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At least 541 records · Page 30Linked to original sources
PubMed1980

An enzyme-linked immunoassay for the detection of antibodies to the mouse mammary tumor virus: application to human breast cancer.

An enzyme-linked immunoassay (ELISA) was developed, using the mouse mammary tumor virus (MMTV) fixed to wells of a microtiter plate, for the determination of antibodies to MMTV. The intensity of the final color change was dependent upon virus or viral antibody concentration. MMTV antibody was readily detectable in sera diluted as much as 1 : 2800. Fixed MMTV bound antibodies to an internal viral protein (p 28) as well as to viral envelope components (gp 52, gp 34), demonstrating that the virus was rendered permeable by our procedure. Applying this assay to human sera, significant differences (P less than 0.005) in IgG binding to MMTV were detected between sera of breast cancer patients, benign breast disease patients and healthy individuals. 26% of breast cancer-derived sera contained MMTV binding antibody; 10% of benign sera or 8% of normal sera were also positive. The reactivity of human IgG with MMTV was blocked by prior incubation of the virus with antisera to gp 34 or, to a lesser extent, with gp 52. The results demonstrate that MMTV antibodies can be quantitated by this simple, rapid and inexpensive procedure.

Animals↗
PubMed1985

Androgen regulates MMTV RNA in the short-term in S115 mouse mammary tumour cells.

This report demonstrates that androgens as well as glucocorticoids can regulate MMTV RNA production in the short term. In S115 mouse mammary tumour cells, MMTV RNA accumulation is regulated within hours by androgen, at a time before any increase in DNA synthesis can be detected, thus providing a marker of an early postreceptor molecular event in steroid action on these cells. Androgen acts via its own receptor and not by cross-binding to the glucocorticoid receptor. The effects are at transcription and not just on stabilisation of RNA because they are blocked by actinomycin D. However, the androgen action shows some partial dependence on simultaneous protein synthesis since cycloheximide is inhibitory. The androgen regulation of MMTV RNA is compared and contrasted with that by glucocorticoids in these cells.

Androgens↗
PubMed1986

Steroid regulation of transfected genes in mouse mammary tumour cells.

The regulation of mouse mammary tumour virus (MMTV) RNA by glucocorticoid hormones is well-established and has provided much information on how steroid hormones work. However, we have shown that androgens can also control MMTV RNA accumulation in S115 mouse mammary tumour cells. This novel androgen action could be explained on the basis that the MMTV long terminal repeat (LTR) can respond to several classes of steroid if appropriate receptors are present in the cells. We have used transfection experiments to demonstrate that androgens can act directly on the LTR in S115 cells. Hormonal regulation of transfected chimaeric genes into these cells was effected by androgen and glucocorticoid but not by oestrogen or progesterone, corresponding to the receptor status of the cells. Furthermore, hormonal control was also conferred by the LTR on expression of an independent cotransfected adjacent gene under its own separate promoter, suggesting that effects of an LTR can stretch to neighbouring genes in a type of hormone-enhancer insertion mechanism.

Androgens↗
PubMed1989

Glucocorticoids stimulate the release of a viral tumor marker (MMTV gp52) while inhibiting tumor cell growth.

The influence of glucocorticoid treatments on the release of mouse mammary tumor virus (MMTV) envelope antigen (gp52) has been studied in C3H mammary tumor cell cultures and compared to treatment-mediated effects on tumor cell growth. Simultaneous assessment of extracellular viral antigen levels and tumor cell growth has indicated that both are coordinately affected by glucocorticoid treatment. While gp52 release is stimulated by treatment, this effect is accompanied by an inhibition of tumor cell growth. These stimulatory and inhibitory effects are mediated by dexamethasone (DEX) in a dose-dependent fashion, and both effects are more pronounced with the synthetic glucocorticoids DEX or triamcinolone acetonide (TA). Quantitation of media gp52 levels by RIA revealed the following hierarchy of glucocorticoid enhancement: TA greater than DEX greater than prednisolone greater than hydrocortisone greater than triamcinolone. A similar order of activity was observed in terms of inhibition of cell growth. The ability of TA to enhance gp52 release was 2.4-2.7 times greater than DEX, a previously proven stimulator of MMTV expression. Cell density of B9 mammary tumor cells was reduced 73% following 72 h of 10(-8) MTA treatment while C3H Mm5mt/cl mammary tumor cells were reduced by 53%. Hormone-mediated changes in in vitro gp52 release suggest that hormones might also influence plasma levels of MMTV gp52 as a systemic marker for the presence and status of murine mammary tumors. Coordinate stimulatory and inhibitory effects suggest that glucocorticoids may play a complex role in murine mammary tumorigenesis and subsequent mammary disease.

Animals↗
PubMed1982

Comparison of mammary tumorigenesis between litters in relation to mammary tumor virus antigenic expression in the milk of C3H/He mice.

As a possible step to estimate the relationship between mammary tumor virus (MTV) and mammary tumorigenesis in mice, MTV antigenic expression in mother's milk and spontaneous mammary tumorigenesis in their daughters were compared between the 1st, the 2nd and the 3rd litters of the highly inbred strains of C3H/H3 mice with low mammary tumor incidence. While MTV antigenic expression was detected in all undiluted samples at each litter by immunodiffusion test, the amount of antigen as measured by the single radial immunodiffusion method was increased with increasing litter numbers. On the other hand, the development of preneoplastic mammary hyperplastic alveolar nodules was different little between litters and mammary tumor incidence by 13 months of age was very low with no difference in all litters. The pattern of estrous cycles and plasma prolactin level were also similar in each litter. The results suggest that spontaneous mammary tumorigenesis in mice is not always affected quantitatively by the amount of MTV when endocrine and genetical conditions are similar.

Animals↗
PubMed1989

Levels of viral glycoprotein provide a dose-dependent measure of tumor cell inhibition.

A chemosensitivity assay utilizing small replicate Mm5mt/c1 C3H mammary tumor cell cultures was developed to determine whether changes in viral antigen expression and release into culture fluids could be utilized as an in vitro measure of chemotherapeutic drug effect. The 52,000 MW viral envelope glycoprotein (gp52) of the mouse mammary tumor virus (MMTV) was measured in culture fluids of control and drug-treated cultures while cell density was simultaneously determined by cell staining and OD 664 mu determination. While extracellular gp52 levels and cell density both progressively increased over 72 hours for control cultures, treatments with doxorubicin resulted in dose-dependent declines in both parameters at 24, 48, and 72 hours. Comparison of doxorubicin dosages for 50% reduction (ED50s) in both parameters (0.68uM and 1.1uM) revealed a similar coordinate reduction in both cell density and MMTVgp52. When gp52 levels were further examined as a general measure of effect for a broad spectrum of 6 drugs with differing mechanisms of action, coordinate declines in cell density and MMTVgp52 provided a time and dose-dependent dual measure of effect for each of the drugs tested. Coordinate declines resulted in the same following hierarchy of concentration-dependent drug potency: methotrexate greater than 5-fluorouracil greater than doxorubicin greater than N [phosphonacetyl- L aspartic acid] (PALA) greater than cis-platinum greater than cyclophosphamide. The dual measures of therapeutic effect afforded by this assay argue for its use as an in vitro measure of effect for optimizing drug treatments.

Animals↗
PubMed1992

Effects of amphetamine on the development of MTV-induced mammary tumors in female mice.

Female C3H/He mice carrying the mammary tumor virus (MTV) were monitored for mammary tumor incidence and latent periods while submitted to a daily subcutaneous injection with amphetamine (0,4 mg/kg/day). Results show that amphetamine caused an increase in incidence and a decrease in latency of tumors compared with placebo. There was also appreciated a correlation with the lethality of mice.

Amphetamine↗
PubMed1994

Levels of viral glycoprotein reflect enhanced effectiveness of combined drug treatments.

A chemosensitivity assay with small replicate Mm5mt/cl C3H mammary tumor cell cultures was developed to determine whether changes in viral antigen expression and release into culture fluids could be utilized as an in vitro measure of single and combined drug effect. The measurement of drug concentrations required for identical 50% reductions in viral antigen levels (ED50s) allowed the dosage-dependence of the same drug to be compared alone and in combination drug treatments. The 52,000 MW viral envelope glycoprotein (gp52) of the mouse mammary tumor virus (MMTV) was measured in culture fluids of control and drug-treated cultures while cell density was simultaneously determined by cell staining and OD 664 mu determination. While extracellular gp52 levels and cell density increased over 72 hours in control cultures, dose-dependent declines in both parameters provided dual measures of effect for combination CAF treatment [cyclophosphamide: doxorubicin (Adriamycin): 5-fluorouracil], combination CMF treatment [cyclophosphamide: methotrexate: 5-fluorouracil] and single component treatments of these combinations. Comparison of ED50s for gp52 reduction revealed that each drug's ED50 concentration was lower in combination treatment than it was in single treatment. In combined drug treatments, the ED50 of doxorubicin was lowered from 5.17 microM to 0.36 microM, that of 5-fluorouracil was lowered from 0.69 microM to 0.22 microM and that of methotrexate was lowered from 15 nM to 1.65 nM. Reductions of ED50 in combined drug treatments argued for drug synergisms in these combinations. When drug concentrations, rather than gp52 reductions, were fixed at identical levels in single and combined treatments, additional declines in gp52 levels reflected the enhanced effects of CAF and CMF combinations over single drug treatments. When the anti-estrogen, tamoxifen, was added to CAF and CMF treatments, further declines in gp52 levels (below CAF and CMF levels) reflected the fact that these hormone-augmented treatments were more effective than either hormone or combination chemotherapy alone. These results indicate that decreases in extracellular levels of MMTV gp52 can be utilized in this in vitro assay as an alternative measure of chemotherapeutic effect for evaluating the synergistic or antagonistic nature of drug or hormone interactions and as a tool for in vitro optimization of combined drug effect.

Adenocarcinoma↗