Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Quantitative studies on the distribution kinetics of isotope-labeled cells from spontaneous murine mammary tumors injected intravenously or arterially showed that cells were rapidly distributed to all organs examined and indicated that the distribution patterns of metastases from such tumors are not primarily determined by the dose of cells delivered to each organ. The preferential colonization of certain organs is therefore considered to depend as much on differential survival and growth of the disseminated tumor cells in unfamiliar metabolic microenvironments, as on vascular sieving effects in organ capillary networks. Further experiments involved transplantation of pieces of nonpulmonary tissue containing trapped mammary tumor cells into syngeneic mice, followed by observation of the animals for several months. From these studies it is concluded that the absence of tumor colonies in extrapulmonary sites after i.v. inoculation is due to their inability to thrive in the organs concerned and not to early death of the original host from heavy pulmonary tumor growth. These results provide further evidence strengthening the conclusion emerging from several independent lines of investigation (Potter et al., Invasion Metastasis, 3: 221-233, 1983; Tarin et al., Cancer Res., 41: 3604-3609, 1981; Tarin et al., Cancer Res., 44: 3584-3592, 1984; Horak et al., J. Natl. Cancer Inst., 76: 913-922, 1986; Nicolson et al., Int. J. Cancer, 38: 289-294, 1986; Naito et al., Invasion Metastasis, 7: 16-29, 1987) that the growth of disseminated tumor cells is inhibited or even abrogated by many of the organs in which the cells sequester after vascular dissemination.
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PMID:Tumor cell dissemination patterns and metastasis of murine mammary carcinoma. 291 Apr 79

The hormone-responsive mammary tumor 13762NF of the F344 rat was cultured in a collagen gel matrix with the use of a serum-free medium supplemented with hormones and epidermal growth factor (EGF). Hydrocortisone (F) had the greatest effect on cell growth. EGF had no growth-promoting activity when used alone, but it had a significant effect when used with F. There was also a population of cells responsive to progesterone (P) and prolactin (PRL). P synergized with EGF as well as with PRL to promote growth. 17 beta-Estradiol alone or in combination with other hormones had no growth-promoting activity. Receptor levels in the tumor were high for glucocorticoids, intermediate for P and EGF, and low for estrogens. Metastasis in the lung and lymph node showed the same basic hormonal responses as the parent tumor. Cultured cells produced tumors with the same histopathology as the parent tumor when transplanted back into female rats; they had the same receptor levels and when placed back in culture showed a growth response to the same set of hormones. The tumor cells formed colonies that were spherical, which was different from the branching structures formed by normal mammary cells in collagen gel.
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PMID:Effect of hormones and epidermal growth factor on the growth of the hormone-responsive 13762NF rat mammary tumor in collagen gel culture. 300 45

Cystosarcoma phylloides is a breast neoplasm that has a frequently unpredictable clinical course. We made a retrospective study of 25 patients with this disease in an attempt to evaluate the indicators of aggressive behavior. In our series, older patient age, nulliparity, rapid tumor growth, pain, and large size of tumors increased the suspicion of malignancy but were not always reliable indicators of malignancy. Skin ulceration, tumor necrosis, and infiltrating tumor margins were the most ominous characteristics. High-grade tumors, that is, those with increased cellularity, vascularity, mitotic figure, and pleomorphism, often indicated aggressive behavior. Mixed mesenchymal components were sometimes related to a malignant course. We found a 24 percent incidence of associated breast cancer. Carcinoma of the ipsilateral breast was found in four patients and later in the contralateral breast in two patients. Of our 25 patients, 10 (40 percent) had recurrence and 4 (16 percent) died from disease. Recurrences after treatment usually occurred within 3 years. Patients must be followed carefully for local recurrence or metastases, since the clinical course is not predictable. Forty percent of the lesions were diagnosed as being malignant. Local excision was associated with recurrence in six of eight patients and was clearly inadequate treatment. Quadrantectomy was effective for benign peripheral lesions when a generous margin could be obtained. From these data, we believe that mastectomy is indicated in all patients with malignant lesions and in those with large benign lesions.
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PMID:Prognostic indicators in cystosarcoma phylloides. 303 Jan 51

Inflammatory breast cancer is the most aggressive breast neoplasm and one of the most ominous solid tumors. Because of distinct clinical characteristics, diagnosis can usually be made on clinical grounds. Biopsy including the overlying skin may demonstrate dermal lymphatic invasion, although the absence of dermal lymphatic invasions should not deter aggressive therapy. Surgery or irradiation alone has little effect on the natural history of this disease since lymphatic invasion and distant metastases are often present at presentation. Inflammatory breast cancer should be considered a systemic disease. Accordingly, aggressive combined modality therapy including multi-drug chemotherapy, surgery, and irradiation have prolonged disease-free survival and overall survival.
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PMID:Inflammatory breast cancer: advances in therapy. 307 91

Staphage lysate (SPL), a preparation of Staphylococcus aureus obtained by bacteriophage lysis, is an interferon-inducer and stimulator of T and B lymphocytes. Does SPL, as an immunopotentiator, have an effect on the growth and metastases of an intradermal mammary carcinoma? To answer this question, a study using SPL in female Fischer rats injected with 7 x 10(6) viable 13762 mammary tumor cells on the midback were used. Four groups were created with 10 animals in each group. Group I was the control group. They received no treatment. Group II received 0.3 ml of medium in which SPL was carried on alternate days. Group III received 0.3 ml SPL on alternate days. Group IV were sensitized with dead staphylococcal organisms prior to SPL treatment as in Group III. Tumor diameters were recorded on days 10, 13, 17, and 21, and autopsies were performed to determine the extent of metastases. Histologic examination and serum antibody measurements were performed. The mean tumor diameters on day 21 were: Group I: 4.1 +/- 0.2 cm; Group II: 3.80 +/- 0.19 cm; Group III: 3.04 +/- 0.13 cm; and Group IV: 2.97 +/- 0.14 cm. Rats receiving SPL treatment in Groups III and IV had significantly smaller tumors (P less than .001). The incidence of axillary lymph node involvement was: Group I: 100%; Group II: 87.5%; Group III: 62.5%; and Group IV: 40%. Lung metastases were seen in all groups. Groups I and II had 100% incidence of grossly visible nodules, whereas Groups III and IV had 75% and 70% involvement. Gross findings were confirmed by microscopic examination.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunomodulation of intradermal mammary carcinoma using staphage lysate in a rat model. 315 83

Malignant breast cancers appear to metastasize first via the lymphatics to colonize regional lymph nodes, and then via the blood circulation to colonize distant organs. Using a rat mammary tumor model based on the 13762NF adenocarcinoma, evidence is presented that malignant cell subpopulations spread lymphatically to regional lymph nodes, then become blood-borne and metastasize to lungs. Using chromosome and cytokeratin markers to identify specific tumor cell subpopulations, tumor progression in this system appears to be associated with the appearance of a highly specialized, metastatic cell subpopulation. This highly malignant cell subpopulation is completely uncoupled by gap junctions when examined for gap-junctional communication, in contrast with less malignant subpopulations that show varying degrees of cell communication through gap junctions. Loss of cell-cell communication may be one of the epigenetic events that leads to the generation of tumor cell diversification and heterogeneity. In concert with host selective pressures, this could result in the evolution of highly malignant cell subpopulations with unique characteristics.
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PMID:Cytoskeletal and junctional heterogeneity in mammary tumor cells and their possible significance in tumor progression. 322 82

The timing within the estrous cycle of surgical removal of a transplanted murine mammary tumor profoundly influences the frequency of pulmonary metastases. We investigated the potential role of the immune response in this phenomenon by measuring splenic natural killer (NK) cell activity and interleukin-2 (IL-2) production in syngeneic tumor-free mice of two age groups at each of two circadian times and in each of four estrous stages. Estrous stage was determined by assessment of vaginal smear cellularity immediately prior to killing and spleen harvest. In a single-cell splenocyte preparation, NK cytotoxicity against a standard tumor cell target was assessed using a radiolabeled chromium release assay while IL-2 activity was determined in a bioassay utilizing the IL-2-dependent CTLL-2 cell line. Mice from the younger group were found to have eight-fold higher NK activity and 35% greater IL-2 production. After normalization of NK and IL-2 values for age, a highly statistically significant difference in NK activity was found among the four estrous and between the two circadian stages of sacrifice. NK activity was greater during the daily resting span across every estrous stage. IL-2 values were highest in diestrus and proestrus when sampled in the light span and in estrus-metestrus when sampled in the dark. The stages within the fertility cycle associated with lowest metastatic potential (proestrus/estrus) correspond precisely with those of highest splenocyte NK activity. These results indicate that an important component of the cellular immune response varies rhythmically both during the fertility and circadian cycles of the host. The rhythmic changes in NK activity may be in part responsible for the similarly rhythmic frequency of postsurgical metastatic dissemination.
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PMID:Natural killer cell activity: age, estrous- and circadian-stage dependence and inverse correlation with metastatic potential. 326 68

This study describes a differential frequency of spontaneous fusion between metastatic and nonmetastatic subpopulations derived from a single mouse mammary tumor. Subpopulations 66, 66c14 (a variant of 66 which is resistant to both thioguanine and ouabain), 410.4, and 44FTO (a thioguanine-resistant, ouabain-resistant derivative of 410.4) spontaneously metastasize from subcutaneous and mammary fatpad sites. Subpopulations 168, 168FARO (a diaminopurine-resistant, ouabain-resistant derivative of 168), 67, 68H, and 410 do not. The ability of these subpopulation lines to fuse spontaneously in vitro was determined after coculturing a drug-resistant line with a wild-type line in nonselective media. After 16-20 h of coculture, cells were plated in the appropriate media to select for fusion products--either HAT (hypoxanthine, aminopterin, thymidine) plus ouabain or AA (alanosine, adenine) plus ouabain--to determine the number of colony-forming cells (fusion products) present per 10(4) cells plated. When both subpopulations of the pair in the fusion mixture were metastatic, a significantly greater number of fusion products was recovered than if one or both of the subpopulations in the fusion mixture was nonmetastatic, with one exception: line 410 readily fused with both 66c14 and 44FTO. Subline 410 was highly metastatic when originally isolated but lost its metastatic competence after a brief time in tissue culture.
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PMID:Spontaneous fusion between metastatic mammary tumor subpopulations. 335 52

The metastatic murine mammary tumor cell line 410.4 and its nonmetastatic counterpart tumor line 410 were examined for the presence of prostaglandin E2 (PGE2) binding using a 3H-PGE2 ligand binding assay. Inhibition of endogenous prostaglandin synthesis with indomethacin was shown to increase markedly binding of 3H-PGE2. Equilibrium binding data for tumor 410.4 show that specific binding is saturable, reversible by unlabeled PGE2, temperature-dependent and specific. PGE1, PGE2 or 16-16-dimethyl PGE2 compete well with 3H-PGE2 for binding. PGD2 partially inhibits 3H-PGE2 binding, whereas PGA2 does not compete. Scatchard analysis of equilibrium binding data reveals a high affinity (Kd = 3.9 X 10(-9) M) and an average of 33,785 binding sites/cell. In contrast, binding of 3H-PGE2 to nonmetastatic line 410 has a slightly lower affinity (Kd = 8.8 X 10(-9) M) and an average of 368,857 binding sites/cell. 3H-PGE binding to line 410 cells is comparatively nonspecific as PGD2 is nearly as effective as PGE1, PGE2 and an analogue of PGE2 in competing with 3H-PGE2 and PGA2 also inhibits 3H-PGE2 binding.
Invasion Metastasis 1988
PMID:Heterogeneity of prostaglandin E2 binding in murine mammary tumor cells differing in metastatic potential. 342 34

A new method for detecting bloodborne TMT-081 rat mammary tumor cells in buffy coat has revealed dose-dependent variations in the latency period after inoculation of tumor cells, the concentration of circulating tumor cells, and the incidence of metastases. Cells isolated from buffy coat of right ventricular blood were more tumorigenic than tryptically dispersed cells from solid tumors. With the new method circulating tumor cells can be detected at concentrations as low as 3 cells/microliter of buffy coat, or approximately 60 cells/ml of whole blood. The morphologic and ultrastructural features of the primary tumor were generally retained in both the circulating and tryptically dispersed cells, as shown by light and electron microscopy. A sparse distribution of intermediate filaments was revealed by high-voltage electron microscopy, although the filaments were not evident in conventional transmission electron micrographs. They were identified as keratin by immunofluorescence studies.
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PMID:Detection and characterization of circulating rat mammary tumor cells in buffy coat and correlation with metastasis. 342 8


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