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Biomedical subjects

E M Rivera

Publications and source records attributed to E M Rivera.

At least 37 records · Page 2Linked to original sources
PubMed1985

Factors influencing differential growth of rat mammary tumor fragments and cells transplanted in gland-free and gland-containing mammary fat pads.

Transplants from eight primary tumors induced by 7,12-dimethylbenz(a)anthracene were placed into gland-free and gland-containing inguinal mammary fat pads of syngeneic female hosts. Samples were transplanted as 1 mm3 fragments or as cell suspensions of enzymatically dissociated tumors averaging 1.5 X 10(5) cells/ml. Similar differential growth patterns resulted from both types of transplants. In samples from two of eight tumors fragments produced more tumors than did dissociated transplants, regardless of fat pad condition. In one case dissociated transplants gave rise to more tumors than did fragments. Samples from two of eight tumors produced no differences in tumor growth from fragments and dissociated transplants. Samples from the remaining two showed low transplantability. Overall, no significant differences in tumor growth could be attributed to transplant treatment or fat pad condition. Gland-containing fat pads inhibited ductal outgrowth following transplantation while gland-free fat pads favored it. From the data, the greater the lability of the primary tumor, the greater the influence of the host microenvironment on the outgrowth potential of the tumor.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1982

Rat mammary tumors from carcinogen-induced nodules and their responsiveness to ovariectomy.

The research objective was to determine whether DMBA-induced rat mammary tumors derived from transplanted mammary nodules differ in ovarian-responsiveness from tumors originating randomly from in situ mammary parenchyma. Nodule-derived tumors were from hyperplastic alveolar outgrowths in mammary fat pads, which were either first generation outgrowths (primary nodule outgrowths) or generations 3-6 of a tumorigenic nodule line (nodule outgrowth T18). Tumors were induced in primary outgrowths by secondary exposure to DMBA in vivo or in vitro. The nodule line was not re-exposed to DMBA because of its high oncogenicity (80-85%). Despite the histological similarity of the tumor derivatives, primary nodule outgrowths and the nodule outgrowth line developed a higher proportion of ovarian-independent to ovarian-dependent tumors (1:3 and 3:4 respectively) than did in situ mammary tissues (1:9). These results are consistent with the observation that nodule outgrowths were themselves ovarian-independent.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1982

Proliferation of ductal outgrowths by carcinogen-induced rat mammary tumors in gland-free mammary fat pads.

The purpose of this study was to evaluate the gland-free mammary fat pad as a preferential site for transplantation of 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat mammary tumors, since previous studies indicated their frequent failure to grow when transplanted in ectopic sites. Accordingly, samples from 14 primary mammary tumors (9 randomly selected and 5 ovarian-independent) were transplanted into the inguinal pairs of gland-free mammary fat pads of syngeneic female Lewis rats (9-12 wk of age). Although the percentage of takes was high (88%), the growth and morphogenetic capabilities of the transplants were strikingly different. Whereas transplants of ovarian-independent tumors consistently developed palpable carcinomas, transplants of all but 1 of the tumors selected at random (most of which were presumably ovarian-dependent) gave rise mainly to apparently normal ductal and hyperplastic outgrowths. The growth behavior of the transplants could not be correlated with the presence or absence in the tumors of mononuclear cells of the immune system. Unless the mammary fat pad selected against the growth of tumor cells, it seemed that the main alternative to tumor formation by the transplants was the proliferation of nontumorous outgrowths. These results draw attention to differences in the phenotypic stability of primary mammary tumors induced by DMBA and open up for further study the question of whether these differences reflect their cellular heterogeneity or their potential to undergo differentiation.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1981

Organ culture passage enhances the oncogenicity of carcinogen-induced hyperplastic mammary nodules.

The purpose of this study was to determine whether culturing hyperplastic mammary nodules in hormone-free medium would enhance their oncogenicity following subsequent transplantation into mammary fat pads. The underlying hypothesis is that the proliferation of transformed cells within the nodules is inhibited by hormone-dependent normal cells also present in the nodules. Accordingly, both primary hyperplastic nodules and tissues from a hyperplastic outgrowth of a primary nodule were maintained as organ cultures for varying periods in hormone-free Medium 199. The results show that whereas noncultured nodules developed mammary tumors at an incidence of only 15%, those passaged in organ culture gave rise to mammary tumors at an incidence of 40 to 43%. This threefold enhancement in the oncogenicity of mammary nodules is interpreted to be due, at least in part, to a reduction in the normal mammary cell content of nodules. Consistent with this interpretation is the observation that cultured nodules gave rise to mammary outgrowths that were predominantly hyperplastic, whereas noncultured nodules generated outgrowths with varying proportions of hyperplastic and normal ductal mammary tissue.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1966

Stimulation by insulin of the formation of ribonucleic acid and protein by mammary tissues in vitro.

1. Insulin is one of the hormones that are essential for successful tissue culture of explants of the mammary glands of pregnant mice. We report here effects of insulin on RNA and protein formation by mammary tissue from pregnant mice and rats incubated in tissue-culture medium 199. 2. The incorporation of [(14)C]adenine over 3hr. into the RNA of explants of the mammary glands of pregnant mice was increased by an average of 68% when the medium contained 5mug. of insulin/ml. Under similar conditions the incorporation into the RNA of slices of the glands of pregnant rats was increased by an average of 61%. Incorporation into the RNA of slices from lactating rats was stimulated to a smaller extent. 3. Adipose tissue was separated from the glands of pregnant mice and the effect of insulin on the incorporation of adenine into its RNA was studied. In whole explants the incorporation of adenine, both with and without insulin, is almost entirely into the RNA of the mammary parenchyma and not of the adipose tissue. 4. Insulin also stimulated by 38% the incorporation of [(14)C]leucine over 3hr. into the proteins of slices of the glands of pregnant rats. It had no significant effect on slices from lactating rats. 5. Actinomycin D (10mug./ml.) decreased the incorporation of [(14)C]adenine into the RNA of slices of the glands of pregnant rats by an average of 97%. Though it also decreased the incorporation of [(14)C]leucine into the proteins by an average of 25%, the percentage stimulation by insulin of this incorporation remained unchanged.

Animals↗