prostatic neoplasms/tyrosine

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Inhibitors of tyrosine kinase inhibit the production of urokinase plasminogen activator in human prostatic cancer cells.

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Urokinase-type plasminogen activator (uPA) seems to be an important protease in prostate cancer invasion, and tyrosine phosphorylation is thought to play a role in the regulation of its production. The amount of uPA was measured with a synthetic peptide substrate after treatment with various

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

The invasive behaviour of prostatic cancer cells is suppressed by inhibitors of tyrosine kinase.

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Proteolytic enzymes, and especially urokinase plasminogen activator (uPA), play an important role in tumour invasion and metastasis. Previously we demonstrated that the production of urokinase plasminogen activator (uPA) was decreased by several tyrosine kinase inhibitors (TKI) in two prostatic

Tyrosine kinase inhibitors alter adhesivity of prostatic cancer cells to extracellular matrix components.

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Tyrosine kinase inhibitors (TKIs) are thought to have potential as a new generation of anti-cancer drugs. Since invasiveness, the main characteristic of malignant behaviour, is believed to depend on altered cell-matrix interactions, we investigated the effect of two potent TKIs, genistein and

Effect of an EGF-R selective tyrosine kinase inhibitor and an anti-androgen on LNCaP cells: identification of divergent growth regulatory pathways.

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BACKGROUND The effect of an EGF-R selective tyrosine kinase (EGF-RTK) quinazoline inhibitor ZM252868 was determined on the androgen-sensitive human prostatic tumour cell line LNCaP, which can also respond via the EGF-R-regulated growth pathway for cell proliferation. Potential interaction or

Microwave assisted synthesis of tyrosine protected gold nanoparticles for dual (colorimetric and fluorimetric) detection of spermine and spermidine in biological samples.

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In this work, tyrosine-protected gold nanoparticles (Tyr-Au NPs) were fabricated by one-step reduction of Au3+ ion using Tyr as a reducing and capping agent under microwave irradiation. The Tyr-Au NPs were successfully used as a dual probe for colorimetric and fluorescence turn-on assays of spermine

Synergistic antiproliferative and apoptotic effects induced by epidermal growth factor receptor and protein kinase a inhibitors in human prostatic cancer cell lines.

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Our results revealed that the blockade of epidermal growth factor receptor (EGFR) tyrosine kinase and protein kinase A (PKA) signaling pathways by specific inhibitors (PD153035 and Rp-cAMPs) leads to a synergistic inhibition of EGF- and serum-stimulated growth of human prostatic cancer cells (LNCaP,

Association of biliary glycoprotein with protein tyrosine phosphatase SHP-1 in malignant colon epithelial cells.

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Biliary glycoprotein (Bgp) is a member of the immunoglobulin superfamily and the carcinoembryonic antigen family. Previous studies have shown that Bgp functions as an intercellular adhesion molecule and a canalicular bile salt transporter. Moreover, we and others demonstrated that Bgp can inhibit

Urokinase plasminogen activator receptor (uPAR) expression is reduced by tyrosine kinase inhibitors.

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Previously we reported that tyrosine kinase inhibitors (TKI) produced a reduction in uPA expression in prostatic cancer cells, and that TKI-treated cells were less invasive compared to untreated cells. Nevertheless, no change in cell migration was observed when TKI-treated cells were supplied with

Multiple responses to EGF receptor activation and their abrogation by a specific EGF receptor tyrosine kinase inhibitor.

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BACKGROUND Epidermal growth factor receptor (EGF-R) autophosphorylation is essential for its intracellular mitogenic signaling via the MAPK pathway and for interaction in other cellular processes. Inhibition of this activity in tumor cells that predominantly utilise EGF-R therefore offers an

Differential sensitivity of human prostatic cancer cell lines to the effects of protein kinase and phosphatase inhibitors.

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We investigated the effect of protein kinase and phosphatase inhibitors on the growth of six human prostatic cancer cell lines: DU145, PC3, ND1, LNCaP, ALVA31 and JCA1. We studied okadaic acid and sodium orthovanadate as serine/threonine and tyrosine protein phosphatase inhibitors, respectively, and

Direct inhibitory effect of somatostatin on the growth of the human prostatic cancer cell line LNCaP: possible mechanism of action.

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The effects of somatostatin-14 (S) on the proliferation of the human prostatic cancer cell line (LNCaP, lymph node carcinoma of the prostate) and on the amount of proteins secreted by these cells have been studied. LNCaP cells were treated for 3 days with different doses of S. The hormone

Growth factors in steroid-responsive prostatic tumor cells.

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Androgens stimulate the growth of prostatic carcinoma, possibly by modulating the activity of locally expressed growth factors. Recently, we have shown that an LHRH (or LHRH-like) system exerting an inhibitory action on cell proliferation is present in the human androgen-dependent prostatic tumor

Tumor antigen and acid phosphatase isoenzyme in prostatic cancer.

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Plasma and prostatic fluid from man, dog, and baboon were measured for carcinoembryonic antigen (CEA) by a radioimmunoassay technique. No CEA was detected in plasma, prostatic fluid, or seminal fluid in 12 dogs and three baboons. Elevated CEA (less than 2.5 ng/ml) was found in 13 of 20 human

PET with O-(2-18F-Fluoroethyl)-L-Tyrosine in peripheral tumors: first clinical results.

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O-(2-18F-Fluoroethyl)-L-Tyrosine (18F-FET) PET has shown promising results in brain tumor diagnosis. The aim of this prospective study was to evaluate 18F-FET PET in comparison with 18F-FDG PET in patients with peripheral tumors. METHODS Forty-four consecutive patients with suspected malignant

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