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)

Experimental and clinical evidence is here assembled in support of the concept that the development of a solid tumor progresses from a prevascular phase to a vascular phase. The prevascular tumor does not induce angiogenesis, is limited in size, and rarely metastasizes. The vascularized tumor induces host microvessels to undergo angiogenesis, has the potential to rapidly expand its cell population, and has a propensity to metastasize. Thus, angiogenesis is necessary but not sufficient for tumor growth and metastasis. Neovascularization of a tumor requires that a critical number of its cells have switched to the angiogenic phenotype. The mechanisms by which tumor cells become angiogenic, subjects of current study, are reviewed here. At least two general categories are recognized: (i) angiogenic activity arises from the tumor cell itself in the form of the release of angiogenic molecules such as basic fibroblast growth factor; (ii) angiogenic activity arises from host cells recruited by the tumor (e.g. macrophages), or is mobilized from the extracellular matrix, or requires concomitant loss of physiological inhibition of endothelial cell proliferation. Accumulating evidence indicates that for most tumors, the switch to the angiogenic phenotype depends upon the outcome of a balance between angiogenic stimulators and angiogenic inhibitors, both of which may be produced by tumor cells and perhaps by certain host cells.
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PMID:The role of angiogenesis in tumor growth. 137 11

To determine whether an association exists between abnormal pulmonary function tests (PFT) before bone marrow transplantation (BMT) and the rate of pulmonary complications after BMT, we retrospectively reviewed all transplants performed in our center between March 1984 and December 1990. A total of 163 patients, 15 years of age and older, with a hematologic malignancy or a solid tumor were treated with intensive therapy and autologous (118) or allogeneic (55) BMT. Sixty patients (37%) developed a pulmonary complication which contributed to patient death in 29 transplants (18%). Patients with pulmonary metastases, prior thoracotomy, or prior radiation to the chest had a higher frequency of abnormal PFT. By univariate analysis, patients with abnormal FVC, FEV1, or TLC before BMT had a significantly increased rate of pulmonary complications (p < 0.005). By multivariate analysis, the rate of pulmonary complications was significantly associated (p = 0.004) with abnormal FEV1 only: in the first 2 months after transplantation the rate was 65% in patients with FEV1 < 70% in contrast to 34% in patients with FEV1 > or = 70% (risk ratio = 1.9). There was no association, however, between abnormal pretransplant PFT and fatal pulmonary complications. We conclude that patients with pretransplant ventilatory defects have a higher risk of pulmonary complications after BMT, but the incidence of fatal complications was not significantly increased, although we cannot exclude a diminished study power due to the sample size. We believe that patients with abnormal PFT should not be excluded from transplantation if the anticipated anti-tumor effect is estimated to be substantial, but additional preventive measures may be necessary.
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PMID:Evaluation of pulmonary complications after bone marrow transplantation: the role of pretransplant pulmonary function tests. 142 92

The efficacy of present day antineoplastic regimens depends upon the delivery and penetration of therapeutic agents through the tumor vascular and interstitial spaces to the tumor cell target. The distribution of relevant molecules or cells in a solid tumor is often poor and heterogeneous and is believed to be due to a number of pathophysiological factors, including elevated interstitial fluid pressure (IFP). Using the wick-in-needle technique, IFP was measured in primary breast and colorectal carcinomas as well as their respective metastases to the lymph nodes and liver in a total of 17 patients. IFP was also measured in one recurrent renal cell carcinoma, one melanoma metastasis to the lymph nodes, and another melanoma metastasis to the lung. IFP varied from 4 to 50 mm Hg with a mean +/- SD of 20 +/- 13 mm Hg in the neoplasms (n = 41 measurements; n = 21 tumors), while IFP in normal tissues had a mean of 2 +/- 4 mm Hg (n = 11). The mean IFPs for metastatic melanoma, primary breast carcinoma, and liver metastases from a colorectal primary were found to be 33 +/- 14, 15 +/- 9, and 21 +/- 12 mm Hg, respectively. In the renal cell carcinoma, the pressure was 38 mm Hg. These results agree with the findings of our 3 previous studies examining IFP in human superficial melanomas (14.3 +/- 12.5 mm Hg, n = 12), cervical carcinomas (15.7 +/- 5.7 mm Hg, n = 12), and head and neck tumors (13.2 +/- 8.8 mm Hg, n = 19), and indicate that in all types of human tumors studied to date, IFP was significantly elevated above that of normal tissue. This observation may be useful in localizing tumors during needle biopsy.
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PMID:Interstitial hypertension in human breast and colorectal tumors. 142 83

The influence of the 70% methanolic extract (RMe) from Red Ginseng (a steamed and dried root of Panax ginseng C. A. Meyer) on the antitumor activity of mitomycin C (MMC) against rat ascites hepatoma AH 130 was investigated. In the case of a solid tumor, RMe at oral doses of 200, 500 mg/kg showed an inhibitory effect, but RMe was ineffective in the case of an ascites tumor. MMC combined with RMe showed a stronger antitumor effect than MMC alone. Moreover, RMe inhibited the pulmonary metastases of the tumor cells, as well as the decrease of blood platelet counts and of the fibrinogen level induced by the infusion of the tumor cells in rats. Furthermore, RMe promoted the uptake of MMC into the tumor cells and enhanced in vitro the cytotoxicity of MMC against the cultured tumor cells.
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PMID:[Pharmacological study on Panax ginseng C. A. Meyer. XIV. Effect of 70% methanolic extract from red ginseng on the cytocidal effect of mitomycin c against rat ascites hepatoma AH 130]. 148 50

The effect of allogeneic blood transfusions on solid tumor growth and pulmonary metastases was examined in two different strains of mice. Recipient mice (C57B1 or DBA/2) were given transfusions from allogeneic donors (Balb/c or B6AF1, respectively). The effect of allogeneic blood transfusion on solid tumor growth (B16 in C57B1 mice and P815 in B6AF1 mice) as well as the number of pulmonary metastases (B16 in C57B1 mice) was examined utilizing inoculations of varying numbers of tumor cells. In both solid tumor models, allogeneic transfusion resulted in significant enhancement of tumor growth when smaller (1.25 x 10(5), 2.5 x 10(5)) numbers of tumor cells were inoculated into the host animal. In contrast, no effect of allogeneic transfusion on tumor growth was observed when higher (4.5 x 10(5)) numbers of tumor cells were inoculated. Similarly, increased numbers of pulmonary metastases following allogeneic blood transfusion were observed when lower numbers (1 x 10(5)) of B16 tumor cells were administered; whereas no effect was observed with higher (4.5 x 10(5)) tumor cell numbers. The data in the present study suggest that the number of tumor cells inoculated into the recipient animal has a strong bearing in the allogeneic blood-transfusion-induced tumor growth effect.
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PMID:Effect of allogeneic blood transfusion on solid tumor growth and pulmonary metastases in mice. 154 81

Long-term therapy of oncology patients has been facilitated by permanent indwelling central venous catheters, but catheter-related infections remain a serious complication of their use. Using a retrospective matched cohort design, we compared the risk of catheter-related infection in 47 adult solid tumor patients with right atrial Hickman catheters and 94 patients with totally implanted port catheters. Patients were matched for primary solid tumor, presence of metastases, age, gender, and date of catheter insertion. Seven of 47 patients with Hickman catheters developed catheter-related infection (1.8 infections/1,000 catheter days at risk) compared with 10 of 94 patients with implanted port catheters (0.4/1000 catheter days, P less than 0.0002). Hickman catheters were used more often for terminally ill patients than were port catheters which was a potential source of bias, but results were unchanged after stratifying patients on lifespan. Our study suggests that there are fewer infections in port than in Hickman catheters in adult patients with solid tumors, but prospective randomized studies are needed.
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PMID:Comparison of infections in Hickman and implanted port catheters in adult solid tumor patients. 154 89

Neoplastic cells require an appropriate pericellular environment and new formation of stroma and blood vessels in order to constitute a solid tumor. Tumor progression also involves degradation of various extracellular matrix (ECM) constituents. In this review we have focused on the possible involvement of ECM-resident growth factors and enzymes in neovascularization and cell invasion. We demonstrate that the pluripotent angiogenic factor, basic fibroblast growth factor (bFGF) is an ECM component required for supporting cell proliferation and differentiation. Basic FGF has been identified in the subendothelial ECM produced in vitro and in basement membranes of the cornea and blood vessels in vivo. Despite the ubiquitous presence of bFGF in normal tissues, endothelial cell (EC) proliferation in these tissues is usually very low, suggesting that bFGF is somehow sequestered from its site of action. Our results indicate that bFGF is bound to heparan sulfate (HS) in the ECM and is released in an active form when the ECM-HS is degraded by cellular heparanase. We propose that restriction of bFGF bioavailability by binding to ECM and local regulation of its release, provides a novel mechanism for regulation of capillary blood vessel growth in normal and pathological situations. Heparanase activity correlates with the metastatic potential of various tumor cells and heparanase inhibiting molecules markedly reduce the incidence of lung metastasis in experimental animals. Heparanase may therefore participate in both tumor cell invasion and angiogenesis through degradation of the ECM-HS and mobilization of ECM-resident EC growth factors. The subendothelial ECM contains also tissue type- and urokinase type- plasminogen activators (PA), as well as PA inhibitor which may regulate cell invasion and tissue remodeling. Heparanase and the ECM-resident PA participate synergistically in sequential degradation of HS-proteoglycans in the ECM. These results together with similar observations on the properties of other ECM-immobilized enzymes and growth factors, suggest that the ECM provides a storage depot for biologically active molecules which are thereby stabilized and protected. This may allow a more localized, regulated and persistent mode of action, as compared to the same molecules in a fluid phase.
Cancer Metastasis Rev 1990 Nov
PMID:Extracellular matrix-resident growth factors and enzymes: possible involvement in tumor metastasis and angiogenesis. 170 86

In this short essay, we have taken the opportunity to review briefly the history of anticancer drug screening, consider the changes that have been made throughout that history, and reflect on the suitability of current screening practices and the models employed. A major change in emphasis in drug discovery has influenced the development and selection of new model tumor systems as well as screening practices. This new direction, a search for drugs that are selective for particular tumor histotypes, especially solid tumors, was stimulated by the paucity of drugs that have clinical solid tumor activity. The new approach to drug discovery and screening is in itself an experiment. Only time will tell if this approach is successful.
Cancer Metastasis Rev 1991 Oct
PMID:Tumor models in drug development. 176 68

Magnetic resonance imaging (MRI) was performed in 126 children with malignant solid tumor between April 1984 and December 1990. The criteria of tumor visualization, localization, staging, prediction of kidney preserving and monitoring treatment were compared by MRI and CT for 47 children with neuroblastoma, Wilms' tumor, hepatoblastoma, rhabdomyosarcoma and teratoma, MRI and CT were viewed together and an assessment was made as to whether the studies yielded equivalent information or whether one study was superior to the other. 1) The tumor were better visualized in 47% cases by MRI than CT. 2) MRI was superior to CT in 43% cases in evaluating the local spread of tumor. 3) There was little difference between MRI and CT in identification of lymph node metastases. 4) Without requiring the injection of intravenous contrast agents, MRI accurately defined displacement, invasion of renal vessels by neuroblastoma. MRI was excellent in prediction of kidney preserving. 5) MRI was useful to detect bone marrow metastases in neuroblastoma. The best imaging plane for a demonstration of bone marrow involvement was coronal in lower limbs.
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PMID:[The role of magnetic resonance imaging for treatment in children with malignant solid tumor]. 194 73

Renal cell carcinoma (RCC) represents an unusual solid tumor for which no treatment other than surgical therapy has been effective. The remarkable heterogenous behavior of this tumor and the documented rare spontaneous regressions suggest an unusual sensitivity to host immunologic control. In recent years, exciting developments in molecular genetics, growth factors, modulators of invasion of metastases, and cytokine-lymphocyte interactions have produced new hypotheses and a wealth of information regarding the origin, behavior, and control of RCC. Interest in the immunotherapy of metastatic RCC has recently increased with the demonstrated reproducible tumor responses obtained with recombinant human interferon-alpha or interleukin-2. Durable clinical remissions in some patients with advanced RCC can now be achieved by using cytokine therapy alone or in combination with activated killer cells. This article reviews the current understanding of the basic biology of RCC, surgical approaches to localized RCC, and biologic therapy for advanced disease.
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PMID:Renal cell carcinoma: basic biology and current approaches to therapy. 194 36


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