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proteinase inhibitor/neoplasms

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BACKGROUND It is thought that the quantitative imbalance between proteases and their inhibitors is a causative factor in invasion and metastasis of cancer cells. We previously reported on a number of androgen-dependent advanced prostate cancer (PCa) patients in which serum alpha2-macroglobulin
All malignant tumors shed cells into the circulation. The number of circulating tumor cells bears no relation to the extent of secondary growth. This is determined by the number of tumor cells that cross the vessel wall and implant in extravascular sites. The rate of cellular emigration is regulated
We have isolated a cDNA clone, designated GTI, by screening a tobacco genetic tumor cDNA library with a tumor-specific "subtracted" cDNA probe. The cDNA contained the entire coding sequence for a 94-amino-acid polypeptide that exhibited significant homology to members of the proteinase inhibitor I
The change in glycosylation of the two acute-phase proteins, alpha-1-proteinase inhibitor (API) and haptoglobin (Hp), in progressive ovarian cancer is different. This has been shown by monosaccharide analysis and lectin-binding studies of proteins purified from serum. In the glycan chains of API,

Serum alpha-1-proteinase inhibitor with abnormal properties in ovarian cancer.

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It was previously reported that sera from ovarian cancer patients contained abnormal forms of alpha-1-proteinase inhibitor (API) that predicted unresponsiveness to chemotherapy. These molecules were detected by extracting the sera with the fucose-specific lectin, lotus tetragonolobus, and analysing
Proteolytic enzymes could be very important in spread of cancer, but the role of the body's natural inhibitors of these enzymes in this process is unknown. One such inhibitor is the serum glycoprotein, alpha-1-proteinase inhibitor (API). In previous studies we showed that the fucose-specific lectin,

Anesthetic agents modify tissue proteinase inhibitor content and tumor behavior.

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Anesthetic agents may modify the tissue content of low molecular weight proteinase inhibitors (mol wt less than 50,000) and affect the colonization and proliferation of B16-F10 melanoma cells in lungs. Lungs of female mice exposed to halothane in oxygen had significantly greater low molecular weight
OBJECTIVE Photodynamic therapy (PDT) and inhibition of cathepsin B proteases by cystatin (cysteine proteinase inhibitor, CPI) are potential new tumour treatment modalities. We have investigated the efficacy of PDT and CPI alone and in combination on a solid mammary carcinoma transplanted into Wistar
The differential effects on primary tumor growth and on the formation of spontaneous pulmonary metastases have been determined for a series of proteinase inhibitors. The substances included the gold compounds, aurothioglucose and aurothiomalate, D(-)penicillamine, phosphoramidon and an egg-white

Are proteinase inhibitors potentially useful in tumor therapy?

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Within the last 15 years a vast literature has arisen, which associates increased levels of proteinase activity with most in vitro transformed malignant cells and many tumor cells in vivo. As a consequence, proteinase inhibitors have been widely proposed as potential candidates for therapeutic use.

Effect of proteinase inhibitor in experimental tumors.

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Aprotinin, a wide range proteinase inhibitor, was given alone to tumor-bearing mice and life span and several tumor growth parameters were recordered. Aprotinin showed anti-tumor effects in Hepatoma 22 and Lewis lung carcinoma, remaining ineffective in Sarcoma 37, Leukemia L1210 and Ehrlich ascitic
Amphibian venom-derived peptides have high potential in the field of anticancer drug discovery. We have isolated a novel Bowman-Birk proteinase inhibitor (BBI)-type peptide from the skin secretion of Pelophylax esculentus (PE) named PE-BBI, and evaluated its bio-functions and anti-cancer activity in
The concentration of stefin A (cystatin A in mice) was measured in animals with experimental tumors (LS lymphosarcoma, HA-1-hepatoma, and Lewis lung carcinoma) during effective antitumor therapy. In mice with these tumors serum concentrations of stefin A increased, while the concentration of
It has been proposed that a cysteine proteinase inhibitor (CPI) found in the ascitic fluid of Sarcoma 180 tumor-bearing mice is a kind of kininogen (Itoh, N., Yokota, S., Takagishi, U., Hatta, A., and Okamaoto, H. (1987) Cancer Res. 47, 5560-5565). The first 40 NH2-terminal residues and 54 residues
A thiol proteinase inhibitor (TPI) has been purified from the ascitic fluid of Sarcoma 180 tumor-bearing mice. The molecular weight of the inhibitor was estimated to be 67,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the substance inhibited papain, cathepsins B and L, but
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