Search PubMed⌕ Search

Biomedical subjects

D Medina

Publications and source records attributed to D Medina.

At least 217 records · Page 12Linked to original sources
PubMed1976

Microcytotoxicity assay of immune responses to non-mammary tumor virus-induced, preneoplastic, and neoplastic mammary lesions in BALB/c mice.

Using a microcytotoxicity assay we have studied the immune responses to the preneoplastic, hyperplastic alveolar nodule (HAN) lines D1 and D2 and to the mammary tumors arising spontaneously from them in BALB/c mice. Lymph node cells (LNC) from mice bearing HAN implants, or from mice whose implants had been removed greater than 1 week prior to testing, failed significantly to inhibit survival of HAN cells in culture. Specific inhibition of HAN cells was found, however, in 9 of 28 experiments with LNC from mice whose implants had been removed within the week of testing, and not with LNC from sham-operated controls. On the other hand, increased survival of HAN cells was also seen with LNC from sensitized, as opposed to normal, mice. This was more frequent for tests with D1 than with D2 HAN cells (38 versus 9%) and when the LNC donors were still bearing HAN IMPLANTs (60% of tests versus 27% when implants removed). Following sensitization by implantation and subsequent removal of D1 or D2 tumors, LNC-mediated inhibition of tumor cell survival, specific for each tumor, was found in about 25% of the tests. Increased survival of tumor cells, however, was seen in 30 to 40% of the tests. This increased survival cross-reacted between D1 and D2 tumors and between D1-D2 and mammary tumor virus-induced tumors, but not between D1-D2 and chemically induced mammary tumors or fibrosarcomas. Increased survival could be blocked by sera from sensitized mice. In contrast to mammary tumor virus-induced mammary lesions, the immune responses to D1 and D2 HAN lines and tumors are "weak" and indeed perhaps stimulate hyperplastic and neoplastic cell survival.

Animals↗
PubMed1976

Preneoplastic lesions in murine mammary cancer.

The current model for murine mammary tumorigenesis indicates that discrete, morphologically identifiable preneoplastic lesions precede and give rise to mammary tumors. The hyperplastic alveolar nodule is the primary lesion that precedes and gives rise to mammary tumors in mice infected with the mammary tumor virus (Bittner) or its variants. In mice fed 7,12-dimethylbenzanthracene or urethan, hyperplastic alveolar nodules are present but infrequent, and the major mammary dysplasias present are ductal hyperplasias. The ductal hyperplasias can be divided into four general morphological types: (a) simple terminal duct hyperplasia; (b) lobular hyperplasia; (c) papillary hyperplasia; (d) end-bud hyperplasia. All types of ductal hyperplasias are characterized by intraductal epithelial hyperplasia and have been shown to give rise to mammal adenocarcinomas in situ or by transplantation into the mammary gland-free fat pads of syngeneic mice. Our current hypothesis is that murine mammary cancer can evolve through one of several intermediate stages. The intermediate stages can be either alveolar or ductal hyperplasias. The latter resemble, in many instances, ductal lesions seen in human breast cancer.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1975

Nuclear magnetic resonance studies on human breast dysplasias and neoplasms.

The ability of nuclear magnetic resonance (NMR) spectroscopy to distinguish normal, diseased non-neoplastic, and neoplastic human breast tissues was investigated with T1 and T2 relaxation times used. The results indicated that NMR relaxation times could distinguish between the mean values of breast neoplasms and other diseased or normal tissues, with P values less than 0.001. Given a single sample, the probability of classifying it nonneoplastic or carcinoma could be accomplished with 85% confidence. For human breast tissues, the relaxation time T2 may be more discriminating that T1. These results support the view that the use of NMR spectroscopy in cancer detection may be of significant value and warrants considerable more interest and effort to determine the beneficial applications and limits of this technology.

Adenocarcinoma↗
PubMed1975

Unlimited division potential of precancerous mouse mammary cells after spontaneous or carcinogen-induced transformation.

Serial transplantation of normal mouse mammary gland in young, isogenic hosts results in progressive loss of division potential, and the transplant line is eventually lost. This is interpreted as an expression of senescence at the cell and tissue level, and it inevitably occurs even though experimental conditions for growth are judged to be optimal. An indefinite extension of mammary growth span can be accomplished by transformation of these normal cells into precancerous cell types, which grow as a benign tissue but which may, however, occasionally undergo a second transformation into a malignant carcinoma. All precancerous tissues tested displayed unlimited growth potential, regardless of whether they occurred spontaneously, or were induced by oncogenic viruses or by administration of chemical carcinogens. Precancerous tissues of both ductal and lobuloalveolar morphology grew continuously. These results indicate that release from cell aging, as measured by the acquisition of unlimited growth potential, is associated with the precancerous state per se, and occurs as an early event in the transition from normal to malignant mammary cells.

Adipose Tissue↗
PubMed1975

Hormone dependence and estradiol receptors in the D series of mammary nodule outgrowth lines and tumors.

Preneoplastic mammary nodule outgrowth lines were examined for their ability to grow and produce tumors in ovariectomized BALB/c mice. In addition, these nodule outgrowth lines and tumors derived from them were investigated for cytoplasmic estrogen receptor proteins by qualitative and quantitative techniques. Early ovariectomy, performed within 4 weeks after transplantation, slightly delayed but did not permanently block the ability of three different nodule lines to completely fill the fat pad with nodule tissue. Ovariectomy performed later than 4 weeks after transplantation or adrenalectomy performed early or late had no effect on nodule growth. Neither early nor late ovariectomy or adrenalectomy had an effect on the maintenance of the nodule alveolar phenotype. Ovariectomy performed 3 weeks after transplantation had little effect on the tumor potential of the low oncogenic line D1 or the high oncogenic line D2. Samples of nodule outgrowths transplanted from ovariectomized mice responded to a chemical carcinogen in a similar manner, as did nodule outgrowths transplanted from control experiments. Thus, the altered hormonal environmenment in ovariectomized mice apparently did not select for subpopulations of nodule cells with altered tumorigenic potentials. The ovarian independence of the nodule lines and tumors derived from them was correlated with a very low level of cytoplasmic estrogen receptor. These results, along with other data, illustrate the nature of the independence on ovarian hormonal control for tumorigenesis in these mammary tumor virus-free nodule lines.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1972

Distinction between the preneoplastic and neoplastic state of murine mammary glands.

We have, using nuclear magnetic resonance spectroscopy, measured the relaxation times and diffusion coefficient of water protons in primary mammary adenocarcinomas of mice. In our biological model, three morphological stages were defined: (a) mammary gland tissue from pregnant mice, (b) preneoplastic nodules, and (c) neoplastic tissue. It was found that neoplastic tissues could be distinguished from normal and prenoeplastic tissue. Spin-spin and spin-lattice relaxation times and the diffusion coefficient of water protons are increased in the neoplastic tissue relative to mammary gland tissue from pregnant mice and preneoplastic nodule tissue.

Adenocarcinoma↗