putrescine/kanker

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Effects on tumor induction, growth, metastasis and histology of concurrent administration of putrescine and its metabolizing inhibitor alpha-difluoromethylornithine in nickel tumorigenesis in soft tissue.

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The effects of putrescine and the inhibitor of its biosynthesis alpha-difluoromethylornithine (DFMO) on nickel tumorigenesis in soft tissue was studied. Three groups of female F-344 rats were injected i.m. with 10 mg of nickel subsulfide (NiSS) in the right hind leg, after which one group was

Imaging prostate derived tumors with PET and N-(3-[18F]fluoropropyl)putrescine.

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Because of the high uptake of polyamines by the prostate and by prostate derived tumors, polyamines have been considered as potential imaging agents for metastatic prostate cancer. We now report the successful PET imaging of the Dunning R3327H prostatic carcinoma with

alpha-Difluoromethylornithine enhancement of 14C-putrescine uptake by an androgen-dependent prostatic tumor.

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Putrescine is a potential scanning agent for metastases of prostatic carcinoma. We examined the in vivo uptake of [14C]-putrescine by the Dunning R3327H Copenhagen rat prostatic tumor and by other tissues, and conclude that: The uptake of [14C]-putrescine by the tumor was higher than that of the

Aloe arborescens extract inhibits TPA-induced ear oedema, putrescine increase and tumour promotion in mouse skin.

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The ethyl acetate extract of the acetone-soluble Aloe arborescens fraction was found to inhibit 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ear oedema, putrescine increase and tumour promotion in mouse skin. Chromatographic analyses of this extract revealed that phenolic compounds such as

Growth-inhibitory effects of the chemopreventive agent indole-3-carbinol are increased in combination with the polyamine putrescine in the SW480 colon tumour cell line.

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BACKGROUND Many tumours undergo disregulation of polyamine homeostasis and upregulation of ornithine decarboxylase (ODC) activity, which can promote carcinogenesis. In animal models of colon carcinogenesis, inhibition of ODC activity by difluoromethylornithine (DFMO) has been shown to reduce the

Effect of D,L-alpha-difluoromethylornithine (DFMO) enhanced [3H]putrescine uptake on 9L tumor cell growth and colony forming efficiency.

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OBJECTIVE This study explored the possible use of D,L- alpha-difluoromethylornithine (DFMO) to enhance the uptake of [3H] putrescine in order to selectively kill brain tumor cells. METHODS Gliosarcoma cells (9L) were grown for 4 or 20 day periods in monolayer cultures with or without [3H] putrescine

Is [1-11C]putrescine useful as a brain tumor marker?

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Our experience with 11C-putrescine underscores the difficulty of finding a selective brain tumor tracer, uniquely incorporated by neoplastic glia or metastatic cells within brain, but not by the proliferating, nontransformed cells which constitute a normal pathophysiological reaction to various

Effects of methylacetylenic putrescine, an ornithine decarboxylase inhibitor and potential novel anticancer agent, on human and mouse cancer cell lines.

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Sensitivity of several human and mouse cancer cell lines to methylacetylenic putrescine (MAP) was evaluated using clonogenic, sulforhodamine B and cell counting assays. The effects of MAP on cell morphology, cell cycle phase distribution and changes in polyamine metabolism of xenografted MCF-7 and

Inhibition by putrescine of the induction of epidermal ornithine decarboxylase activity and tumor promotion caused by 12-O-tetradecanoylphorbol-13-acetate.

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The induction of epidermal ornithine decarboxylase (EC 4.1.1.17) (ODC) following topical application of the tumor-promoting agent 12-O-tetradecanoylphorbol-13-acetate (TPA) to mice can be inhibited by topical application of putrescine, the product of the enzyme. The degree of inhibition depended on

Macrophages induce resistance to 5-fluorouracil chemotherapy in colorectal cancer through the release of putrescine.

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The development of chemoresistance to 5-fluorouracil (5-FU) is a major obstacle for sustained effective treatment of colorectal cancer (CRC), with the mechanisms being not fully understood. Here we demonstrated that tumor associated macrophages (TAMs) became activated during treatment with 5-FU and

Putrescine-1,4-dicinnamide from Pholiota spumosa (Basidiomycetes) inhibits cell growth of human prostate cancer cells.

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Previously, it was isolated from the fruiting bodies of the gilled mushroom Pholiota spumosa (Basidiomycetes, Strophariaceae), putrescine-1,4-dicinnamide, a phenylpropanoid derivative conjugated with polyamine putrescine never isolated before as a natural compound. Recently, polyamine analogs that

Low-dose deoxycholic acid stimulates putrescine uptake in colon cancer cells (Caco-2).

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Deoxycholic acid (DCA) has long been implicated as tumour-promoting agent in the colon. Polyamines are necessary for cell proliferation, they are accumulated in high amounts in colon cancer cells, and their concentrations in the colonic lumen can reach millimolar levels. The aim of this study was to

Thirty years of polyamine-related approaches to cancer therapy. Retrospect and prospect. Part 1. Selective enzyme inhibitors.

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As soon as the natural polyamines (PAs), putrescine (Put), spermidine (Spd) and spermine (Spm), were recognized as ubiquitous constituents of eukaryotic cells, their involvement in growth-related processes attracted particular interest. The high activities of ornithine decarboxylase (ODC) and

Pharmacological and dietary agents for colorectal cancer chemoprevention: effects on polyamine metabolism (review).

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Chemoprevention is the long-term use of different chemical agents, both synthetic and natural, to prevent or delay the onset of disease. Since colorectal cancer has a significant environmental component, it is an ideal disease in which to evaluate the potential benefits of chemopreventive agents.

Tumor angiogenesis and polyamines: alpha-difluoromethylornithine, an irreversible inhibitor of ornithine decarboxylase, inhibits B16 melanoma-induced angiogenesis in ovo and the proliferation of vascular endothelial cells in vitro.

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alpha-Difluoromethylornithine (DFMO), an irreversible inhibitor of ornithine decarboxylase, inhibited B16 melanoma-induced angiogenesis in chick embryo chorioallantoic membrane and subsequently the growth of the tumor on the chorioallantoic membrane. These inhibitions were reversed by exogenous

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