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S Mondal

Publications and source records attributed to S Mondal.

At least 55 records · Page 3Linked to original sources
PubMed1980

Probabilistic view of the transformation of cultured C3H/10T1/2 mouse embryo fibroblasts by 3-methylcholanthrene.

When C3H/10T1/2 cells are treated with a given concentration of a chemical carcinogen, the transformation frequency can vary over 4 orders of magnitude, depending primarily upon the number of cells plated. To explain this phenomenon, we have developed a probabilistic theory of the formation of transformed foci in this system. We define p1 as the probability that a cell will be activated by carcinogen treatment, p2 as the probability per cell generation that an activated cell will be transformed, and p3 as the probability per cell generation that an activated cell will be deactivated. The equation we have derived: log (F/N) = log [2p1p2(1 -- p3)/2(1 -- p3) -- 1]+ n log (1 -- p3) describes focus formation; F is mean number of loci per dish after carcinogen treatment, N is number of cells in a dish at confluence, and n is number of cell generations to confluence. This equation has been verified experimentally; p3 = 0.24 and p1p2 = 3.8 X 10(-6) at a single concentration of 3-methylcholanthrene. This relationship explains previously inexplicable effects of cell density on transformation frequency.

Animals↗
PubMed1980

Inhibition of induced differentiation of C3H/10T 1/2 clone 8 mouse embryo cells by tumor promoters.

C3H/10T 1/2 cells were induced to differentiate into muscle cells by treatment with 5-azacytidine, and the effects of tumor promoters, nonpromoters, and inhibitors of tumor promotion on this induced differentiation were investigated. Cell morphology was dramatically changed within 30 min after treatment with phorbol ester-related tumor promoters and mezereine but not with other tumor promoters. There was a good correlation between the tumor-promoting activity of the compounds and their inhibitory action on differentiation except in case of phenobarbital; this promoter of liver carcinogenesis did not inhibit differentiation. Inhibitors of tumor promotion, dexamethasone, fluocinolone acetonide, retinoic acid, and antipain, also inhibited the 5-azacytidine-induced differentiation. When the cells were treated after induction of differentiation with 12-O-tetradecanoylphorbol-13-acetate, a potent tumor promoter, and simultaneously with one of those inhibitors of tumor promotion, the inhibitory action of 12-O-tetradecanoylphorbol-13-acetate was not affected. From these facts, it is evident that using a single phenomenon produced by one class of tumor promoter as a criterion for screening environmental tumor promoters is not justifiable.

Animals↗
PubMed1980

Effect of 12-O-tetradecanoylphorbol-13-acetate on the morphology and growth of C3H/10T1/2 mouse embryo cells.

The effects of the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) on the morphology and growth properties of C3H/10T1/2 clone 8 cells were examined. The morphology of these cells was changed within 30 min following treatment with 0.1 microgram of TPA per ml; they became smaller and refractile with long beady processes. Such changes were observed in both logarithmic and confluent cultures and lasted about 72 hr. Subsequent treatments were much less effective in inducing these changes. Scanning electron microscopy showed cell retraction and rounding as the most significant immediate effects of TPA treatment; many cells remained partially rounded 48 hr afterwards. Long-term surface modifications ascribable to TPA treatment were not detected. TPA had only minor effects on the growth of cultured C3H/10T1/2 cells in the presence of 10% fetal calf serum. Slight increases in plating efficiencies and saturation densities were generally observed in the presence of TPA but not with the related non-tumor-promoting compound phorbol. The cells grew slowly in 1% fetal calf serum and demonstrated serum batch-dependent alterations in their growth properties when exposed to TPA. Under conditions that produce doubling times of 70 hr or greater, TPA, but not phorbol, reduced the doubling time to about 50 hr. Saturation densities were also increased by TPA in 1% fetal calf serum. The effects of TPA on the growth of an oncogenically transformed variant of C3H/10T1/2 were quite different. While minimal effects of TPA were observed quite different. While minimal effects of TPA were observed when transformed cells were treated in the presence of 10% total calf serum, TPA treatment in 1% fetal calf serum significantly inhibited cell growth.

Animals↗
PubMed1979

Establishment of epithelial cell lines from adult mouse regenerating liver.

A simple technique for developing epithelial cell lines from regenerating mouse liver has been described. Twenty-one epithelial cell lines have been developed and can be divided into four groups according to their morphology. All these near diploid cell lines have the capacity to metabolize diverse classes of chemical carcinogens (3-methylcholanthrene, 2-acetylaminofluorene, dimethylnitrosamine and aflatoxin B1) to cytotoxic metabolites. It is not yet possible to determine which ones of these cell lines originated from hepatocytes. Studies are in progress to further characterize and to use these cell lines as lethally irradiated feeder layers for cell-mediated activation of various classes of chemical carcinogens and mutagens with C3H/10T1/2 mouse embryo fibroblasts as indicator cells.

2-Acetylaminofluorene↗
PubMed1979

Sporotrichosis.

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Female↗
PubMed1978

Enhancement of oncogenesis in C3H/10T1/2 mouse embryo cell cultures by saccharin.

Impure and pure samples of saccharin (2 milligrams per milliliter) did not produce oncogenic transformation of C3H/10T1/2, clone 8, mouse embryo fibroblasts. However, after treatment of the cells with a nontransforming initiating dose (0.1 microgram per milliliter) of 3-methylcholanthrene, continuous treatment with either sample of saccharin (100 micrograms per milliliter) led to significant transformation. It is concluded that in this system saccharin is a cocarginogen, probably functioning as a promoting agent that is 1000-fold less active than the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate.

Animals↗
PubMed1978

Effect of doxycycline on transmission of Vibrio cholerae infection among family contacts of cholera patients in Calcutta.

Doxycycline was used among the family contacts of hospitalized cholera patients in Calcutta to determine its effectiveness in controlling transmission of V. cholerae infection. A total of 137 such contacts were given a single oral dose of doxycycline in graded doses according to age. A similar group of 139 contacts received a single dose of multivitamins as placebo. All 276 contacts were examined bacteriologically daily for 10 days for the presence of V. cholerae in their stools. The results showed that doxycycline was effective in significantly reducing the load of V. cholerae infection for up to 5 days following treatment.

Adolescent↗
PubMed1978

Enhancement of X-ray transformation by 12-O-tetradecanoyl-phorbol-13-acetate in a cloned line of C3H mouse embryo cells.

A phorbol ester promoting agent, 12-O-tetradecanoyl-phorbol-13-acetate, enhances X-ray transformation in vitro in a two-stage fashion similar to that shown previously for ultraviolet radiation and chemical carcinogens. In studies with a mouse embryo-derived cell line (C3H/1OT 1/2 clone 8), there were clear interactive effects between X-radiation and 12-O-tetradecanoylphorbol-13-acetate. These were particularly marked when a minimally transforming X-ray dose (50 or 100 rads) was followed by 12-O-tetradecanoylphorbol-13-acetate treatment beginning either immediately after the radiation exposure or 48 to 96 hr later.

Animals↗
PubMed1978

Ultraviolet light in the oncogenic transformation of cultured C3H/10T1/2 mouse embryo cells.

Skin tumors are produced in rats, mice, and humans by exposure to UV light. We developed a mouse embryo fibroblast line C3H/10T1/2, which can be transformed by chemical carcinogens, X-irradiation, UV radiation, and oncornavirus. When we irradiated these cells with 10, 25, 50, 100, 150, or 200 ergs/mm2 of UV light, neither transformation nor cytotoxicity was observed at the two lower doses. When the irradiated cells were cultured in medium containing 0.1 micrograms TPA/1 ml (a potent tumor promoter) starting from 0-120 hours after irradiation, a high frequency of transformation was always produced. When the cells were initiated with subeffective concentrations of 0.1 micrograms MCA/ml followed by UV radiation at different intervals, no transformation occurred; however, these initiated cells were transformed after TPA treatment. When we treated the cells with multiple exposures to UV light, no transformation occurred then nor when the cells were treated with TPA followed by UV irradiation at different intervals. Thus UV in our system acts as a pure initiator in the two-stage process of oncogenic transformation.

Animals↗
PubMed1977

Effects of promoters on DNA synthesis in C3H/10T1/2 mouse fibroblasts.

The synthesis of DNA has been studied by autoradiography and by measurements of tritiated thymidine ([3H]TdR) incorporation in cultured C3H/10T1/2 mouse embryo fibroblasts. The cells were first treated with 3-methylcholanthrene as an initiator and then with promoters according to schedules that produce oncogenic transformation. The levels of 3-methylcholanthrene used did not affect the growth or [3H]TdR incorporation of the cells. Treatment during the log phase of growth with 12-O-tetradecanoyl-phorbol-13-acetate, phorbol didecanoate, or 4alpha-phorbol didecanoate produced a transient inhibition of [3H]TdR incorporation with the maximum at 12 hr after treatment. This resulted in a temporary delay of growth followed by recovery of the normal cell-doubling time. Phorbol did not produce these effects, suggesting that the inhibition of DNA synthesis is associated with the process of promotion. Although treatment of the cells with 12-O-tetradecanoyl-phorbol-13-acetate during stationary phase resulted in a 2- to 3-fold stimulation of [3H]TdR incorporation, multiple treatments spanning log and stationary phases were found to be necessary for promotion.

Animals↗
PubMed1976

Oncogenic transformation of C3H/10T1/2 clone 8 mouse embryo cells by halogenated pyrimidine nucleosides.

Oncogenic transformation has been induced in vitro in the C3H/10T1/2 clone 8 line of mouse cells by exposure to 5-fluoro-2'-deoxyuridine (FUdR) or 5-fluorouracil. This transformation is both dose and time dependent and can be markedly decreased by simultaneous exposure of the cells to thymidine. The transformation induced by 5-fluorouracil is probably due to its intracellular conversion to FUdR or its monophosphate. Transformation by FUdR was found to be cell cycle dependent with maximum sensitivity to transformation occurring in early S phase. Cell lines that produced sarcomas in antithymocyte-treated syngeneic mice were isolated from FUdR-transformed cultures. Trifluorothymidine, 5-bromo-2'-deoxyuridine, and 5-iodo-2'-deoxyuridine induced no transformed foci in the C3H/10T1/2 clone 8 cell line. Thus, not all mutagens produce oncogenic transformation nor does the lack of mutagenicity, as classically measured, completely exclude the possibility that a given agent is oncogenic. Also, there was no evidence of the "switch on" of oncornaviral information in the FUdR-transformed cell lines.

Animals↗