phorbol/neoplasms

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Phorbol esters in seed oil of Jatropha curcas L. (saboodam in Thai) and their association with cancer prevention: from the initial investigation to the present topics.

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OBJECTIVE In 1988, we first reported the complete chemical structure of a new type of phorbol ester, abbreviated to DHPB, found in seed oil of Jatropha curcas L. (Saboodam in Thai) and its tumor-promoting activity on mouse skin. Although this seed oil contains toxic phorbol ester, it was planned to

Tumor-promoting phorbol esters induce angiogenesis in vivo.

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It has been hypothesized that tumor growth is dependent on the concomitant growth of its vascular supply, and thus agents that stimulate angiogenesis may help support tumor growth. Phorbol esters are potent tumor promoters that induce a variety of biochemical effects in cells, including activation

Retinoids inhibit the mitogenic activity of tumour-promoting phorbol esters on human lymphocytes.

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The tumour-promoting agents 12-0-tetradecanoylphorbol-13-acetate (TPA) and phorbol-12, 13-dibutyrate (PDB) I are potent mitogens for human peripheral blood lymphocytes. In contrast, the non-cocarcinogenic substance phorbol lacks lymphocyte-activating properties. Non-toxic levels of retinoic acid

Effects of structural changes on the tumor-promoting activity of phorbol myristate acetate on mouse skin.

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4a alpha-Phorbol-9,9a-didecanoate, 4a alpha-phorbol-9-myristate-9a-acetate, and phorbol-9-myristate-9a-acetate-3-aldehyde were tested for skin tumor-promoting activity by using 7,12-dimethylbenz(a)anthracene as the initiating agent. There were 30 female ICR/Ha mice/group, and tests were continued

Cytotoxic action of phorbol esters on human pancreatic cancer cells.

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We previously showed that phorbol esters are cytotoxic to human thyroid epithelial cells expressing a mutant RAS oncogene. Here we explore the generality of this finding using cells derived from pancreatic cancer, which, like thyroid, shows a high frequency of RAS mutation, but is a much greater

Inhibition of intercellular communication by tumor-promoting phorbol esters.

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Cocultures were established of mouse epidermal cells (HEL/37) and mouse fibroblast cells (PG-19) deficient in the enzyme hypoxanthine-guanine phosphoribosyltransferase. Metabolic cooperation between the cocultured cells was detected as labeling of PG-19 cells on incubation of cocultures with

Influence of tumor-promoting phorbol esters on the phosphorylation of membrane proteins in lymphocytes.

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Treatment of bovine lymphocytes with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) (10(-8) M) for as little as 5 min significantly alters the ability of membrane-particulate fractions to phosphorylate proteins using in situ protein kinases and exogenous [gamma-32P]ATP. After 20 min of treatment, the

Modulation of oxidant formation in mouse skin in vivo by tumor-promoting phorbol esters.

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The pathways of oxidant generation in mouse epidermis were investigated by 32P-postlabeling analysis of diastereomeric DNA adducts derived from oxidation of (7S,8S)-dihydroxy-7,8-dihydrobenzo(a)pyrene ((+)-BP-7,8-diol). The pattern of deoxynucleoside-3'-5'-bis-phosphate adducts in epidermal

Comparison of the biological activity of the tumor promotor phorbol myristate acetate and a metabolite, phorbolol myristate acetate, in the cell culture.

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Phorbolol myristate acetate, a metabolite of the tumor promotor phorbol muristate acetate in mouse skin, has one-fiftieth the potency of the parent molecule for the induction of cell division in stationary cultures of BALB/c-3T3 mouse embryo cells. Similarly, in a mixed cell culture assay devised

Tumor promoter phorbol-12-myristate-13-acetate induces poly(ADP)-ribosylation in fibroblasts.

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The tumor promoter phorbol-12-myristate-13-acetate (PMA) causes an increase in pol(ADP)-ribosylation in mouse and human fibroblasts via the intermediate formation of active oxygen. In contrast to poly(ADP)-ribosylation induced by the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine, de novo

Limb mesenchymal cells inhibited from undergoing cartilage differentiation by a tumor promoting phorbol ester maintain expression of the homeobox-containing gene Msx1 and fail to exhibit gap junctional communication.

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Tumor promoting phorbol esters are potent inhibitors of the chondrogenic differentiation of limb mesenchymal cells, but the mechanism by which these agents elicit their antichondrogenic effect is unknown. Here we report that limb mesenchymal cells inhibited from undergoing chondrogenesis by a tumor

Plasminogen activator induction and platelet aggregation by phorbol and some of its derivatives: correlation with skin irritancy and tumor-promoting activity.

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Phorbol and eight of its derivatives were investigated for their ability to stimulate the synthesis of the enzyme plasminogen activator in cultured chick embryo fibroblasts and to aggregate human blood platelets and have been assayed for tumor, promoting and skin, irritant activities. Over a range

Differential effects of bryostatin 1 and phorbol ester on human breast cancer cell lines.

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The effects of the protein kinase C (PKC) activators, phorbol ester 12-O-tetradecanoyl-13-phorbol acetate (TPA) and the marine natural product, bryostatin 1, on the growth and morphology of human breast cancer cell lines were examined. TPA (1 to 100 nM) inhibited growth of four of six cell lines by

Regulation of nucleoside transport by lipopolysaccharide, phorbol esters, and tumor necrosis factor-alpha in human B-lymphocytes.

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Nucleoside transport systems and their regulation in human B-lymphocytes have been characterized using the cell lines Raji and Bare lymphoma syndrome-1 (BLS-1) as experimental models. These cells express at least three different nucleoside transport systems as follows: a

Nonpromoting 12-deoxyphorbol 13-esters inhibit phorbol 12-myristate 13-acetate induced tumor promotion in CD-1 mouse skin.

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Prostratin and 12-deoxyphorbol 13-phenylacetate (dPP) form a new class of protein kinase C activators of unique biological activity. Although they bind to and activate protein kinase C, in mouse skin they either fail to induce typical phorbol ester (PMA) effects (e.g., hyperplasia) or induce only

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