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At least 127 records · Page 7Linked to original sources
PubMed1983

Sera from irradiated rats contain antibodies to a ubiquitous tumour-associated antigen.

Female rats of the inbred strains BN/BiRij and WAG/Rij were irradiated with 30 kV X-rays, or 15 MeV or 0.5 MeV fast neutrons. Sera were collected several months after irradiation and found to be negative for antibodies reacting with the murine mammary tumour virus as tested by a solid-phase radioimmunoassay and an immunofluorescence absorption test. We found, however, that in an immunofluorescence assay several sera from irradiated rats reacted with a cytoplasmic antigen in rat mammary, ureter and skin carcinoma cell lines as well as a mouse mammary tumour and a transformed BALB/3T3 mouse fibroblast line. No reaction was found with normal fibroblast cell lines of rat or murine origin. Endpoint titres of the sera on tumour cells ranged from 1:20 to 1:160. Of 48 sera from unirradiated rats 18 also stained tumour cells, but usually at the low dilution of 1:10. Irradiation seems to enhance antibody activity to a ubiquitous tumour-associated antigen.

Animals↗
PubMed1979

Molecular relationship of the DNA and RNA of intracytoplasmic A particles to mouse and mammary tumour virus genomes.

We have directly tested the hypothesis that single-stranded cytoplasmic A particle-associated DNA (ss CAP DNA) is a murine mammary tumour virus (MMTV) proviral intermediate by hybridizing 125I-labelled ss CAP DNA to MMTV RNA or to MMTV complementary DNA (cDNA). 125I-labelled CAP DNA did not form duplexes with either MMTV RNA or MMTV cDNA. In contrast, CAP RNA hybridized readily with MMTV cDNA. CAP RNA contained all the MMTV virus sequences, but at lower concentrations than in MMTV virus particles. Single-stranded CAP DNA hybridized readily with mouse DNA from several sources. A study of the rate of hybridization of CAP DNA to cell DNA at various driver to probe ratios showed that its rate of hybridization is similar to that of tumour cell DNA reassociation. Further, in reassociation studies accelerated by using the phenol emulsion reassociation technique (PERT), CAP DNA originally isolated as single-stranded DNA was shown to reanneal (70%), to protect 125I-cell DNA to the same extent (67%) and to do so with kinetics of reassociation equivalent to that of mouse DNA. Although CAP DNA isolates were slightly enriched for MMTV specific sequences when compared to total cellular DNA, we conclude that the majority of ss CAP-associated DNA is equivalent to a random sample of total tumour cell DNA.

Animals↗
PubMed1978

Prevalence of murine mammary tumor virus antibody and antigens in normal and tumor-bearing feral mice.

Approximately 20% of normal male and female feral mice (Mus musculus) from areas with populations having either high [Lake Casitas (LC) and La Puente] or low (Bouquet Canyon) spontaneous lymphoma incidence expressed murine mammary tumor virus (MuMTV) gp52 in specific tissues. Sera from a low percentage (6%) of mice from the same trapping areas contained precipitating antibody specific for MuMTV. Although moderate to high levels of MuMTV gp52 were expressed in mammary tumor tissues of 3 of 7 LC mice and 3 of 3 (C57BL/10ScSn X LC)F1 mice, the same animals showed no detectable MuMTV-precipitating antibody. Neither MuMTV antibody nor tumor-associated MuMTV gp52 was defected in 10 LC mice bearing lymphomas or in 5 LC mice bearing hepatomas. Low levels of MuMTV gp52 expression and MuMTV antibody were also detected in subspecies of M. musculus and in the more distantly related species M. cervicolar. Compared with normal and tumor-bearing inbred mice of high (C3H/HeN) and low (C3H/HeN foster-nursed on NIH Swiss) mammary tumor strains, normal and tumor-bearing feral mice express MuMTV gp52 and MuMTV-precipitating antibodies at low frequency.

Animals↗
PubMed1977

Considerations on the preneoplastic lesions of the mammary gland.

The general characteristics of the preneoplastic lesions of the human mammary gland, as they are known through histologic description, are outlined, and data obtained from the experimental analysis of mammary gland preneoplasia in five areas of endeavor are discussed. Results obtained with transplantation procedures and aimed at defining the growth potential of hyperplastic outgrowths are reported. Information derived from the study of events able to induce benign hyperplastic outgrowths or their malignant transformation in the murine mammary gland is summarized. Attempts to predict neoplastic transformation in morphologically hyperplastic epithelium of human and rodent glands are discussed. The present status of efforts toward the prophylaxis of preneoplastic lesions of the mammary gland is described. Considerations of the relationship between preneoplasia and tumor dormancy conclude the presentation.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1987

Interaction of different steroid hormones during progression of tumour cells to steroid autonomy.

Progression to steroid insensitivity poses a major problem in therapy of breast cancer, but studies of the origin of steroid-insensitive cells have been few and have concentrated in any one system on the loss of response to only one steroid. Since both normal and tumour mammary cells have complex endocrine requirements, we wondered how different steroids might interact during loss of steroid sensitivity. Cloned cells from the androgen-responsive Shionogi 115 mouse mammary carcinoma respond in vitro to both androgens and glucocorticoids in terms of both cellular and molecular parameters but, following prolonged absence of any steroid, these cells become unresponsive. We show here that 2 steroids can interact to prevent the progression to steroid insensitivity since the S115 cells can be protected against any loss of response to either androgen or glucocorticoid with either steroid alone. Androgen protects against loss of glucocorticoid sensitivity and glucocorticoid protects against loss of androgen sensitivity. The clinical implications are discussed.

Animals↗
PubMed1987

Hormonal regulation of mouse mammary tumor growth.

In view of reports that human breast cancer cells secrete growth factors that can replace estradiol in sustaining tumor growth [1], we have investigated whether hormone independent (HI) GR mouse mammary tumors can sustain growth of estrogen-depleted hormone dependent (HD) tumors. HD GR mammary tumor TSl 106 was grafted subcutaneously in the right flank of estrone plus progesterone treated castrated (020 X GR)F1 mice. After 2 weeks the estrone treatment was stopped and the mice received 50, 100 or 150 mg HI GR mammary tumor TSl 104 in the left flank. However, the regression of the HD tumor due to estrone depletion was not prevented or retarded by the HI grafts. In other experiments we investigated integrations of mouse mammary tumor virus (MMTV) proviral DNA in the DNA of GR mammary tumors. We could demonstrate the presence of two cell populations in tumor TSl 96, both HD but differing in MMTV DNA integration events. Our data indicate that exogenous integrations of MMTV proviruses can take place in mouse mammary tumor DNA without loss of hormone dependency of the tumors. Like in GR/Mtv-2+ mice, mammary tumor transplants differing in MMTV proviral integrations are also observed in 020/Mtv-2+ mice.

Animals↗
PubMed1988

Different int-1 region DNA rearrangements within different zones of a single mouse mammary tumor.

Fragments were taken from separate parts of hormone-dependent (HD) primary GR mouse mammary tumors and serially transplanted in estrone plus progesterone treated or hormonally untreated castrated mice. The transplants were examined with respect to int-1 DNA rearrangement, proviral integrations of the murine mammary tumor virus (MMTV), and estrogen and progesterone receptor content. One of the fragments (b) taken from the primary tumor of line TSI 96 produced transplants that showed int-1 rearrangement in one allele and also MMTV proviral integrations not at the int-1 gene, whereas transplants from another fragment (a) only had the normal germ-line int-1 arrangement and no extra MMTV provirus. These respective genotypes were retained when the tumors became hormonally independent during further transplantations. The results indicate that int-1 rearrangement was not present in the originally transformed cell but occurred in a HD cell during growth of the tumor. Furthermore they indicate that loss of hormonal dependence in GR mammary tumors is due to a mutational event, unrelated to int-1 rearrangement.

Animals↗
PubMed1987

Progression to steroid insensitivity can occur irrespective of the presence of functional steroid receptors.

A major problem in treatment of cancers arising in steroid-sensitive cells is their inevitable progression to a steroid-insensitive state; current therapies are based on the assumption that hormone insensitivity is associated with loss of receptor. We demonstrate for the first time that breast tumor cells can progress to steroid insensitivity in spite of functional steroid receptors. Transfection of the steroid-inducible LTR-C3 gene into unresponsive S115 mouse mammary tumor cells results in full inducibility of that gene with both androgen and glucocorticoid. Thus, although all known endogenous inducible parameters are lost, the steroid sensitivity of a transfected exogenous gene demonstrates that the machinery for steroid responsiveness is still fully functional. Furthermore, these transfected genes retain steroid sensitivity only while steroid is present; on prolonged withdrawal of steroid, they lose responsiveness, implying an epigenetic mechanism is involved.

Androgen-Binding Protein↗