�ber leuk�mogene und immunosuppressive Wirkungen von Phorbol bei AKR-M�usen

Gericke, D; Kovac, W; Hecker, Erich

doi:10.1007/bf00304057

Cited by 8 publications

(5 citation statements)

References 4 publications

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“…In AKR/J mice, phorbol treatment did not affect the pattern of spontaneous (viral) leukaemia development: analogous to the results of Gericke, Kovac and Hecker (1974), who failed to induce leukaemias by i.p. phorbol administration in their AKR subline, in which spontaneous leukaemia incidence is extremely low.…”

Section: Discussionsupporting

confidence: 82%

Smooth-muscle-associated contractile protein in renal mesenchymal tumour cells and in transformed cells from DMN-injected rats

Toh¹,

Hard²,

Cauchi³

et al. 1976

Br J Cancer

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Summary.-Phorbol, the unesterified parent alcohol of the skin promoter TPA, was administered i.p., twice weekly, throughout the lifetime of mice of 7 inbred strains: males and females of AKR/J, C3Heb and BALB/c, and females of SJL/J, DBA/2, SWR and C57BL. A striking difference in strain response was observed, with a pronounced leukaemogenic effect in SWR, a significant shortening of the latent period for spontaneous reticulum cell sarcomas (RCNB) in SJL/J, and no demonstrable effect in the other strains. When mice of 3 of the above-mentioned strains (SWR, SJL/J and AKR/J) were thymectomized prior to the beginning of phorbol treatment, different patterns of response were again observed. Thymectomy did not influence the leukaemia incidence in SWR mice, slightly inhibited RCNB development in SJL/J mice and converted phorbol into a leukaemogenic agent for AKR/J mice.

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Section: Discussionsupporting

confidence: 82%

Smooth-muscle-associated contractile protein in renal mesenchymal tumour cells and in transformed cells from DMN-injected rats

Toh¹,

Hard²,

Cauchi³

et al. 1976

Br J Cancer

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“…In view of these data, it does not appear surprising that phorbol did not act as a. virus inducer in AKR mice (20).…”

Section: Discussionmentioning

confidence: 86%

Tumor initiators and promoters in the induction of Epstein—Barr virus

Hausen

Bornkamm

Schmidt

et al. 1979

Proc. Natl. Acad. Sci. U.S.A.

213

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The effect of various tumor initiators and promoters on induction of persisting Epstein-Barr virus (EBV) in different lines of lymphoblastoid cells was analyzed. Neither five polycyclic aromatic hydrocarbons, amongst them potent tumor initiators (e.g., 7,12-dimethylbenz[a]anthracene), nor the potent (ultimate) liver carcinogen N-acetoxy-N-2-acetylamino-fluorene induced EBV. A series of compounds, representing three classes of tumor-promoting diterpene esters (e.g., 12-O-tetradecanoylphorbol-13-acetate), efficiently induced EBV in persistently infected cells. The concentration required for maximal induction ranged between 0.5 and 100 nM. Some nonpromoting diterpenes (phorbol, 4alpha-phorbol-12,13-didecanoate, and ingenol) did not induce EBV. However, the nonpromoters, resiniferatoxin and 12-deoxyphorbol-13-decatrienoate, were effective, whereas anthralin, a tumor promoter, did not induce EBV. In three lines of EBV genome-carrying cells (Raji, NC-37, and RPMI 64-10) only abortive induction was noted, leading exclusively to synthesis of early antigen. In cells of lines with low spontaneous virus release (P3HR-1, B95-8, and QIMR-Wil), upon treatment with tetradecanoylphorbol acetate, approximately 20-40 times more viral DNA was recovered as compared to untreated controls. Viral DNA from tetradeca-noylphorbol acetate-induced cultures revealed the same restriction endonuclease cleavage pattern as viral DNA obtained from noninduced cells. Within 10 days after induction, release of infectious virus increased approximately by one order of magnitude. Prostaglandins, reported to be released after treatment with tumor promoters, were ineffective in virus induction under the conditions tested.

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“…1), suppresses a distinctive function of two categories of cells considered major par ticipants in natural antitumor defense, i.e., the tumoricidal capacity of macrophages and of NK cells [27], Remarkably enough, phorbol ( fig. 1), the polyfunctional diterpene par ent of TPA, exhibited neither leukemogenic nor immunosuppressive activities in AKR mice [11] nor did it suppress the natural cel lular antitumor activity of macrophages [27].…”

mentioning

confidence: 99%

Tumor-Promoting Diterpene Esters Prevent Macrophage Activation and Suppress Macrophage Tumoricidal Capacity

et al. 1982

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The efficacy of varied diterpene ester type tumor promoters in suppressing the acquisition as well as the manifestation of cytolytic activity by macrophages was investigated. These mechanisms, believed to be basic to natural antitumor resistance, were markedly suppressed not only by the phorbol ester, TPA, but also by several other tumor promoters of the polyfunctional diterpene ester type covering tigliane, ingenane, and daphnane derivatives. The promoters were particularly effective in preventing the lymphokine-induced enhancement of natural cytolytic activity in resting macrophages. Moreover, the same promoters suppressed the manifestation of cytotoxicity by previously activated macrophages. Their influence on the effector phase was less pronounced than on the activation phase. In sharp contrast, typical solitary carcinogens of the polycyclic aromatic hydrocarbon type exerted little or no activity in the macrophage test systems. Since TPA had already been shown to suppress the natural killer activity in vitro and to abrogate host tumor resistance in vivo, the present findings lend further support to the interpretation that tumor promoters, apart from directly stimulating the outgrowth of transformed cells, may function via interference with natural antitumor effector systems.

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�ber leuk�mogene und immunosuppressive Wirkungen von Phorbol bei AKR-M�usen

Cited by 8 publications

References 4 publications

Smooth-muscle-associated contractile protein in renal mesenchymal tumour cells and in transformed cells from DMN-injected rats

Smooth-muscle-associated contractile protein in renal mesenchymal tumour cells and in transformed cells from DMN-injected rats

Tumor initiators and promoters in the induction of Epstein—Barr virus

Tumor-Promoting Diterpene Esters Prevent Macrophage Activation and Suppress Macrophage Tumoricidal Capacity

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