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)

The effect of a high-fat (HF) diet (23% corn oil) on the growth and metastasis of the 13762 mammary tumor in Fischer 344 retired breeder (RB) and young virgin (YV) female rats was studied. The RB (10-12 mo old) and YV (8 wk old) rats were fed the HF or low-fat (LF) diet (5% corn oil) prior to and following tumor implantation for a total of at least 10 weeks. The growth rate of the primary tumor in the intact RB and YV was not affected by the HF diet. In RB rats ovariectomized 4 weeks prior to tumor implantation, the tumor grew significantly faster in the HF group as compared to the LF group. The total volume of metastatic tumor nodules in the lungs of the HF groups was significantly higher than that in the the lungs of the LF groups in both the intact and ovariectomized RB. In the YV, there was no difference in pulmonary metastatic burden between the HF and LF groups. The weights of the HF intact and ovariectomized RBs were higher than those of the LF animals. However, when pulmonary metastatic tumor burden was compared to body weight at implant or at sacrifice, there was no significant correlation in either the HF or LF groups. These results suggest that an HF diet enhanced the growth of pulmonary metastases in the intact and ovariectomized RB but not the YV rats and that the effect of the HF diet on pulmonary tumor burden cannot be attributed entirely to increased body weight.
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PMID:Stimulatory effect of high polyunsaturated fat diet on lung metastasis from the 13762 mammary adenocarcinoma in female retired breeder rats. 347 66

A difference in the expression and metabolism of sulfated glycosaminoglycans between rat mammary tumor cells derived from a primary tumor and those from its metastatic lesions has been observed. Cells from the primary tumor possessed about equal quantities of chondroitin sulfate and heparan sulfate on their cell surfaces but released fourfold more chondroitin sulfate than heparan sulfate into their medium. In contrast, cells from distal metastatic lesions expressed approximately 5 times more heparan sulfate than chondroitin sulfate in both medium and cell surface fractions. This was observed to be the result of differential synthesis of the glycosaminoglycans and not of major structural alterations of the individual glycosaminoglycans. The degree of sulfation and size of heparan sulfate were similar for all cells examined. However, chondroitin sulfate, observed to be only chondroitin 4-sulfate, from the metastases-derived cells had a smaller average molecular weight on gel filtration chromatography and showed a decreased quantity of sulfated disaccharides upon degradation with chondroitin ABC lyase compared to the primary tumor derived cells. Major qualitative or quantitative alterations were not observed for hyaluronic acid among the various 13762NF cells. The metabolism of newly synthesized sulfated glycosaminoglycans was also different between cells from primary tumor and metastases. Cells from the primary tumor continued to accumulate glycosaminoglycans in their medium over a 72-h period, while the accumulation of sulfated glycosaminoglycans in the medium of metastases-derived cells showed a plateau after 18-24 h. A pulse-chase kinetics study demonstrated that both heparan sulfate and chondroitin sulfate were degraded by the metastases-derived cells, whereas the primary tumor derived cells degraded only heparan sulfate and degraded it at a slower rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered expression of glycosaminoglycans in metastatic 13762NF rat mamma adenocarcinoma cells. 356 53

The ability to metastasize via the bloodstream of mammary tumors occurring in Balb/cfC3H and Balb/cfRIII mice (two substrains of identical Balb/c genotype carrying milk-transmitted C3H or RIII murine mammary tumor virus (MuMTV) infection, respectively) has been compared in MuMTV-free Balb/c virgin female recipients given intravenous tumor cell suspensions or subcutaneous solid tumor transplants from mammary tumor-bearing Balb/cfC3H and Balb/cfRIII breeding female donors. Tumor cell suspensions different for MuMTV inducing variant, growth rate, tumor size, and clinical duration, injected intravenously to Balb/c virgin female recipients, have been compared with respect to the foci of lung colonization induced in recipient hosts. The results obtained indicate that MuMTV variant, growth rate and clinical duration of the primary mammary tumor, but not the size of the primary tumor, significantly influence the lung colonization. Similar results were obtained with solid subcutaneous transplants of the same mammary tumors. The significance of these results for the understanding of the general mechanisms of tumor metastases is discussed.
Invasion Metastasis 1987
PMID:Lung colonization and metastasis of murine mammary tumors: relationship to various characteristics of the primary tumors. 367 42

A new murine mammary tumor cell line (BALB/c-MC) was established from a spontaneous mammary tumor in a 17-mo.-old female mouse of the low mammary cancer strain BALB/cHe. The cell line was derived from a papillary adenocarcinoma. In monolayer culture the line exhibits a pavementlike arrangement of cells and forms "domes" or "hemicysts" as the cells become confluent. The cell line rapidly forms tumors when transplanted into young syngeneic BALB/cHe mice. The subcutaneous injection of 10(6) cells resulted in the development of mammary tumors (typical papillary adenocarcinomas) in 33 of 37 (87%) recipients within 2 to 3 mo. after injection. These mammary tumors also metastasize to lung [14 of 33 (42%) of recipients] during this time. The number of chromosomes in this cell line is hyperdiploid (average of 43, range 39 to 44).
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PMID:Establishment and characterization of a new murine mammary tumor cell line, BALB/c-MC. 368 Jan 3

Young, virgin female Fischer 344 rats bearing the 13762 transplantable mammary tumor were fed diets containing either 5% (low-fat group) or 23% (high-fat group) corn oil for five weeks before and six weeks after tumor implantation. Animals in the two diet groups gained weight at comparable rates throughout the experiment. There was no significant difference between the low-fat and high-fat groups with respect to average tumor diameter measured twice per week for six weeks. At the time of death (6 weeks after tumor implantation), the lungs of all rats in both diet groups contained some metastatic tumor deposits; the volume of the metastases in the lungs varied widely in both groups. Numbers of metastases to regional lymph nodes and kidneys appeared unaffected by the fat content of the diet. Thus, both growth of the 13762 mammary tumor itself and metastatic spread from the tumor were comparable whether the young rats were fed a high-fat or a low-fat diet.
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PMID:The influence of dietary fat on mammary tumor metastasis in the rat. 373 22

A variant of metastatic mouse mammary tumor line 410.4 was produced which is resistant to both 60 microM thioguanine and 3 mM ouabain. Occult tumor cells which result from the metastatic spread of this subline are detected by plating cell suspensions from host tissues in selective media containing thioguanine and ouabain (TO). Only the tumor cells survive and form colonies. Tumor cell colonies were recovered when as few as 6 tumor cells mixed with 1 X 10(6) lymph node cells or normal lung cells were plated in TO. Thus, the method potentially will detect the presence of clonogenic tumor cells when the host tissue contains less than 0.0006% tumor cells. Results suggest that, within 15 min of intravenous injection, less than 10% of the injected cells are clonogenic. In addition, clonogenic tumor cells can be detected in draining lymph nodes prior to the appearance of a palpable tumor implant in the subcutis.
Invasion Metastasis 1986
PMID:Use of drug resistance markers to recover clonogenic tumor cells from occult metastases in host tissues. 375 60

This study was designed to determine whether treatment with the nonsteroidal antiestrogens analog II and tamoxifen given three times per week, 2 weeks before and 2 weeks after tumor cell transplantation, influenced the metastasis of a transplantable, metastatic rat mammary tumor, DMBA-4. Following transplantation of 2,000 viable tumor cells into the fifth and sixth mammary fat pads of 50-day-old inbred, female WF rats, all rats in all 3 groups displayed primary tumors by 5 weeks post tumor transplant. Analog II delayed the primary tumor development when compared to the time of the primary tumor development in either the control (untreated) or tamoxifen-treated groups. No metastatic tumors were found in the analog II-treated group 5 weeks after tumor transplantation, and only 1 animal in the tamoxifen-treated group had a secondary tumor, whereas 50% of the control animals had metastatic tumors. Six weeks after tumor implantation, palpable secondary tumors had developed in 40% of the analog II-treated group and 80% of the tamoxifen-treated group, whereas 60% of the control animals had developed secondary tumors. By the end of the study (7 wk) no differences existed between primary or secondary tumor incidences or between control and antiestrogen-treated groups. Both antiestrogens were effective in delaying the development of secondary tumors, especially during the time of treatment. Following cessation of treatment, analog II prevented metastatic tumor development for up to a month and tamoxifen, for 3 weeks. Further studies are indicated to determine if continuous treatment can effectively inhibit metastatic tumor development indefinitely.
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PMID:Effects of nonsteroidal antiestrogens, analog II and tamoxifen, on a metastatic transplantable rat mammary tumor. 391 97

Spontaneous mutation rates were determined in mouse mammary tumor subpopulation lines that differ in metastatic phenotype. Although there was almost a 9-fold difference in spontaneous rates to ouabain resistance among the three lines tested, the difference did not correlate with ability to metastasize. Similarly a 10-fold difference in spontaneous rates to 6-thioguanine resistance did not correlate with metastatic ability. In contrast, the frequency of ethyl methanesulfonate-induced mutations was associated with metastatic potential. Thus, ethyl methanesulfonate only induced significant numbers of 6-thioguanine resistant colonies in 66 and 410.4 cells, the only 2 of 5 lines tested that spontaneously metastasize at high frequency, and of ouabain resistant colonies in 66, 410.4, and 168 cells, the only lines tested that produce experimental lung metastases after i.v. injection. Differential sensitivity to induced mutation was not correlated with differences in plating efficiency, wild type sensitivity to ethyl methanesulfonate, 6-thioguanine, or ouabain toxicity, ploidy, cell shape, cell size, or ability to engage in metabolic cooperation.
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PMID:Correlation of frequency of induced mutation and metastatic potential in tumor cell lines from a single mouse mammary tumor. 402 98

The M3 mammary tumor was transplantable in syngeneic BALB/c mice, and metastasized spontaneously into the lungs. When primary tumors were resected in early stages of evolution (10 days), the number of mice with lung metastasis decreased. When specific soluble tumor extracts, tumor cell culture supernatant or formalinized tumor cells were inoculated 2 and 4 days after surgery, an enhancement of lung metastasis was observed. When splenectomy was performed at the time of tumor resection, this enhancement was abrogated. These results suggest that tumor plasma cell membranes or the products released by them play an important role in dormant metastases growth, but only in the presence of the spleen, suggesting its involvement in the mechanism of the metastatic process.
Invasion Metastasis 1985
PMID:Enhancement of the incidence of metastasis in tumor-resected mice. Influence of soluble tumor extract and splenectomy. 403 Feb 47

Approximately 1/3 of all mammary carcinomas are hormone-dependent. Therefore in approximately 30% of these cancer patients transient regression of the tumor may be obtained by means of endocrine therapy. Ablative procedures such as ovariectomy, adrenalectomy, hypophysectomy, roentgen castration, and destruction of the hypophysis by isotope implantation have been used. Administration of such hormones as estrogens, androgens, and corticosteroids and of hormone antagonists have been attempted. Remissions have been observed under the influence of L-dopa. A method to determine the hormone dependency of a mammary tumor is now available. The presence of estrogen receptors in human mammary carcinomas has a distinct correlation with the response to adrenalectomy. In the absence of receptors the chance of success of hormone therapy is minimal. Currently 51 patients have been found suitable for analysis. Remissions occurred in 21 of 24 patients with receptor-positive tumors but in only 3 of 27 with receptor-negative tumors. It was noted that those with cutaneous metastases more often respond favorably to endorcrine therapy than do those with skeletal or visceral metastases. No complete parallelism was found between hormone dependency and the presence of receptors. In 2 of the 3 receptor-positive patients who did not show an objective remission, a distinct subjective remission was noted. It is recommended that receptor determinations be done in every mammary tumor case operated on in the primary stage.
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PMID:Human breast cancer and estrogen receptor. 477 76


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