mouse model of mouse prostatic cancer.
3  the management of the clinical evolution of prostatic cancer.
4  for patients with bone pain from metastatic prostatic cancer.
5 ves as potential agents for the treatment of prostatic cancer.
6  their potential utility in the treatment of prostatic cancer.
7 oor survival in patients with pancreatic and prostatic cancers.
8 C differ from those of the nonlethal primary prostatic cancers.
9 in lung, gastric, colorectal, pancreatic and prostatic cancers.
10  immunodeficient (SCID) mouse model of human prostatic cancer and an immunocompetent mouse model of m
11 ed by high levels of hormones (e.g. probably prostatic cancer and breast cancer).
12 gene is involved in the progression of human prostatic cancer and possibly lung and breast cancer.
13 est that CD44 is a metastasis suppressor for prostatic cancer and that decreased expression of the st
14 wn-regulated during the progression of human prostatic cancer and that this down-regulation does not
15 a potential role in breast cancer as well as prostatic cancer and will be the impetus for further stu
16  high selectivity for sensitive detection of prostatic cancer biomarkers spermine and spermidine in r
17 nfer increased risk for breast, ovarian, and prostatic cancers, but it is not clear why the mutations
18 on between birth weight and high stage/grade prostatic cancer cannot be excluded.
19 ffects of androgen on PCNA expression in the prostatic cancer cell line LNCaP.
20 me 16 into the highly metastatic Dunning rat prostatic cancer cell line, AT6.1.
21  this purpose, we used an androgen-dependent prostatic cancer cell line, LNCaP-FGC, as an in vitro mo
22 enic activity in cultures of the LNCaP human prostatic cancer cell line.
23  GBX2, are overexpressed in a panel of human prostatic cancer cell lines (ie., TSU-pr1, PC3, DU145, a
24 c hyperplasia specimen (BPH-1), and in three prostatic cancer cell lines (LNCaP, PC-3, and DU145).
25                           In addition, three prostatic cancer cell lines treated with recombinant mas
26 antisense GBX2 transfectants from both human prostatic cancer cell lines was inhibited by more than 7
27  expressed to different degrees in the human prostatic cancer cell lines.
28                                        LNCaP prostatic cancer cells are characterized by having a PTE
29 ogic levels of Ca2+ (i.e., >600 micromol/L), prostatic cancer cells are not contact inhibited by E-ca
30 defined (SFD) medium, what grows out are not prostatic cancer cells but basally derived normal transi
31  spontaneous metastatic ability of AT6.1 rat prostatic cancer cells by greater than 30-fold.
32  These findings suggest a mechanism by which prostatic cancer cells can achieve metastatic potential
33 t the growth rate and biological behavior of prostatic cancer cells can be altered to a more aggressi
34  of CK2alpha using pcDNA6-CK2alpha protected prostatic cancer cells from TRAIL-mediated apoptosis by
35                               We have tested prostatic cancer cells in culture for the presence of ch
36 owth of the normal transit-amplifying versus prostatic cancer cells is due to the differential effect
37 t R3327G), the androgen-stimulated growth of prostatic cancer cells occurred identically in both AR-n
38                        LNCaP cells are human prostatic cancer cells that have a frame-shift mutation
39           Indeed, exposure of radiosensitive prostatic cancer cells to low non-cytotoxic concentratio
40 an chromosomes into highly metastatic rodent prostatic cancer cells to map the location of a metastas
41 the proliferation of hormone-dependent human prostatic cancer cells were determined in vitro and in v
42 y, GBX2-overexpressing TSU-pr1 and PC3 human prostatic cancer cells were transfected with a eukaryoti
43 her, they may favor the metastatic spread of prostatic cancer cells without decreasing their growth p
44 n antisense C-FABP transcript into the PC-3M prostatic cancer cells yielded two transfectant lines: P
45                                           In prostatic cancer cells, but not in non-transformed cells
46 t metastatic dissemination of pancreatic and prostatic cancer cells.
47 iple signaling pathways for proliferation of prostatic cancer cells.
48 ation, invasiveness, and metastasis of human prostatic cancer cells.
49 ptor (AR) in the growth and the apoptosis of prostatic cancer cells.
50 ulate the proliferation of hormone-dependent prostatic cancer cells.
51 ignal-transducing capability, inhibits human prostatic cancer cells.
52 al cells but complete absence of staining in prostatic cancer cells.
53 y mAb225 inhibited the growth of DU145 human prostatic cancer cells.
54  small gap junctions in human pancreatic and prostatic cancer cells.
55 animals on test, the cumulative incidence of prostatic cancer development at 28 weeks of age in 16 un
56 gen ablation with Linomide enhances the anti-prostatic cancer efficacy compared to either monotherapi
57 ormone-related disorders, including advanced prostatic cancer, endometriosis, and precocious puberty.
58 is in stromal cells, as a survival factor of prostatic cancer epithelial luminal cells, and as a supp
59 varian, endometrial, breast, colorectal, and prostatic cancers exhibit increased endogenous fatty aci
60 reast, ovarian, endometrial, colorectal, and prostatic cancers express elevated levels of fatty acid
61      Human breast, ovarian, endometrial, and prostatic cancers express receptors that can mediate the
62 regulated in more than 70% of the 49 primary prostatic cancers from untreated patients.
63 EGFR) may contribute to androgen-independent prostatic cancer growth at both primary and metastatic s
64 lation therapy, more than 90% of the primary prostatic cancers had downregulation, with 60% having no
65 l therapeutic compounds for the treatment of prostatic cancer has been the goal of many researches.
66 d conventional radiation doses for localized prostatic cancer is feasible when delivered with three-d
67 nging their phenotype, and the few available prostatic cancer lines do not increase bone formation in
68  of theranostics and especially the field of prostatic cancer management.
69            In contrast, using four different prostatic cancer models (i.e., human PC-82, human LNCaP,
70 , similar to that encountered with end-stage prostatic cancer or a catastrophic stroke that leaves a
71  KAI1 occurs during the progression of human prostatic cancer, protein expression, mutation, and alle
72 utocrine systems operating in pancreatic and prostatic cancers, SCLC is exemplified by multiple, redu
73 certain highly metastatic Dunning R-3327 rat prostatic cancer sublines, such as AT6.1, without metast
74 c potential within the Dunning system of rat prostatic cancer sublines.
75 yase which has been used in the treatment of prostatic cancer, the steroidal compounds 20, 24, and 27
76 rm of CD44 is involved in the progression of prostatic cancer to a metastatic state.
77  and retardation of the growth of human PC-3 prostatic cancer tumors.
78 scuss the current understanding of AR in non-prostatic cancer types and summarize ongoing AR-directed
79 ependency of the normal prostate and of most prostatic cancers upon androgens and the fact that tumor
80                                              Prostatic cancers were mostly P-cadherin negative, but s
81  the androgen-responsive PC-82 and A-2 human prostatic cancers when grown in severe combined immunode
82  activity, and to identify patients with non-prostatic cancer who might benefit from targeting this p
83 lly, two different androgen-responsive human prostatic cancer xenograft models (i.e., PC-82 and A-2)
84  abilities against a series of rat and human prostatic cancer xenografts growing in vivo.
85 R22) and androgen-independent (CWR22R) human prostatic cancer xenografts, the acute response of CWR22
86 pressing the in vivo growth of rat and human prostatic cancer xenografts.