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At least 145 records · Page 8Linked to original sources
PubMed1981

Mammary tumorigenicities of three chemically induced mouse kidney cell lines in syngeneic female hosts.

Three chemically induced, mammary tumour virus (MMTV) and leukemia virus (MuLV) producing, baby mouse kidney (BMK) cell lines derived from respectively strains BALB/c (-/HeA and -/CrglA) and C57BL/LiA were investigated for their mammary tumour (MT) evoking potentials in syngeneic female hosts. An i.p. inoculated virus-enriched fraction from A3 cells (BALB/c/HeA) had a similar oncogenic effect as i.p. and s.c. inoculated whole A3 cells. The average MT ages were reduced in all 3 groups. Cell lines BBM (BALB/c/CrglA) and BB (C57BL/LiA) were tested as i.p. inoculated whole cells. Again, the average MT age was reduced in thus treated BALB/c/Crgl females. In the case of C57BL/LiA the percentage of animals with MT was strongly increased in the BB cell inoculated group (1 MT in control group). Bioassay results corrected for intercurrent death cases (including leukosis) were statistically significant. It is concluded that the endogenous MMTV variants of the 3 mouse (sub-)strains are virulent MT evoking viruses in autologous hosts when they are induced.

Animals↗
PubMed1991

Functional abnormality of glucocorticoid receptor in Shionogi carcinoma 115 cells as evidenced by gene transfer experiments.

The assay systems for steroid receptor functions in steroid-sensitive cells (SC-3 cells) were developed in which hormone-responsive element linked to a reporter gene [chloramphenicol acetyl transferase (CAT) gene] was transfected by the electroporation technique. Stimulation with androgen of SC-3 cells transfected with mouse mammary tumor virus promoter-CAT gene (MMTV-CAT) resulted in clear enhancement of CAT activity, whereas glucocorticoid required abnormally high concentrations to obtain significant stimulation. The simultaneous addition of glucocorticoid surprisingly inhibited androgen-induced CAT activity in SC-3 cells, whereas glucocorticoid and androgen acted together synergistically to activate CAT activity in T 47D cells. When SC-3 cells were cotransfected with the expression vector of human glucocorticoid receptor (GR) gene, inhibition with glucocorticoid of androgen-enhanced CAT activity was abolished. These results would suggest that SC-3 cells contain functionally abnormal GR.

Animals↗
PubMed2000

Genetically engineered mouse models of mammary intraepithelial neoplasia.

Foci of atypical mammary epithelium have been associated with breast cancer in many species including mouse and man. The advent of targeted genomics has led to the creation of numerous genetically engineered mice (GEM) which display focal atypical lesions associated with mammary cancer. Some early lesions in GEM have a remarkable morphological similarity to pre-cancers in humans. While the malignant potential of atypical foci have been thoroughly documented in the non-GEM by tissue transplantation, a review of the literature reveals that precursor lesions in GEM remain incompletely described and only partially documented. Their validation as appropriate models of human breast preneoplasia awaits classical transplantation studies. Here, we review the literature characterizing early lesions of GEM models of mammary cancer, discuss the principles of the Focality, Atypia, and Association and present an introduction of mammary transplantation for model Validation.

Animals↗
PubMed1978

Detection of viral proteins in mouse mammary tumors by immunoperoxidase staining of paraffin sections.

An indirect immunoperoxidase method is described, which can readily detect viral antigens in paraffin sections of primary, transplanted, and metastatic mammary tumors of mice. In addition to having the obvious advantage of not being limited to fresh specimens, immunoperoxidase staining of paraffin sections proved to be superior in many respects when compared with immunofluorescence and frozen sections. Immunoperoxidase staining of paraffin sections is permanent and provides the kind of histological detail required for precise cytological identification and localization with light microscopy. All of 25 tumors and 4 metastatic lesions showed evidence of glycoprotein gp52 as well as other mouse mammary tumor viral antigens. The pattern and intensity of the stain were related to the degree of histologic differentiation of the tumor. Wide variations in expression of viral antigens by individual malignant cells were observed within the same tumor.

Animals↗
PubMed1996

Effects of two dietary fat levels and four dietary linoleic acid levels on mammary tumor development in Balb/c-MMTV mice under ad libitum feeding conditions.

The relationship between dietary fat intake (level and type) and the development of breast cancer in humans is a matter of concern in Western society. A high fat intake is associated with a greater mammary cancer risk in humans and in animal models. Higher intake of polyunsaturated fatty acids in humans shows little or no association with mammary tumor development in epidemiologic surveys. From literature data, it appears that a higher intake of polyunsaturated fatty acids (linoleic acid) is related to an increase in mammary tumorigenesis in animal studies in which chemical carcinogens like dimethylbenz[a]anthracene are used as tumor initiator. Mostly the latency period of these chemically induced models in rather short. In this study, the Bald/c-MMTV (mouse mammary tumor virus) mouse strain was chosen as an animal model: MMTV leads to tumor initiation, and dietary factors influence tumor promotion over a relatively long latency period. The mice were fed diets with two fat concentrations: a high [36% of energy (en%)] or low (16 en%) fat level; fat was isocalorically replaced by carbohydrates (cornstarch). At both dietary fat levels, linoleic acid was given at four levels: 2, 3, 6, and 10 en%. Linoleic acid-rich fat was isocalorically replaced by oleic acid-rich fat. The diets were consumed ad libitum over a lifetime. Animals were euthanized as soon as mammary tumor diameter was > or = 1 cm or when the animals were in a poor clinical condition. The incidence of mammary tumors at 18 months was significantly higher in one group only: 36 en% fat and 2 en% linoleic acid. This group also showed the shortest mean latency period for mammary tumor development. Mean mammary tumor incidence was higher and mean onset time shorter in the four high-fat groups than in the low-fat groups. No (linear) dose-response relationship between dietary linoleic acid concentration and mammary tumor incidence and latency period was observed. This indicates that a higher dietary linoleic acid intake does not increase the incidence or shorten the latency period of breast cancer in the Balb/c-MMTV mouse strain at two different dietary fat levels.

Animals↗
PubMed1977

Plasma levels of a viral protein as a diagnostic signal for the presence of mammary tumor: the effect of tumor removal.

We have previously shown (1, 2) that mice with mammary tumors can always be identified by their very high plasma levels of gp52, a 52,000 mol wt glycoprotein of the mouse mammary tumor virus (MMTV). The present investigation demostrates that the tumor is the principal source of the plasma gp52 since surgical excision is invariably followed in the first 9 days by a sharp decreasing (10-100-fold) of the gp52 levels. Control animals in which the tumors were left in place by a "sham" surgical procedure maintained their high level of gp52, which continued to increase as the disease progressed. The behavior of the gp52 after surgical removal suggests that gp52 plasma concentrations are diagnostically and prognostically informative, as indicated by the following finding: (a) All tumor recurrences were correctly diagnosed by increases in gp52 levels, and some were detected 4-7 days before they were found by palpation. (b) Tumor regrowths were accompanied by continued increases in plasma gp52 concentrations at rates that usually matched the speed of tumor development. (c) The only animals that remained tumor free at the termination of the experiment were those that maintained their gp52 levels at or below 15 ng/ml. (d) The probability of a tumor-free animal relapsing within 2 wk is much higher if its gp52 level is above the mean. (e) More remarkably, the plasma levels of gp52 at the time of surgery are superior to the size of the tumors removed as prognostic indicators of eventual surgical "cures". The availability of a specific and sensitive systemic measure of disease status should augment the usefulness of the murine mammary tumor model by catalyzing a more rapid acquisition of information on the therapeutic effectiveness of the new and varied drug combinations being tested for adjuvant chemotherapy.

Animals↗
PubMed1993

Progression of androgen-sensitive mouse tumor (Shionogi carcinoma 115) to androgen-insensitive tumor after long-term removal of testosterone.

Shionogi Carcinoma 115 (SC115) is an androgen-sensitive transplantable mouse tumor. To study the mode of progression from androgen-sensitive to -insensitive tumor, cloned SC115 cells were serially cultured without androgen. Shortly after withdrawal of androgen, SC115 cells showed markedly decreased growth, but growth resumed gradually with loss of response to androgen and the cells 60 weeks after androgen removal [A(-)60 cells] grew faster than SC115 cells cultured in the presence of androgen. A(-)60 cells showed malignant phenotype with morphological changes and tumorigenicity in male and female mice. Although mRNA and binding capacity of androgen receptor were maintained, the cells after removal of androgen rapidly lost expression of mouse mammary tumor virus-related gene and the loss was irreversible in A(-)60 cells. The stimulating effect of basic fibroblast growth factor (bFGF) temporarily decreased, then recovered to the initial level after long-term androgen removal. This fluctuation of response to bFGF was accompanied with changes in the number of bFGF receptors and amount of bFGF-like substance(s) secreted. The substance(s) seemed to be an FGF-like growth factor different from known factors. It was concluded that progression of SC115 cells to androgen-insensitive ones under an androgen-deprived condition proceeded with adaptation by means of increases in production of an FGF-like growth factor and in binding capacity to this factor.

Androgens↗
PubMed1978

Modulation of mouse mammary tumor virus production in the MJY-alpha cell line.

Implantation of the mouse mammary tumor virus (MMTV)-producing mammary tumor cell line MJY-alpha into isogeneic mice elicited both humoral and T-cell responses against MMTV virion antigens. The carcinosarcomas which developed from the implanted cells showed a significant decrease in MMTV synthesis, compared with cells remaining in culture, which was detectable as early as 7 days after implantation and for five transplant generations. Electron microscopic examination of thin sections of the tumors revealed that intracytoplasmic A particles, budding particles, and cell-free MMTV B particles were all affected. However, immunofluorescence assays of tumor sections demonstrated the presence of MMTV viral antigens in the cells. Cell cultures initiated from first-, third-, and fourth-generation tumors were morphologically identical to the original in vitro cell line, although virus production was barely detectable. Analysis of the cultures by electron microscopy revealed a significant increase in MMTV virions after in vitro passage 3. Polypeptide profiles obtained by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of virions purified from these cultures were identical to MMTV. Immunodiffusion demonstrated the cross-reactivity between these virions and MMTV particles obtained from mouse milk. In vitro treatment of MJY-alpha cell cultures with rabbit anti-MMTV antiserum resulted in a reduction of extracellular MMTV virions, as well as alterations in their sodium dodecyl sulfate-polyacrylamide gel electrophoretic polypeptide patterns.

Animals↗
PubMed2004

Activation of Akt-1 (PKB-alpha) can accelerate ErbB-2-mediated mammary tumorigenesis but suppresses tumor invasion.

Elevated expression of Akt-1 (PKBalpha) has been noted in a significant percentage of primary human breast cancers. Another frequent event in the genesis of human breast cancers is amplification and overexpression of the ErbB-2 receptor tyrosine kinase, an event which is associated with activation of Akt-1. To directly assess the importance of Akt-1 activation in ErbB-2 mammary tumor progression, we interbred separate strains of transgenic mice carrying mouse mammary tumor virus/activated Akt-1 and mouse mammary tumor virus/activated ErbB-2 to derive progeny that coexpress the transgenes in the mammary epithelium. Female transgenic mice coexpressing activated Akt-1 and ErbB-2 develop multifocal mammary tumors with a significantly shorter latency period than mice expressing activated ErbB-2 alone. This dramatic acceleration of mammary tumor progression correlates with enhanced cellular proliferation, elevated Cyclin D1 protein levels, and phosphorylation of retinoblastoma protein. These bitransgenic mammary tumors also exhibit lower levels of invasion into the surrounding tissue and more differentiated phenotypes. Consistent with these observations, female mice coexpressing activated Akt-1 and ErbB-2 developed significantly fewer metastatic lesions than the activated ErbB-2 strain alone. Taken together, these observations suggest that activation of Akt-1 during ErbB-2-induced mammary tumorigenesis may have opposing effects on tumor growth and metastatic progression.

Animals↗
PubMed1994

Pregnancy dependence of mammary tumours in DDD mice congenic for Mtv-2, DDD/1-Mtv-2/Mtv-2.

Mammary tumours developed in 110 (95.7%) of 115 DDD/1-Mtv-2/Mtv-2 (DDD/1-Mtv-2) and 24 (47.1%) of 51 DDD/1fDDD/1-Mtv-2 (DDD/1fMtv-2) force-bred female mice during a one-year period. The mean tumour age +/- SE was 220 +/- 7 and 269 +/- 7 days, respectively. These tumours were examined for responsiveness to pregnancies by comparing their growth after transplantation between virgin and breeding recipients. Of 73 tumours from DDD/1-Mtv-2 mice, 9 (12%) were completely pregnancy-dependent (CPD), 3 (4%) pregnancy-dependent (PD), 9 (12%) pregnancy-responsive (PR), and 52 (71%) pregnancy-independent (PI), and of 25 tumours from DDD/1fMtv-2 mice, one (4%) was CPD, one (4%) PR, and 23 (92%) PI. Although most tumours were heterogeneous in morphology and there was no clear relation between morphology and PD properties, most CPD tumours were type P and considered to be connected with mammary plaques. When 9 CPD tumours from DDD/1-Mtv-2 mice were serially transplanted in breeders, 6, 2 and one progressed to lose pregnancy dependence within 3, 8 and 18 generations, respectively. DDD/1-Mtv-2 mice will provide a model for studies on progression of mammary tumours from hormone-dependent to autonomous states.

Animals↗
PubMed1984

Factors affecting spontaneous tumor incidence rates in mice: a literature review.

The recent increased use of mice for lifetime oncogenicity testing has resulted in concern for the modulating effects on spontaneous tumor incidence rates by factors other than the test article and the high variability of spontaneous tumor incidence rates in control mice. The various factors shown to affect spontaneous tumor incidence rates in mice must be considered in the planning and conduct of oncogenicity studies with this species if biologically meaningful results are to be achieved. This review reports the results of investigations conducted during the past 50 years to determine the effects of various environmental, dietary, hormonal, viral, and genetic factors on spontaneous tumor incidence rates for mice.

Altitude↗
PubMed1977

Levels of mammary tumor virus in hormone-dependent and -independent mouse mammary tumor cells.

Levels of mammary tumor virus particles (types A and B) and levels of the virus antigen were assayed in hormone-dependent and -independent mammary tumors of GR mice. Various transplant generations of seven separate tumor lines were investigated. The results indicated that the tumors consisted of different cell clones, each of which exhibited a separate progressive expression and subsequent loss of the mammary tumor virus. When the tumors were transplanted, levels of B particles first declined in the hormone-dependent cells, but in later transplant generations, the B particle content of the autonomous cells also dropped. In some tumor lines, this was accompanied by a decrease in viral antigens and/or A particles, but in other lines these concentrations remained high. One tumor line (line V) that remained hormone-dependent throughout nine transplantations was practically devoid of B particles but contained high levels of A particles and mammary tumor antigen.

Animals↗