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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution, antibody-induced redistribution, and shedding of murine mammary tumor virus (MuMTV) antigens and the surfaces of GR mouse ascites leukemia (GRSL) cells were studied by the immunoferritin technique and compared with the same activities of thy 1.2 and H-2.8 antigens. MuMTV antigens were redistributed easily and then largely shed from the cell surface; in contrast, H-2.8 antigen moved easily and probably was partially released from the plasms membrane and Thy 1.2 antigen moved slowly and was some what interiorized. The complement-dependent cytotoxicity test was used to study the possibility of antigenic modulation for these cell-surface antigens from the surface of the GRSL cells could be modulated by preincubation with anti-MuMTV serum, in contrast to H-2.8 and Thy 1.2 antigens. The results obtained with the immunoferritin technique and the cytotoxicity test correlated well and sug-ested that the shedding of MuMTV antigens from the cell surfaces may occur in vivo, providing the tumor a way to escape from the immune defense of the host. Thy 1.2 and H-2.8 antigens were present on the envolope of B and C particles, which suggested that these viruses do not select a Thy 1.2 or H-2.8-negative area of the GRSL cell surface as amaturation site.
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PMID:Antibody-induced modulation and shedding of mammary tumor virus antigens on the surfaces of GR ascites leukemia cells as compared with normal antigens. 18 12

We used the mouse mammary tumor and its associated virus (murine mammary tumor virus) to examine the possibility of using plasma levels of a viral protein (gp52, the glycoprotein of 52,000 molecular weight) as a diagnostic indicator of the presence of a solid tumor. The following features have emerged from our studies: (a) tumor-bearing animals show markedly elevated (100-1000 ng/ml) plasma levels of gp52 and the mean concentration increases with tumor size; (b) mammary tumor tissues located outside the mammary gland are also detected by the elevated plasma gp52; (c) low (2-10 ng/ml) plasma levels of gp52 are found in tumor-free mice, whether they are derived from strains characterized by high or low frequencies of spontaneous mammary tumors; (d) tumor-free lactating females exhibit the normally low levels of plasma gp52 despite the fact that their milk contains an average of 20,000 ng/ml of this antigen; (e) thus, high levels of plasma gp52 are found only in the presence of tumor and are not induced by either predisposition for the disease or by normal production of the antigen during lactation; (f) the circulatory clearance time of gp52 is sufficiently rapid to require continued replenishment to maintain the high levels observed in tumor-bearing animals, a feature implying that the gp52 concentration can be a responsive parameter of disease status. The information obtained suggests that plasma gp52 is a potentially useful and specific systemic indicator of the presence and extent of murine mammary neoplasia.
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PMID:Plasma levels of a viral protein as a diagnostic signal for the presence of tumor : the murine mammary tumor model. 18 89

The mammary tumor virus (MuMTV) in the milks of 7 mouse strains and substrains was titrated for infectivity in 4 strains. The data indicated that: 1) Each strain shed a different MuMTV and some genetic strains carried two MuMTV's, each discernible by its mouse strain preference in infectivity tests. 2) Less than 5% of RIIIf and about 10% of Af mice shed detectable MuMTV antigen in their milks after the third parturition. After the sixth parturition, 33% of RIIIf and 50% of Af, and after the ninth parturition, 60% of RIIIf and 90% of Af mice shed viral antigen in their milks. The MuMTV's in milks of high-parity mothers were most infectious in mouse strains different from those most susceptible to MuMTV in RIII and A milks of low-parity mothers. Therefore, RIII and A mice each harbored two viruses, one that was removed by foster-nursing and the other that was not. 3) The susceptibility incidence of RIIIfC57BL mice to RIII virus changed gradually from about 10% in 1970 to about 70% in 1975. Susceptibility of C57BL mice to RIII virus did not change appreciably over this period, and the natural tumor incidence in RIIIfC57BL remained unchanged (about 10%). In addition to their susceptibility to RIII virus, C57BL mice were also susceptible to GR virus; they were relatively resistant to other strains tested. They were especially resistant to RIIIf virus, to which Af and BALB/c mice were very susceptible. 4) Approximately 90% of C3HfC57BL and C3HfBALB/c mice shed antigen in their milks after the third parturition, although the tumor incidence was less and occurred later than in C3H mice. No clear-cut differences could be detected in infectivities between low-parity C3H milk and high-parity C3Hf milks tested in several assay strains.
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PMID:Biologic characteristics of some mouse mammary tumor viruses. 18 80

Newborn female mice of three strains--BALB/cfC3H [mammary tumor virus (MuMTV)-infected], BALB/c, and C57BL (both virus-free)--were given injections of 17beta-estradiol or testosterone, alone or in combination with ovine prolactin, for the first 5 days of life. Half of each group of mice were ovariectomized at 40 days of age, and all mice were killed between 6 and 16 months of age. Mammary glands of BALB/cfC3H mice receiving steroid hormones were better developed than those of mice not receiving steroids. Androgen induced a higher incidence of grossly dilated ducts and secretion-filled alveoli. Mammary nodule and tumor incidences were higher in steroid-treated mice than in controls; androgen resulted in higher incidences than did estrogen. The age of onset of mammary tumors was also earlier after neonatal steroid treatment. In BALB/c mice, neonatal injections of estrogen induced some alveolar development of the mammary gland; neonatal injections of ovine prolactin had a greater effect. The mammary glands of C57BL mice did not show any evidence of stimulation by neonatal hormone treatment, which indicated the probability of strain differences. However, no nodules or tumors occurred in these MuMTV-free strains. Therefore, MuMTV was essential for neoplastic mammary responses to neonatal hormone treatment. Ovariectomy prevented alveolar development and abnormal changes in the mammary glands of all groups, thus indicating that ovary-independent alterations in the mammary gland were not induced by neonatal steroid treatment. We concluded that neonatal steroid exposure resulted in increased mammary tumor risk in mice, but only in the presence of both MuMTV and ovaries.
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PMID:Long-term effects of neonatal steroid exposure on mammary gland development and tumorigenesis in mice. 18 88

The effects of neonatal and perinatal thymectomy on mammary tumorigenesis in (C57BL X I)F1fC3H hybrid female mice were determined. When hybrid females were neonatally thymectomized by controlled suction, a procedure that removes thymic lobes completely, a large proportion of animals developed stigmas of a fulminant wasting disease and died before tumors developed. However, when hybrid females were subjected to neonatal thymectomy by continuous suction, a procedure that resulted in retention of thymic remnants, they survived and manifested a significant prolongation of latent period before tumorigenesis. When complete removal of the thymus was carried out in the perinatal period, the effect on mammary tumorigenesis was critically dependent on the age at surgery. The procedure was without effect when performed at 1, 3, and 8 weeks of age. However, when it was performed at 9-12 days of age, there was a delay or a decrease in the appearance of mammary tumors. The extent of T-cell depletion and/or its timing in relationship to the introduction of murine mammary tumor virus appeared to play a critical role in determining the effect on eventual tumor development.
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PMID:Inhibition of mammary tumors by incomplete T-cell depletion. 19 Apr 16

The effect of prolactin in supporting the growth of 7, 12-dimethylbenz(a)anthracene-induced mammary tumor in adult female Sprague-Dawley rats was investigated when estrogen receptors were blocked by the nonsteroidal antiestrogen, Tamoxifen, ICI 46,474. Following an oophorectomy-induced remission, perphenazine, which stimulates endogenous prolactin release, was able to restore tumor growth whether or not Tamoxifen was added. A second course of perphenazine treatment, instituted after the tumors were allowed to shrink, was again effective in stimulating tumor growth. After a regression in tumor size induced by oophorectomy and daily administration of Tamoxifen, perphenazine was able to restore original tumor size despite continued treatment with Tamoxifen. In intact rats, after regression was obtained by daily administration of Tamoxifen and the prolactin inhibitor, lergotrile mesylate, perphenazine induced tumor growth when the latter was discontinued, even though Tamoxifen was continued for 50 days. Estrogen receptors measured at the time of maximum stimulation by perphenazine were undetectable. On the other hand, estradiol did not stimulate tumor growth when serum prolactin was depressed to undetectable levels by lergotrile. These results indicate that prolactin supports the growth of 7, 12-dimethylbenz(a)anthracene-induced rat mammary tumor and that estrogen receptors are not required under these conditions.
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PMID:Predominant role of prolactin in stimulating the growth of 7, 12-dimethylbenz(a)anthracene-induced rat mammary tumor. 19 Nov 82

The hormone-dependent 7,12-dimethylbenz(a)anthracene rat mammary tumor has been shown to regress when administered pharmacological doses of testosterone propionate. Tumor regression was correlated with estrogen receptor before and 15 to 20 days following testosterone therapy. A dramatic decline of receptor occurred in all regressing tumors, whereas those administered sesame oil alone maintained both growth and receptor content. Although receptor in regressing tumor was significantly less than in the untreated biopsies, the small amount of remaining receptor maintained the same binding affinity to estradiol, showing that testosterone affects the number and not estrogen affinity of the estrogen receptor. These studies suggest that testosterone depletion of estrogen receptor may be causally related to tumor regression.
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PMID:Estrogen receptors in androgen-induced breast tumor regression. 19 56

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.
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PMID:Plasma levels of a viral protein as a diagnostic signal for the presence of mammary tumor: the effect of tumor removal. 19 30

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.
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PMID:Levels of mammary tumor virus in hormone-dependent and -independent mouse mammary tumor cells. 19 32

Indirect immunoferritin and fixed immunofluorescence tests were carried out on (a) sera of mice hyperimmunized with isologous mouse mammary tumor virus (MMTV) particles or isologous MMTV-producing mammary tumor cells grown in tissue culture and (b) sera of mammary tumor-bearing and tumor-free mice of several inbred strains. Sera were tested against MMTV produced by C3H/HEJ/Tex tissue culture cells (MMT-1). Mammary tumor-bearing A/Dm, C3H/HeTex, and RIII/Dm mice and apparently tumor-free A/Dm mice were found to develop naturally occurring nonprotective anti-MMTV antibodies, whereas sera of tumor-free C3H/HeTex, RIII/Dm, and C57BL/6/Tex female mice and A/Dm, C3H/HeTex, and RIII/Dm male mice did not contain anti-MMTV antibodies. Indirect immunoferritin and fixed immunofluorescence labeling of MMTV particles was prevented by absorbing sera with purified MMTV particles. The results demonstrate the relationship of naturally occurring anti-MMTV antibodies in mouse sera to the presence of mammary tumors, confirm previous reports that mice are not tolerant to MMTV, and further establish the usefulness of the indirect immunoferritin procedure in studies of the immune response of mice.
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PMID:Immunoelectron microscopic studies of antibodies in mouse sera directed against mouse mammary tumor virus. 19 33


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