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

Characteristics of [3H]progesterone-binding components were studied in cell-free preparations of two hormonally responsive tumors: the R3230AC mammary adenocarcinoma and 9,10-dimethyl-1,2-benzanthracene-induced mammary tumor of the rat. Progesterone-binding macromolecules from cytosols of both mammary neoplasms exhibited sedimentation coefficients of 3.5 to 4.0 S on sucrose gradients of either low or high ionic strength. From Scatchard analyses of titration data, apparent dissociation constants of 4 to 6 X 10(-8) M were determined for ligand-binding protein complexes from either tumor. Specific progesterone-binding capacities varied considerably, ranging from 150 to 650 fmoles/mg of cytosol protein. Optimal binding of [3H]progesterone was reached by 2 to 3 hr at 3 degrees, pH 7.4, and then decreased rapidly. Specificity studies indicated that cortisol, corticosterone, and triamcinolone acetonide competed effectively for [3H]progesterone-binding. This suggested that [3H] progesterone was bound largely to a macromolecule distinct from transcortin, which does not bind glucocorticoids containing 9alpha-fluoro groups. Aldosterone, as well as several androgens and estrogens, were weak competitors of binding except at high concentrations. The nature of the inhibition of progesterone-binding sites by triamcinolone acetonide and corticosterone was competitive. Concurrent titrations of [3H]progesterone and [3H]triamcinolone acetonide-binding sites demonstrated that their binding capacities were similar, considering the relative stabilities of the complexes. These results, which indicated that progesterone and glucocorticoids compete for the same binding site, suggest that these hormones may influence mammary gland differentiation and development by a common mechanism.
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PMID:Characteristics of progesterone-binding components in neoplastic mammary tissues of the rat. 17 35

Neuraminidase treatment of mouse mammary tumor virus, Rauscher murine leukemia virus, and Mason-Pfizer monkey virus resulted in loss of their capacity to inhibit hemagglutination of influenza virus. Hemagglutination-inhibition activity of these RNA tumor viruses could be restored by in vitro resialylation catalyzed by sialyl transferase. The major glycoprotein in the intact envelope of desialylated and, to some extent, native virions could be specificallly labeled in vitro with CMP-(14C) sialic acid. These studies further characterize the individual glycoproteins of mouse mammary tumor virus, Rauscher murine leukemia virus, and Mason-Pfizer monkey virus.
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PMID:Sialylatin of glycoproteins of murine mammary tumor virus, murine leukemia virus, and Mason-Pfizer monkey virus. 17 11

Cystosarcoma phylloides (c.p.) is a rare fibroepithelial neoplasm of the mammary gland exhibiting considerable histological variations ranging from the aspect of hypercellular fibroadenoma to that of pleomorphic sarcoma. In this study, 58 cases of c.p. were graded according to their histology into 3 groups of increasing malignancy-benign tumors: 23 cases (42%), borderline tumors: 16 cases (27%) and malignant tumors: 18 cases (31%). Their clinical properties and evolution have been compared. These tumors were found exclusively in women, most often during the 5th and 6th decade of life (age range from 19 to 81 years). In two thirds of the cases, the history of the disease was shorter than 6 months. The symptoms were generally scant. Only in 2 cases were severe local lesions observed. The postoperative clinical course has been followed for at least 5 years in 32 instances. Recurrences were observed in 5 patients, the histology being as a rule the same as that of the primary tumor. The 12 patients with benign tumors are well 5 years or more after operation. One of the patients presenting a malignant tumor died of lung embolism soon after mastectomy. 2 out of 10 patients with borderline tumors died within 6 years with metastases of the mammary tumor. Our analysis confirms the experience that c.p. are relatively benign but often recurring neoplasms that rarely disseminate. As far as prognosis and treatment are concerned, tumors of questionable dignity should be considered malignant. To avoid such vague terms as "benign or malignant c.p." we support OBERMANN'S suggested separation of c.p. into "cellular fibroadenoma" and "periductal fribrosarcoma". Wide local excision for small and benign tumors is recommended. All other forms require simple mastectomy. Prophylactic dissection of the axillary lymph nodes is not necessary as these tumors usually disseminate hematogenously. Roentgen therapy or chemotherapeutic agents are not useful in treatment.
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PMID:[Cystosarcoma phylloides of the breast. Analysis of 58 cases]. 17 36

Specific radioimmune precipitation assays were utilized to demonstrate the presence of precipitating antibodies to mouse mammary tumor virus (MMTV) in the high-spontaneous mammary tumor strains of mice: C3H/HeN+, GR/N, BALB/cfC3H, and C57BL/6 X C3H F1 (hereafter called B6C3F1). Antibody titers in C3H/HeN+ mice increased with age, with highest titers observed in tumor-bearing animals. MMTV-precipitating antibodies were not detectable by radioimmune precipitation assay in low-mammary tumor strains (AKR, BALB/c C57BL/6, and C3H/HeN-) but were detectable in MMTV-inoculated BALB/c mice. Appearance of antibodies preceded palpable tumor formation, and antibody titers were directly correlated to virus dose. Natural antibody to MMTV in C3H/HeN+ and B6C3F1 mice coexists with the murine leukemia virus natural antibody as determined by competition radioimmunoassays.
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PMID:Autogenous immunity to mouse mammary tumor virus in mouse strains of high and low mammary tumor incidence. 17 9

Mouse mammary tumor virus (MMTV) proviral sequences were detected in the cellular DNA of mammary tumors and livers of RIII and C3H mice by molecular hybridization with radioactively labelled MMTV 60-70S RNA or tritiated MMTV complementary DNA (cDNA). By means of DNA:DNA reassociation kinetics, the DNA of the mammary tumor cells of these two mouse strains were found to contain more MMTV proviral sequences than the DNA of liver cells of these same tumor-bearing mice. Evidence is also presented that the DNA of the liver cells lacks a part (approximately 25%) of the MMTV proviral sequences found in the mammary tumor cells of these mouse strains. The relationship of the extra MMTV proviral sequences found in mammary tumor cells to the early mammary tumor-igenesis seen in these mouse strains is discussed.
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PMID:A biochemical approach to the study of the transmission of mouse mammary tumor viruses in mouse strains RIII and C3H. 18 34

The immunogenicity of 6C3HED lymphosarcoma ascites tumor cells was greatly enhanced upon treatment with Vibrio cholerae neuraminidase. As a result, mammary tumor virus (MTV)-free C3H mice which had been repeatedly immunized with the treated cells resisted a challenge of 10(6) untreated viable cells inoculated i.p., whereas all control animals died after receiving less than 10 lymphosarcoma tumor cells. In contrast, there was no increase in the refractoriness to challenge when MTV-infected C3H mice were immunized. Incubation of 6C3HED lymphosarcoma cells with serum of splenic lymphocytes from the immunized MTV-free C3H mice neutralized their tumorigenicity and protected recipient MTV-free and MTV-infected C3H mice against the disease. As shown by the 51Cr microcytotoxicity assay, the complement-dependent cytotoxic antibody titer reached 1,024; 29% of the target cells were lysed by lymphocytes obtained from immune MTV-free C3H mice. When the immune lymphocytes were pretreated with anti-theta serum they lost their ability to neutralize the tumorigenicity of the lymphosarcoma, failed to be stimulated by the T cell mitogens, phytohemagglutinin and concanavalin A, and failed to achieve cytolysis of the lymphosarcoma target cells in vitro. These observations establish the central role of the theta-antigen-bearing immune lymphocytes in cell-mediated immunity in this system. Failure of the immune system in the immunized MTV-infected C3H mice to cope with the challenging lymphosarcoma, even at low cell numbers, was reflected, not in the absence of humoral response, but in the relatively low level of cell-mediated immunity. This was manifested in both the neutralization and in the vitro cell-mediated immunity assays. This apparent immunological deficiency observed in the MTV-infected C3H mice could be countered by the transfer of lymphocytes from MTV-free C3H mice immunized with neuraminidase-treated 6C3HED lymphosarcoma cells. The recipient MTV-infected C3H mice then rejected a subsequent challenge with lymphosarcoma tumor grafts.
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PMID:Characteristics of immunity induced by neuraminidase-treated lymphosarcoma cells in C3H (MTV+) and C3H (MTV-) mice. 18 51

Prolactin reverses the inhibitory effects of pharmacological doses of androgen on 7,12-dimethylbenz(a)anthracene-induced mammary tumor growth (Quadri, S.K., Kledzik, G.S., and Meites, J.J. Natl. Cancer Inst., 52: 875-878,1974). To determine whether this effect is due to an alteration in the ability of the tumor cell to bind prolactin, we have quantitated prolactin receptors in androgen-responsive and nonresponsive tumors. Prolactin receptors were measured with 125I-labeled ovine prolactin in a subcellular fraction which reproducibly contained 60 to 80% of the total receptor present in tumor homogenates. Prolactin binding was reversible, reached a steady state in 9 hr, and was completed by excess unlabeled prolactin. Prolactin bound to its receptor with a Kd of approximately 1 X 10(-10) M. Growing tumors were biopsied, and rats bearing regrown tumors were given injections of 4 mg testosterone propionate twice a week. Prolactin receptors were reduced in most of the tumors, which regressed after testosterone treatment by an average of 63% compared to the pretreatment biopsy specimens. Nonresponsive tumors and vehicle-injected controls showed no signifcant alterations in receptor content. This reduction of prolactin receptors is probably insufficient to account for androgen-induced mammary tumor regression.
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PMID:Prolactin receptors and androgen-induced regression of 7,12-dimethylbenz(a)anthracene-induced mammary carcinoma. 18 48

Cells producing type C (avain sarcoma virus) or type B (mouse mammary tumor virus) RNA tumor viruses contain small amounts of RNA complementary to the viral genomes. The negative strands are complementary to at least 30 to 45% of the viral genomes and are found as RNA-RNA duplexes in the nucleus and cytoplasm of infected cells and in mature virions.
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PMID:RNA complementary to the genome of RNA tumor viruses in virions and virus-producing cells. 18 16

Five different mouse mammary tumor cell lines were propagated in a serum free medium. Evaluation of growth characteristics, including logarithmic growth, cell population increase, protein production and days to confluency, showed serum-free medium comparable to serum-containing medium. Mouse mammary tumor virus expression and production, in C3H and GR tumor cell lines, as determined by virus particle counting and RNA dependent DNA polymerase assays, subsequent to dexamethasone stimulation revealed equivalent to higher levels of virus in serum-free medium as compared to serum-containing medium.
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PMID:Propagation of mouse mammary tumor cell lines and production of mouse mammary tumor virus in a serum-free medium. 18 96

When BALB/cfC3H females are subjected to continous suction thymectomy, a procedure that results in retention of thymic remnants, the latent period before tumor development is significantly prolonged. However, when BALB/cfC3H females are thymectomized by control suction, a procedure which removes thymic lobes completely, there is no effect on mammary tumorigenesis. Our results show that incomplete T cell depletion causes premature onset of non-T cell cytotoxicity, an augmentation of T cell cytotoxicity, and an alteration in a serum-blocking activity to mammary tumor target cells as tested in microcytotoxicity assay. On the other hand, complete neonatal thymectomy effectively and completely abrogates immune response to mammary tumor target cells. The inability of completely thymectomized mice to generate an immune response to MTV suggests (but does not prove) that MTV-induced mammary tumor target cell surface antigens are thymus-dependent.
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PMID:Stimulation of immune mechanisms against mammary tumors by incomplete T cell depletion. 18 35


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