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carcinogenesis/protease

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Secretory leukocyte protease inhibitor modulates urethane-induced lung carcinogenesis.

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Secretory leukocyte protease inhibitor (SLPI), 11.7 kDa serine protease inhibitor, is produced primarily in the respiratory tract, but it is often elevated in lung, head/neck and ovarian cancers. SLPI expression in relation to cancer progression, metastasis and invasion has been studied extensively

Estrogen-induced lysosomal proteases secreted by breast cancer cells: a role in carcinogenesis?

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In an attempt to understand the mechanism by which estrogens stimulate cell proliferation and mammary carcinogenesis, metastatic human breast cancer cell lines (MCF7, ZR75-1) were found to secrete a 52,000 dalton (52K) protein under estrogen stimulation. Following its purification to homogeneity,

Protease inhibitor-induced stabilization of p21(waf1/cip1) and cell-cycle arrest in chemical carcinogen-exposed mammary and lung cells.

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In previous studies, we have shown that human breast and lung carcinoma cells and mouse nontransformed type II lung cells fail to undergo cell-cycle arrest in G(1) phase in response to treatment with hydrocarbon carcinogens but rather accumulate in the S phase with damaged DNA. This situation may
The effect of the potent synthetic protease inhibitor [N,N-dimethylcarbamoylmethyl 4-(4-guanidinobenzoyloxy)-phenylacetate] methanesulfate (FOY-305) on skin carcinogenesis in ddY mice was examined over a total observation period of 105 days. Administration of 0.1% FOY-305 in the diet suppressed the

Cell Surface Human Airway Trypsin-Like Protease Is Lost During Squamous Cell Carcinogenesis.

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Cancer progression is accompanied by increased levels of extracellular proteases that are capable of remodeling the extracellular matrix, as well as cleaving and activating growth factors and receptors that are involved in pro-cancerous signaling pathways. Several members of the type II

Keratinocyte-specific onset of serine protease BSSP expression in experimental carcinogenesis.

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Malignant transformation of mouse skin by chemical carcinogens and tumor promoters, such as the phorbol ester 12-O-tetradecanoylphorbol-13-acetate, is a multistage process leading to the formation of squamous cell carcinomas. In an effort to identify target genes whose expression is associated with

Selective DNA-amplification induced by carcinogens (initiators): evidence for a role of proteases and DNA polymerase alpha.

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Inhibitors of DNA polymerase alpha (aphidicolin, phosphonoacetic acid, phosphonoformic acid) efficiently inhibit initiator-induced amplification of SV40 DNA sequences in the SV40-transformed Chinese hamster cell line CO631. Amplification is also inhibited by various protease inhibitors (antipain,

Induction of a novel Ca2+-dependent serine protease in rat liver treated with various promoters of liver carcinogenesis.

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The induction of a novel Ca2+-dependent protease in rat liver treated with various liver promoters, as well as its increase in preneoplastic lesions during liver carcinogenesis, was demonstrated. Six groups of male Fischer 344 rats (150 g body weight) were fed separately diets containing one of the

Inhibition of carcinogen-induced chromosomal aberrations by an anticarcinogenic protease inhibitor.

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It was hypothesized that chemicals- and radiation-induced carcinogenesis might require at least two specific chromosomal events that must coincide within a single target cell: (i) induction of chromosomal changes, possibly mutations, that are recessive and therefore latent in diploid somatic cells

Inhibition of oral carcinogenesis by a protease inhibitor.

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The effect of the Bowman-Birk inhibitor (BBI) and soybean trypsin inhibitor (SBTI) on experimental 7,12-dimethylbenz[a]anthracene [(DMBA) CAS: 57-97-6]-induced oral carcinogenesis in Syrian male hamsters was examined. All treatments were applied topically on both cheek pouches for 20 weeks, and the

Protease inhibitor suppression of colon and anal gland carcinogenesis induced by dimethylhydrazine.

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In the present study, we examined the ability of chymostatin, a highly specific inhibitor of chymotrypsin, to suppress dimethylhydrazine-induced colon carcinogenesis, and the dose-response relationship for an extract of soybeans containing the Bowman-Birk inhibitor (BBI) to suppress

Effects of various preparations of dietary protease inhibitors on oral carcinogenesis in hamsters induced by DMBA.

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We studied the ability of a soybean extract containing the Bowman-Birk protease inhibitor (BBI), referred to as BBI concentrate (BBIC), purified BBI (PBBI), and the chymotrypsin inhibitor from potatoes to suppress oral carcinogenesis in hamsters induced by 7,12-dimethyl-benz[a]anthracene (DMBA).

Prevention of carcinogenesis by protease inhibitors.

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Protease inhibitors are very effective in their ability to suppress carcinogenesis in many different in vivo and in vitro assay systems. One particularly effective protease inhibitor, the soybean-derived Bowman-Birk inhibitor, has been extensively studied in our laboratory. Our results have

Suppression of dimethylhydrazine-induced carcinogenesis in mice by dietary addition of the Bowman-Birk protease inhibitor.

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In the present study the effect of feeding the soybean-derived Bowman-Birk protease inhibitor (BBI) on dimethylhydrazine (DHM)-induced gastrointestinal tract and liver carcinogenesis in mice was examined. In this investigation we found the addition of 0.5 or 0.1% semipurified BBI or 0.1% purified

Promoter hypomethylation of protease-activated receptor 2 associated with carcinogenesis in the stomach.

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OBJECTIVE Trypsin acting at protease-activated receptor 2 (PAR2) contributes to a progression of malignant tumors. An abnormal DNA methylation has been recognized as an important molecular mechanism for the genesis of various types of cancers. We attempted to clarify the relationship between the
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