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 purpose of this study was to determine whether dietary (n-3) fatty acids would affect mammary tumor growth and metastasis. Weanling female BALB/c mice were fed diets that contained 10% corn oil (CO), linseed oil (LO) or a fish oil-corn oil mix (FO) for 3-8 wk prior to receiving subcutaneous injections of one of two syngeneic mammary tumor cell types (410 and 410.4). Tumor growth was assessed by monitoring mean tumor diameter and tumor weight upon removal. Feeding LO, but not FO, reduced the growth (p less than 0.05) of 410.4 mammary tumors compared with growth in those fed CO. Metastasis data paralleled the tumor growth rate. Feeding LO and FO enhanced (p less than 0.005) incorporation of (n-3) fatty acids into tumors. Tumor prostaglandin E (PGE) production was reduced (p less than 0.005) by LO and FO, compared with CO. FO feeding reduced 410.4 tumor PGE synthesis more (p less than 0.05) than LO feeding, yet tumor growth was only inhibited by LO. These data suggest an inhibitory effect of dietary linolenic acid [i.e., 18:3 (n-3)] on mammary tumor growth and metastasis. However, this effect did not directly correlate with diet-induced changes in PGE synthesis.
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PMID:Effect of dietary alpha-linolenic acid on growth, metastasis, fatty acid profile and prostaglandin production of two murine mammary adenocarcinomas. 197 7

Tumor subpopulations 66c14, 168FARN, and 4T07 are drug-resistant variants selected from sister subpopulations derived from a single mouse mammary tumor. These subpopulations are heterogeneous in their capacities to form experimental metastatic growth in the lungs and liver. Initial survival kinetics of arrested cells, determined by the clearance of 125IUdR-labelled cells, and subsequent growth rates, determined by sequential recovery of clonogenic tumor cells from occult metastases, both correlated with organ-colonizing potential as determined by necropsy. The growth rates of these 3 subpopulations were determined in vitro in monolayer and in situ in the subcutis, in the liver following intrasplenic injection, and in the lung following intravenous injection. Clonogenic potential of all 3 lines was similar in vitro (54-59%). Growth rates in vitro (population doubling times 16.5-21 hr) and in the subcutis (tumor volume doubling times 5.2-7.4 days) were similar for the 3 subpopulations, but differed significantly in the liver and lungs. For line 4T07, the most metastatic line to both lung and liver, population doubling times in vitro and in the lung and liver were similar, ranging from 17 to 26 hr. For lines 66c14 and 168FARN, the growth rates in lungs and livers were much slower than in vitro. Line 66c14, which is relatively more metastatic to the lungs, grew much faster in the lung (39 hours) than in the liver (91 hr), but line 168FARN, which is relatively more metastatic to the liver, grew at a faster rate in the liver (37 hr) than in the lung (63 hr). Thus, 3 tumor subpopulations (seeds) derived from a single tumor were differentially affected by host organ factors (soil) at 2 distinct stages in the metastatic process.
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PMID:Differential influence of organ site on three subpopulations of a single mouse mammary tumor at two distinct steps in metastasis. 199 57

Our previous studies using randomly integrated plasmid DNA as unique clonotypic markers of SPI mouse mammary tumor cells transplanted into syngeneic CBA/J or nude mice demonstrated reproducible selection and eventual overgrowth of the primary transplant tumors by genotypically distinct metastatic subclones. Two independent metastatic SPI clones, neo5 and ras1, were shown to exhibit "clonal dominance" relative to the non-metastatic SPI tumor-cell population. These results suggested that the capacity for preferential growth within the tumors may be related to cellular properties associated with metastatic ability. To investigate the clonal interactions of metastatic SPI clones present within the same tumor mass, we have analyzed tumors composed of paired mixtures of neo5 and ras1. The tumors were monitored for the relative proportion of each clone by Southern blot analysis. The ras1 clone was found to dominate over the neo5 clone in the majority of tumors examined, even when present as 1% of the mixed inoculum. This represents a 20- to 50-fold enrichment of ras1, while the proportion of neo5 within the tumors was reduced at least 5-fold. No evidence for selection of either clone was seen during co-culture in vitro. Neo5 and ras1 are indistinguishable with respect to tumorigenic and metastatic potential when inoculated separately into different mice, suggesting that clonal dominance is independent of metastatic ability. Analysis of the metastases resulting from mixed inocula indicates that it is possible for a subpopulation representing less than 1% of the primary tumor mass to give rise to metastases. This also suggests that the process of metastasis within metastatic tumors is independent of clonal dominance.
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PMID:Clonal selection within metastatic SP1 mouse mammary tumors is independent of metastatic potential. 200 57

Two immunomodulatory protocols were evaluated for their ability to inhibit lung colonization by mouse mammary tumor line 4T07. Preimmunization with tumor cells or pretreatment with poly I:C were equally effective at inhibiting lung colonization but a clonogenic tumor cell assay demonstrated that the treatments reduced tumor cell burden at different steps during the metastatic process. Poly I:C pretreatment accelerated tumor cell clearance based on the recovery of clonogenic tumor cells from lungs dispersed within 6 h post-arrest. Preimmunization inhibited the subsequent replication of tumor cells which survived and established in the lung, as indicated by the expansion of clonogenic cell numbers between 1 day and 7 days post-arrest. Histologic examination of serial sections of lungs demonstrated that very few (6%) of the tumor cells were extravascular 6 h post-tumor cell injection. By 24 h and 168 h the percentages of tumor cells which were extravascular had increased to 62% and 86%, respectively. Thus, poly I:C pretreatment appears to enhance killing of tumor cells prior to extravasation, whereas preimmunization appears to inhibit tumor cells after extravasation.
Clin Exp Metastasis
PMID:Inhibition of lung colonization at two different steps in the metastatic sequence. 203 19

Metastatic cells are often considered to be clonal derivatives of one of the primary tumor cell subpopulations. To determine if the cells of spontaneously developed lung nodules in a mammary tumor-bearing mouse represent the major or minor population of the cells in the primary tumor, comparisons were made of the pattern of their mouse mammary tumor virus (MMTV) proviral integrations, and their insertional mutations of the mouse mammary tumor proto-oncogenes, int-1 and int-2. Of the 78 tumor-bearing C3H/He mice sacrificed, seven mice showed metastatic lung nodules, but only four mice had nodule tissues adequate for the present analysis. Examination of the primary tumors and the corresponding lung nodules of these four mice revealed that the number of newly integrated MMTV proviruses and their sites of integration in the genomic DNAs of primary tumors and tumor nodules were variable, and that the int-1 gene was disrupted in three of the primary tumors but not in any of the metastasized tumor tissue. These results support the notion that, at least in some mice, the majority of cells constituting the primary mammary tumors and the corresponding metastases are of different genotypes and raise the possibility that the activation of different int-proto-oncogenes may be involved in the genesis of different cell subpopulations including metastatic cells in the same mouse.
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PMID:Genetic diversity of spontaneously developed primary and metastatic mammary tumor cells in mice. 217 23

We describe the use of enzymes combined with brief, sequential mechanical disruptions in a Tekmar Stomacher blender for the recovery of clonogenic neoplastic cells from solid tumors, lungs, and livers. The method has yielded 3 X 10(8) to 5 X 10(8) total cells and 1.2 X 10(6) to 17 X 10(6) clonogenic cells per gram of tissue from three different mouse mammary tumor subpopulations growing in the subcutis. The clonogenic cell yields represent a 4- to 13-fold increase over our previous best method of tumor disaggregation. The increase in total cells recovered, while not as dramatic (up to 3-fold), was statistically significant for two of the three tumor lines. We were also able to efficiently recover 125I-iododeoxyuridine labelled neoplastic cells from lungs and livers after injecting the cells intravenously. Over half of the total radiolabel present in these organs prior to disaggregation could be recovered in the cell suspensions obtained.
Invasion Metastasis 1990
PMID:Efficient recovery of clonogenic stem cells from solid tumors and occult metastatic deposits. 230 60

This study examines whether oleate may influence the linoleate enhanced metastasis of line 4526 murine mammary tumors. In addition, the in vitro proliferative response of line 4526 to oleate and other selected fatty acids was assessed. Initially, the tumor cells were grown in a defined medium supplemented with palmitate, stearate, oleate, linoleate, linolenate or arachidonate. The unsaturated fatty acids stimulated and the saturated fatty acids inhibited proliferation compared to fatty acid-free medium. Next, we examined the effect of oleate on the linoleate enhanced metastasis of 4526 tumors by substituting oleate for saturated fat in isoenergetic diets containing high or low levels of linoleate. Oleate had no effect on metastasis in mice fed the high linoleate diets but it significantly increased metastasis in mice fed the low linoleate diets. Finally, the fatty acid compositions of tumors and mammary fat pads were compared to diet fatty acid compositions and metastatic frequency. Metastasis corresponded more closely to total unsaturated fatty acids than to total polyunsaturated fatty acids or to any individual fatty acid. These studies suggest that both mono- and polyunsaturated fatty acids may stimulate mammary tumor metastasis. However, the influence of dietary oleate probably depends on the level of linoleate and total unsaturated fatty acids in the diet.
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PMID:Modulation of mouse mammary tumor growth and linoleate enhanced metastasis by oleate. 231 78

This report describes the light (LM) and electron microscopic (EM) features and the results of an indirect immunofluorescence study (IF), the latter using monoclonal and monospecific antibodies to cytoskeletal proteins, of a malignant, invasive and metastatic breast myoepithelioma. A 53-year-old female underwent mastectomy for a large necrotic mammary tumor that had invaded the overlying skin. By LM, the neoplasm was composed of interlacing bundles of large, elongated and interspersed stellate cells with acidophilic cytoplasm. The neoplastic cells displayed a moderate degree of anaplasia, high mitotic activity, and strong tendency for necrosis. Stromal desmoplasia was marked, especially toward the center of the neoplasm. By IF, the tumor cells revealed bright cytoplasmic fluorescence with antibodies to actin, prekeratin, and cytokeratin. A few scattered spindle cells, which stained with the anti-vimentin and anti-actin anti-bodies, most likely represented stromal myofibroblasts. The anti-desmin reaction was negative. By EM, the neoplasm was composed of variably differentiated, elongated and stellate myoepithelial cells connected by desmosomes, enveloped by remnants of basal lamina, and containing pinocytotic vesicles, a well-developed rough endoplasmic reticulum, large Golgi areas, aggregates of intermediate filaments that were often arranged in dense curvilinear bundles (tonofilaments), and bundles of microfilaments with fusiform, dense bodies. The combined LM, EM, and IF study of this mammary tumor establishes its myoepithelial origin and, thus, identifies it as myoepithelial carcinoma distinct from other spindle cell breast tumors. This neoplasms was locally invasive and cytologically malignant; moreover, its malignancy was further confirmed by the development of lung and pleural metastases.
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PMID:Malignant myoepithelioma (myoepithelial carcinoma) of the breast: an ultrastructural and immunocytochemical study. 241

Complementary antitumor treatments are required to increase the cure rate achieved by surgery and/or radiotherapy by avoiding future recurrences and metastases. The growth of most solid tumors, particularly carcinomas, depends upon the simultaneous development of internal tumor vasculature to allow the proliferation of tumor cells. Inhibition of tumor vascularization is an indirect means of limiting tumor expansion. Daily administration of cortisone and maltose tetrapalmitate (MTP) abolished growth of implanted syngeneic C3HBA mammary tumor. Gross and macroscopic examination of these tumors revealed that tumor growth was prevented. Histological examination demonstrated lack of vascularization within the neoplastic tissue. We believe that this combination in an appropriate form could provide a prophylactic treatment regimen after conventional antitumor treatments in humans.
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PMID:Prophylactic antiangiogenic tumor treatment. 247 30

Three cell lines derived from two metastases of a mammary carcinoma in a female dog were analyzed cytogenetically. All three cell lines showed a modal chromosome number of 76, with ranges of 74-77, 72-78, and 73-78. A biarmed chromosome in addition to the X chromosomes was observed in all cells of one cell line, and in a part of the cells of the other two cell lines. Results of banding analyses indicated that this chromosome was identical in the three cell lines, and can thus be considered a clonal marker. Additional biarmed chromosomes have not been reported previously from mammary tumor cells, although their presence is rather common in other canine neoplasms.
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PMID:Cytogenetic analysis of cell lines derived from metastases of a mammary carcinoma in a dog. 247 28


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