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prostatic hyperplasia/tyrosine
L'enllaç es desa al porta-retalls
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[Expression of tyrosine phosphatase containing C-src homology SH-2 in benign prostate hyperplasia].
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OBJECTIVE
To explore the expression of tyrosine phosphatase containing C-src homology SH-2 (SHP-1 and SHP-2) in benign prostate hyperplasia.
METHODS
With En Vision two-step method, the expression of SHP-1 and SHP-2 was detected in 10 cases of normal prostate tissue, 30 cases of BPH, 20 cases of PIN,
PTPIP51 mRNA and protein expression in tissue microarrays and promoter methylation of benign prostate hyperplasia and prostate carcinoma.
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BACKGROUND
Protein tyrosine phosphatase interacting protein 51 (PTPIP51) shows a tissue-specific expression pattern and is associated with cellular differentiation and apoptosis in several mammalian tissues. Overexpression of the full-length protein enhances apoptosis. It is also expressed in
Effect of resveratrol and some other natural compounds on tyrosine kinase activity and on cytolysis.
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Resveratrol is a phytoalexin with several biological and pharmacological activities including the "French paradox". We investigated the effect of resveratrol on cytolytic activity by oxygen reactive species and on soluble and particulate tyrosine kinases from human placenta and human prostatic
Imatinib mesylate (Gleevec) as protein-tyrosine kinase inhibitor elicits smooth muscle relaxation in isolated human prostatic tissue.
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OBJECTIVE
To evaluate the mechanism of action of imatinib mesylate (Gleevec), a protein tyrosine kinase inhibitor on the human prostate with benign prostatic hyperplasia.
METHODS
Prostate samples were obtained from 16 patients with benign prostatic hyperplasia (mean age 68.3 ± 1.9 years), who had
Effect of a vitamin D3 analogue on keratinocyte growth factor-induced cell proliferation in benign prostate hyperplasia.
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Prostate enlargement and function is under the dual control of androgens and intraprostatic growth factors. They regulate, in concert, prostate cell proliferation and apoptosis. An increased signaling of both growth factors and androgens are supposed to underlie benign prostate hyperplasia (BPH),
Expression of a truncated form of the c-Kit tyrosine kinase receptor and activation of Src kinase in human prostatic cancer.
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A truncated form of the c-Kit tyrosine kinase receptor, originally identified in mouse haploid germ cells, is aberrantly expressed in human cancer cell lines of various origin. This alternative transcript originates in the 15th intron of the human c-kit gene. We have previously demonstrated that
[Benign prostatic hyperplasia and growth factors: mechanisms and hypotheses].
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The aetiology and pathogenesis of benign prostate hyperplasia (BPH) are still unresolved questions, although a number of hypotheses have been developed, most of which have still not been confirmed by experimentation. BPH has been regarded as a kind of adenoma, as a stromal disease, as the result of
Quantitative phosphoproteomics reveals the protein tyrosine kinase Pyk2 as a central effector of olfactory receptor signaling in prostate cancer cells.
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The prostate-specific G-protein-coupled receptor 1 (PSGR1) is an olfactory receptor specifically expressed in the prostate gland. PSGR1 expression is elevated both in benign prostatic hyperplasia tissue and in prostate cancer. Stimulation of PSGR1 by the odorant β-ionone leads to an increase in the
The Ron receptor tyrosine kinase positively regulates angiogenic chemokine production in prostate cancer cells.
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Overexpression of the Ron receptor tyrosine kinase has recently been shown in a wide variety of human cancers. However, no studies have examined Ron receptor expression or function during prostate tumorigenesis. In this study we report that Ron is highly expressed in human prostate adenocarcinoma
A tyrosine kinase profile of prostate carcinoma.
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Tyrosine kinases play central roles in the growth and differentiation of normal and tumor cells. In this study, we have analyzed the general tyrosine kinase expression profile of a prostate carcinoma (PCA) xenograft, CWR22. We describe here an improved reverse transcriptase-PCR approach that permits
Autocrine regulation of human prostate carcinoma cell proliferation by somatostatin through the modulation of the SH2 domain containing protein tyrosine phosphatase (SHP)-1.
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The present study was intended to gain additional information on the growth regulation of prostate by somatostatin (SRIF) and the intracellular events involved. The human prostate adenocarcinoma cell lines PC-3 and LNCaP produce SRIF and express subtypes 2 and 5 of SRIF receptors. The secretion of
Polymorphisms of fibroblast growth factor receptor 4 have association with the development of prostate cancer and benign prostatic hyperplasia and the progression of prostate cancer in a Japanese population.
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Fibroblast growth factor receptor 4 (FGFR4) is a member of a family of transmembrane receptors with ligand-induced tyrosine kinase activity. The Glycine (Gly) to Arginine (Arg) polymorphism at codon 388 (Gly388Arg), which encodes an amino acid in the transmembrane part of the FGFR4 gene, was
Protein tyrosine kinase 7 (PTK7) as a predictor of lymph node metastases and a novel prognostic biomarker in patients with prostate cancer.
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Protein tyrosine kinase 7 (PTK7) has been studied in various tumors, but its role in prostate cancer remains unknown. This study is aimed to investigate the prognostic and predictive significance of PTK7 in patients with prostate cancer. PTK7 expression was evaluated by real-time reverse
A small molecule agonist of EphA2 receptor tyrosine kinase inhibits tumor cell migration in vitro and prostate cancer metastasis in vivo.
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During tumor progression, EphA2 receptor can gain ligand-independent pro-oncogenic functions due to Akt activation and reduced ephrin-A ligand engagement. The effects can be reversed by ligand stimulation, which triggers the intrinsic tumor suppressive signaling pathways of EphA2 including
Evaluation of the fibroblast growth factor system as a potential target for therapy in human prostate cancer.
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Overexpression of fibroblast growth factors (FGFs) has been implicated in prostate carcinogenesis. FGFs function via their high-affinity interactions with receptor tyrosine kinases, FGFR1-4. Expression of FGFR1 and FGFR2 in prostate cancer (CaP) was not found to be associated with clinical
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