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Biomedical subjects

D Medina

Publications and source records attributed to D Medina.

At least 199 records · Page 11Linked to original sources
PubMed1978

Effect of chemical carcinogen treatment on the immunogenicity of mouse mammary tumors arising from hyperplastic alveolar nodule outgrowth lines.

The experiments reported herein examined the effects of chemical carcinogen treatment of precursor hyperplastic alveolar nodules on the immunogenicity of subsequent mammary tumors in mice. The results of in vitro immunogenicity assays were compared with those of in vivo transplantation resistance tests. This comparison demonstrated that the in vitro assays predicted qualitatively and quantitatively the results from the in vivo test. In addition, the data suggested that the immunogenicity of a tumor depends on events occurring during the development of precursor hyperplastic alveolar nodules rather than during the development of subsequent mammary tumors.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

Mammary tumor virus oncogenesis and tumor immunogenicity in three sublines of the C3H mouse.

Mammary tumorigenesis and mammary tumor transplantation immunogenicity have been studied and compared in three sublines of the C3H strain: in standard mammary tumor virus (MTV-S)-infected C3H/He mice; in MTV-S-infected C3H/Ki mice; and in MTV-S-free C3Hf/He mice. The age at the appearance of the first tumor, the growth rate of the tumors in their first transplant generation, and the immunogenicity of each tumor in syngeneic female recipients have been determined for the first tumor to appear in each of 25 breeding females from each of the three sublines. Two statistically significant trends were evident among the tumor characteristics compared in the three sublines: (a) an early appearance of tumors was related to the presence of the MTV-S. The genetically dissimilar sublines, C3H/He and C3H/Ki, both infected with the MTV-S, developed mammary tumors at an average age of about 10 months, 11 months before MTV-S-free C3Hf/He mice; (b) the tumor characteristics of immunogenicity and growth stimulation were related to host genetic factors. The genetically similar sublines, C3H/He and C3Hf/He, developed similar proportions of immunogenic and growth-stimulating mammary tumors; the genetically divergent C3H/Ki subline developed tumors that were not immunogenic and tended to be strongly growth stimulating.

Age Factors↗
PubMed1978

Concanavalin A-induced agglutinability of normal, preneoplastic, and neoplastic mouse mammary cells.

The concanavalin A (Con A)-induced agglutinability of normal, preneoplastic, and neoplastic mouse mammary epithelial cells was examined. Cells freshly dissociated from normal mammary glands, hyperplastic alveolar nodules, or primary mammary adenocarcinomas by collagenase digestion in the presence of bovine serum albumin were strongly agglutinated by low concentrations of Con A. After short-term culture in vitro, however, cells from all three types of tissue were only weakly agglutinated by Con A, as measured by both suspension and hemadsorption assays. By comparison, cells of three established mammary tumor culture lines agglutinated strongly in the presence of the lectin. Treatment of the normal, preneoplastic, and neoplastic mammary cells in primary cultures with either trypsin or collagenase had little or no effect on their agglutinability, whereas hyaluronidase significantly increased their reactivity. Studies with fluorescein-tagged Con A indicated that all three cell types were capable of binding the lectin. The results were consistent with previous evidence suggesting that neoplastic transformation of mouse mammary epithelial cells is not manifested in vitro by several of the alterations in growth patterns, intercellular interactions, and surface properties that usually accompany transformation of fibroblastic cells.

Animals↗
PubMed1978

Differential response of cultured mouse mammary cells of varying tumorigenicity to cytochalasin B.

Cultured BALB/c mouse mammary gland epithelial cells of varying oncogenic potential in vivo have been examined for their ability to multinucleate in the presence of cytochalasin B (CB). Highly tumorigenic cell lines derived from mammary tumors with hormonal, viral, or chemical carcinogen etiologies were extensively multinucleated when cultured in CB-supplemented medium. Normal mammary gland cells from either pregnant or lactating animals were predominantly mono- or binucleate under comparable conditions. At low passage levels after cloning, cell lines derived from a chemical carcinogen-induced mammary tumor were weakly oncogenic and remained largely mono-, or binucleated when cultured in CB-supplemented medium. At higher cell passage levels, both the ability to produce tumors in vivo and the degree of multinucleation in CB-supplemented medium increased dramatically with the clonal cell lines. Thus, the response of cultured mouse mammary gland epithelial cells to CB in vitro may be useful as a marker of the oncogenic potential of such cells.

Animals↗
PubMed1977

Angiogenesis: a marker for neoplastic transformation of mammary papillary hyperplasia.

Mouse mammary papillomas elicit new formation of vessels when transplanted onto the rabbit iris. This angiogenic capacity is a property of carcinomas but not of the resting mammary gland. In mouse papillary hyperplasias, however, this property appears much earlier than any morphological or clinical sign of carcinoma. A test for angiogenic capacity may reveal a step in the progression toward clinical malignancy and thus could be used to screen for neoplastic potential of hyperplastic epithelium in biopsy tissues.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1977

Tumor formation in preneoplastic mammary nodule lines in mice treated with nafoxidine, testosterone, and 2-bromo-alpha-ergocryptine.

The tumor potentials of five preneoplastic mammary nodule lines were examined in BALB/cCrgl mice treated with either nafoxidine, an estrogen antagonist; 2-bromo-alpha-ergocryptine, a prolactin suppressant; or testosterone. The inhibitory effect of any of the three agents was dependent on the individual nodule line and was not correlated with the effects of ovariectomy. Nafoxidine inhibited tumor formation only in nodule line D2; testosterone inhibited tumor formation in lines C3 and C4; and 2-bromo-alpha-ergocryptine failed to inhibit tumor formation in any of the nodule lines. These results provided information on the range of responses of mouse preneoplastic mammary tissues to a variety of antihormone treatments and suggested that responses to ovariectomy need not be correlated with responses to specific antihormone treatments.

Animals↗
PubMed1977

Systemic effect of benign and malignant mammary tumors on the spin-lattice relaxation time of water protons in mouse serum.

The spin-lattice relaxation time (T1) for water protons in sera was significantly (P less than 0.001) elevated above that for normal sera in mice bearing benign ductal papilloma and malignant mammary carcinoma. Serum T1 values did not differ significantly in mice with ductal hyperplasia or preneoplastic alveolar nodules. Elevated serum T1's could not be explained on the basis of serum iron levels or serum protein concentrations. This was the first report of a "systemic effect" of serum T1 elevation by a benign tumor.

Animals↗
PubMed1977

Comparison of the growth properties in vitro and transplantability of continuous mouse mammary tumor cell lines and clonal derivatives.

Five continuous mouse mammary tumor cell lines and 12 clonal derivatives have been established from tumors arising in BALB/c or C3H mice either spontaneously or in response to viral (mammary tumor virus), hormonal (17 beta-estradiol), or chemical [7,12-dimethylbenz(alpha)anthracene] stimuli in vivo. The cell lines were examined for the following in vitro growth parameters:plating efficiency, saturation density, population-doubling times, colony formation on plastic surfaces, and anchorage-independent growth in methylcellulose. The majority of the mammary tumor cell lines were transplantable in syngeneic, immunocompetent mice and gave rise to tumors composed of epithelial cells. There was no growth parameter in vitro which invariably correlated with tumorigenicity in vivo. Most of the mammary tumor cell lines appeared to produce C-type virus. Only one, a C3H derivative, appeared to respond to stimulation by glucocorticoids with the enhanced production of B-type virus. Analysis of the growth properties exhibited in culture by transformed mammary epithelial cells revealed marked differences from those previously reported for transformed fibroblasts.

Animals↗
PubMed1977

Enhancement of mammary tumor formation in mice by a cytostatic drug, melphalan.

Melphalan (L-phenylalanine mustard), a cytostatic drug used in treatment of human breast cancer, was injected into mice bearing preneoplastic hyperplastic alveolar nodule mammary outgrowth line D2. Melphalan, doses of either 2.5 or 5.0 mg/kg, markedly enhanced tumor formation in its mammary nodule outgrowth line. Samples of nodule outgrowths in untreated mice produced 13% tumors by 9 months after transplantation, whereas nodule outgrowths in melphalan-treated mice produced 57 and 85% mammary tumors in the lower and higher dose groups, respectively.

Animals↗
PubMed1976

Mammary gland as a morphological end point in carcinogenesis studies.

The murine mammary tumor system is characterized by the presence of intermediate preneoplastic mammary cell populations. The intermediate mammary cell populations are characterized as either alveolar hyperplasias or ductal hyperplasias. The most frequently encountered preneoplastic cell population is the hyperplastic alveolar nodule, which has been extensively characterized with respect to its biological and hormonal properties. While the alveolar hyperplasias are seen predominantly in mice infected with the mammary tumor virus, ductal hyperplasias are seen primarily in mice treated with chemical carcinogens. Both types of lesions can serve as morphological end points for carcinogenesis studies in the mammary gland.

Animals↗
PubMed1976

Mammary tumorigenesis in chemical carcinogen-treated mice. IV. Induction of mammary ductal hyperplasias.

BALB/cCrgl, C57BL/Ki, and (C57BL/Ki X DBAf)F1 mice were treated with 7,12-diemthylbenz[a]anthracene (DMBA) or urethan to determine conditions that would induce a high frequency of ductal hyperplasias in the mammary gland. Among virgin BALB/c mice treated with either 3.0 or 4.0 mg DMBA, ductal hyperplasias and mammary tumors were present in 50% and 31% of the mice, respectively. These ductal hyperplasias were characterized by intraluminal epithelial hyperplasia and capped by endbud-like structures that appeared abnormal. Hyperplastic alveolar nodules were not seen. Most mammary tumors were adenocarcinomas rather than the adenocanthomas observed in DMBA-treated, pituitary isograft-bearing BALB/c mice. The predominant mammary lesions in urethan-treated, pituitary isograft-bearing C57BL and (C57BL X DBAf)F1 mice were terminal duct (lobular) hyperplasias characterized by intraluminal epithelial hyperplasia; the urethan-induced mammary tumors were a mixture of adenocarcinomas (36%), adenoacanthomas (5%), and fibroadenomas (59%). The induction by chemical carcinogens of intraductal hyperplasias in a relatively high incidence, with associated mammary neoplasms, provides a system for study of the process of tumor progression in lesions similar to suspected high-risk lesions occurring in human breast cancer.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1976

Mammary tumorigenesis in chemical carcinogen-treated mice. VI. Tumor-producing capabilities of mammary dysplasias in BALB/cCrgl mice.

Two types of mammary dysplasias occurring in 7,12-dimethylbenz[a]anthracene (DMBA)-treated BALB/cCrgl mice were transplanted into the cleared mammary fat pads of syngeneic mice for an assessment of their growth behavior and tumor potentials. Keratinized nodules, numerous in DMBA-treated, pituitary isograft-bearing BALB/cCrgl mice, produced primarily ductal outgrowth in control mice and very few tumors (7%) 56 weeks after transplantation. Such dysplasias transplanted into mice bearing pituitary isografts exhibited lobuloalveolar development and produced a higher incidence of tumors (32%). Hyperplastic alveolar nodules (HAN), though relatively rare in DMBA-treated BALB/cCrgl mice, produced lobuloalveolar outgrowth in control mice and had a 100% tumor incidence. Four HAN outgrowth lines were developed by serial transplantation of samples of the nodule outgrowths. The tumor potentials of these nodule lines in intact controls and ovariectomized mice was determined over several transplant generations. The tumor potentials of two of the three nodule lines were decreased in the absence of ovarian hormones. However, the growth of 23 mammary tumors derived from these nodule lines and of nine derived from in situ primary tumors was unaffected by the absence of the ovary. These results, along with those published previously, suggest that mammary tumors in chemical carcinogen-treated mice arise from several precursor populations. These preneoplastic populations comprise both alveolar and ductal hyperplasias.

9,10-Dimethyl-1,2-benzanthracene↗