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)

Systemic administration of swainsonine, an indolizidine alkaloid, inhibits the experimental metastasis of B16-F10 murine melanoma cells. This activity can be attributed primarily to swainsonine-mediated enhancement of host natural killer cell activity. As one next step towards investigating the potential therapeutic utility of this drug, its efficacy in enhancing host survival in the same B16-F10 model system has been assessed. In studies employing intravenously injected tumor cells, pretreatment of mice with swainsonine-containing drinking water provided a reproducible protective effect for the host. This prolongation of survival was substantially enhanced when swainsonine was administered in combination with either of two other immunomodulators, polyinosinic: cytidylic acid (poly-IC) or interleukin-2. In studies in which combinations of these agents were administered after intravenous injection of tumor cells, or after subcutaneous implantation, a greatly reduced effect on host survival was observed. However, when used in combination with cyclophosphamide (to block the effects of suppressor T cells), swainsonine did increase mean survival time. The implications of these results for the use of swainsonine in treatment of metastatic or localized disease, together with its potential mechanism(s) of action, are discussed.
Clin Exp Metastasis
PMID:An assessment of the effects of swainsonine on survival of mice injected with B16-F10 melanoma cells. 210 78

From May 1986 until July 1987, oral morphine hydrochloride in water solution was used in terminal patients, under a strict protocol of administration, and complying with the basic principles of Palliative Care. A retrospective study was carried out on the 40 patients who had received the drug for more than three consecutive days. As shown in Table 1, the average age of the treated patients was 70 years. The ambulatory patients represented 27.5% of the sample. The average initial dose was 60 mg, and the average maintenance dose was 120 mg. The median treatment time was 45 days. "Good" results were achieved in 85% of the patients, and "fairly good" in the remainder ("good" results were defined as "satisfactory symptom control, good life quality"--in this group there were some patients who obtained total suppression of the symptoms and optimal life-quality, i.e. "excellent" results; "bad" results were defined as "total absence of therapeutic effect"; and "fairly good" results, the intermediate cases). The more frequently treated symptoms were: 67.5%, pain due to tumor mass; and 20%, pain due to nerve compression-invasion, bone pain, and dyspnoea due to pulmonary metastases or primary lung cancer: total symptoms was more than a hundred per cent, because a number of patients had more than one symptom. Whenever necessary, adjuvant drugs were employed. Side effects were seen in 37% of the patients (specially nausea, vomiting, constipation, and somnolence for more than four days).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Oral morphine in the treatment of patients with terminal disease]. 213 Feb 44

The diagnosis of colorectal carcinoma is based on double-contrast barium enema and endoscopy. However, in contrast to computed tomography (CT), these modalities do not permit a precise preoperative prediction wether a tumour is limited to the bowel wall or has spread into surrounding tissue. To improve the detection of colorectal neoplasms by CT we prospectively studied the use of intrarectally administered water for CT scan in 16 patients with colorectal cancer proved by barium enema and endoscopy. The water repletion technique allowed an improved depiction of the large bowel wall, and the primary tumour was demonstrated by CT in all cases. Furthermore the use of water prevented artifacts which was helpful in the evaluation of the liver for suspected metastases.
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PMID:[The computed tomography of colorectal tumors with water as the contrast medium]. 216 82

The etiology of the paramagnetic relaxation enhancement seen in malignant melanoma on proton magnetic resonance (MR) images has been the subject of many recent investigations and has been ascribed to iron from associated hemorrhage or chelated metal ions, rather than directly due to melanin. The purpose of this study was to correlate proton relaxation times on MR images in malignant melanomas with histopathologic features (i.e., degree of pigmentation, iron deposition, and necrosis), water content, and electron paramagnetic resonance (EPR) spectra to elucidate the etiology of the relaxation behavior demonstrated by these neoplasms. Cultured cells derived from human malignant melanoma metastases were implanted subcutaneously into nude mice. Twelve separate lesions were evaluated in 10 mice. Magnetic resonance imaging was performed in vivo at 1.9 T using spin echo and inversion recovery acquisitions for the purposes of calculating T1, T2, and proton density [N(H)]. Histopathologic examination was performed on specimens resected immediately after imaging, using hematoxylin/eosin, Prussian blue, and Fontana stains to assess tumor necrosis, and iron and melanin content. Dry/wet weight ratios and EPR spectra were also obtained on resected specimens. Our results indicate that T1 shortening correlates with increasing melanin content and not with increasing iron deposition, EPR-active metallic cations, necrosis, or water content. In fact, a presumably unrelated statistical correlation was found between increased iron and T1 prolongation. The T2 relaxation times did not correlate with the presence of any single factor other than proton density. Although the unique relaxation behavior of nonhemorrhagic malignant melanoma in vivo cannot be traced to a single cause, our data suggest that, contrary to previous investigations, it is strongly influenced by the presence of melanin rather than iron or other naturally occurring paramagnetic ions.
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PMID:Human malignant melanomas with varying degrees of melanin content in nude mice: MR imaging, histopathology, and electron paramagnetic resonance. 216 37

Differentiation of benign from pathologic compression fractures of vertebral bodies was evaluated with magnetic resonance imaging in a prospective study of 53 patients. Twenty-six patients had 34 benign posttraumatic compression fractures. Twenty-seven patients had metastatic disease to the vertebral column and seven pathologic fractures. T1- and T2-weighted spin-echo (SE) sequences (1.5 T) were performed in all patients. A presaturation technique was used to obtain "fat" and "water" images to better assess the degree of normal fatty marrow replacement in fractured vertebrae. Short inversion-time inversion-recovery (STIR) images were also obtained. Discrimination between benign and pathologic compression fractures was generally possible with the SE sequences. Chronic benign fractures demonstrated isointense marrow signal intensity (SI), compared with that of normal vertebrae with all sequences. Pathologic fractures showed low SI on T1-weighted images and high SI on T2-weighted images. Fat images revealed complete replacement of normal fatty marrow, shown as absent SI in the involved vertebral body. Water and STIR images showed diffuse high SI in pathologic fractures, with STIR images having the highest contrast between abnormal and normal marrow. Acute benign compression fractures also demonstrated high SI on T2-weighted, water, and STIR images, but the SI was less pronounced and the pattern was generally more inhomogeneous than that of pathologic compressions. In general, fat images showed only partial replacement of normal fatty marrow by low SI, in contrast to the complete absence of marrow SI typical of pathologic fractures.
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PMID:Benign versus pathologic compression fractures of vertebral bodies: assessment with conventional spin-echo, chemical-shift, and STIR MR imaging. 229 58

In selective internal radiation (SIR) therapy of hepatic metastases, tumor vasculature is preferentially embolized with high-energy beta-emitting yttrium-90-labeled microspheres. To enable accurate estimation of the resultant absorbed radiation doses to tissues, an intraoperative beta detection probe is used to scan the liver surface. The validity of the response of this probe to Y-90 and its clinical application were assessed with a phantom containing varying activities and with biopsy samples obtained from patients being treated with SIR therapy. A linear relationship was found between the probe counts taken from the biopsy samples and the calculated tissue radiation doses from the specific activities of each sample. This relationship was repeated with probe counts determined against a water phantom containing various activities of Y-90. The probe was shown to respond minimally to bremsstrahlung. The use of the probe in measuring tissue radiation doses at laparotomy provides the opportunity to control dose administration during SIR therapy. In this way, subtherapeutic exposure of normal tissue can be assured while tumor tissue receives maximal radiation levels.
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PMID:Selective internal radiation therapy: validation of intraoperative dosimetry. 231 90

Lymphokine-activated killer (LAK) cells combined with recombinant interleukin-2 (rIL-2) can produce tumor regression in murine models and in patients with pulmonary metastatic disease. However, the dose escalations of rIL-2 required for optimal therapeutic effect often result in increased vascular permeability ("vascular leak syndrome") and other toxic systemic consequences. To avoid systemic distribution, lung perfusion was used to administer LAK and rIL-2 locally. Preliminary to using these agents to treat tumor-bearing lungs, we used a nonblood-perfused isolated rat lung model to study the localization of radiolabeled rIL-2 and LAK and to characterize effects on normal lung tissue of increasing dosages and exposure times of rIL-2 and LAK cells, individually and combined. Lung function or permeability was assessed by measuring lung weight gain and pulmonary arterial pressure during the perfusion, extravascular lung water by double indicator dilution techniques, and wet weight to dry weight ratio. After perfusion for 1 hour using 200,000 U (1,300 U/ml) rIL-2, injury was detected as visible pulmonary edema, weight gain and increases in wet to dry weight ratio, and extravascular lung water; no injury was detected at lower, clinically appropriate dosages. When 1 X 10(8) LAK cells combined with 100,000 U rIL-2 (666 U/ml) were perfused for up to 2 hours, no injury was ascertained. Uptake and distribution of the radiolabeled rIL-2 or LAK was uniform to all lung lobes and corresponded to the decrease of 12% of the rIL-2 or 50% of the LAK from the perfusate after 1-hour perfusion.
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PMID:Lymphokine-activated killer cells with interleukin-2: dose toxicity and localization in isolated perfused rat lungs. 233 37

Between 1981 and 1987, 53 of 102 patients with malignant diseases of the oesophagus underwent bypass surgery with gastric, colonic or jejunic interposition. To recognise the early or later complications, we used X-ray examination of the chest, water soluble contrast medium and barium meal, real-time sonography and CT. With these methods we found insufficiencies of anastomosis, stenosis, fistulae to the adjacent organs, necrosis, infections, erosions and ulcerations of the anastomosis, pleuropulmonary complications and metastases. Without of early complications were 30%, without of late complications only 8% of all patients.
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PMID:[Peri- and postoperative roentgen diagnosis following esophageal bypass operation]. 237 33

Results of the treatment of spontaneous pulmonary metastases by immunocorrection after tumour resection in mice and the analysis of antimetastatic activity of spleen macrophages (SM) by the method of adoptive transfer are presented. The injection of cytotoxic SM, NK-cells or the use of the biological response (lipid A and MDP-PE) modifiers cause no decrease in the number of lung metastases. The SM of operated mice, as distinct from the SM of immunocorrected mice causes the metastatic spreading in lungs of recipient mice. This effect is supposed to be mediated by the suppressor macrophages secreting prostaglandin E2 (PgE2). The treatment of mice with indometacin (inhibitor of the PgE2-synthesis) in the drinking water resulted in the 7-8-fold decrease in the number of lung metastases in operated mice.
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PMID:[Characteristics of metastasis and antimetastatic activity of macrophages in mice after postoperative immunomodulation]. 237 91

Tamoxifen, an antiestrogen with efficacy in treatment of both estrogen receptor-positive and negative breast tumors, may be immunomodulatory. We tested tamoxifen's ability to augment the antitumor activity of interleukin-2 (IL-2), a lymphokine capable of expanding and activating lymphocytes, in the treatment of established pulmonary metastases of the weakly immunogenic murine fibrosarcoma MCA-106. Age-matched C57BL/6 female mice bearing pulmonary metastases induced by a tail vein injection of MCA-106 tumor suspension (5 x 10(5) cells/mouse) were treated from days 3 through 12 with intraperitoneal saline solution or IL-2 (50,000 units twice a day). Half of the mice in each group received plain and the remainder received tamoxifen-treated (2 units/ml) drinking water ad libitum for the duration of the experiment. All mice were killed on day 18 for enumeration of pulmonary metastases. Compared with saline-treated control mice, IL-2 and tamoxifen reduced metastases by 66% (p less than 0.0002) and 30% (p less than 0.005), respectively. IL-2 and tamoxifen combined reduced metastases 95% (p less than 0.0002), significantly better than did IL-2 (p less than 0.02) or tamoxifen (p less than 0.0003) alone. In vitro, tamoxifen inhibited proliferation of the weakly estrogen receptor-positive MCA-106 tumor by approximately 30%. Tamoxifen had no effect on the generation of 3-day IL-2-activated lymphocyte cytotoxicity against both natural killer-sensitive (YAC) and natural killer-resistant (MCA-106) target cells. Both YAC and MCA-106 tumor became more resistant to lysis with increased concentration of tamoxifen. This is the first demonstration of in vivo potentiation of IL-2 antitumor activity by tamoxifen and suggests its possible use clinically.
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PMID:Tamoxifen potentiates in vivo antitumor activity of interleukin-2. 238 15


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