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)

Metastases from transitional cell carcinoma of the bladder are not widely appreciated radiographically, although they are commonly found at autopsy. Radiographic evidence of metastatic disease was reviewed in 51 patients. Sites included lung, 28; bone, 24; mediastinum, eight; liver, eight; brain, three; urethra, one; abdominal nodes, one; and extradural space, two. The patterns of lung metastases consisted of solitary nodules, multiple nodules, sigmental infiltrates, pulmonary edema, and a Pancoast tumor. A sarcoidlike pattern with hilar and interstitial disease was also seen. One patient had a malignant pleural effusion. Mediastinal lymph node enlargement was isolated or associated with lung involvement. Bone metastases demonstrated either an osteoblastic or a mixed osteolytic-osteoblastic pattern in 47% of the instances. Ivory vertebrae were identified in three patients. Because of the significance of identifying metastatic disease before any extensive curative bladder surgery, we recommend at least a preoperative chest radiograph, a bone scan, and a liver scan.
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PMID:Metastatic transitional cell carcinoma from the bladder: radiographic manifestions. 10 47

Primary cardiac rhabdomyosarcoma is rare and its extension to the mitral valve even rarer. We report a case of left atrial rhabdomyosarcoma involving the mitral valve. The patient was a 62-year-old man who complained of recurrent pre-syncopal episodes, dyspnoea often sudden in onset, asthenia and major weight loss (10 kg in one month). 2-D echocardiography revealed a 4.9 cm2 wide mass attached to the atrial side of the anterior mitral leaflet and to the adjacent inferior interatrial septum, where it seemed to have origin. CT scan and scintigraphy revealed bone, kidney and spleen metastases. The patient underwent emergency cardiac surgery because of increasing pre-syncopal and dyspnoeic episodes due to obstruction by the intracardiac mass. At surgery a tumor was found infiltrating the left atrial wall, the interatrial septum, the mitral anulus and the anterior mitral leaflet up to its tip. Invasion of mitral anulus did not allow mitral valve replacement, so that an excision of the intracardiac mass was performed as extensively as possible. Histology revealed a rhabdomyosarcoma. A post-operative chemotherapy cycle had to be stopped due to onset of atrial fibrillation and dyspnoea. 2-D echo monitoring revealed rapid new growth of the tumor across the basal portion of mitral valve leaflet to the atrioventricular orifice. After several episodes of increasing dyspnoea, the patient had a pulmonary oedema and died.
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PMID:[Primary cardiac rhabdomyosarcoma involving the mitral valve]. 129 26

Interleukin-2 is a glycoprotein physiologically produced by human lymphocytes which is capable of mediating some still unknown immunologic reactions. In vitro, interleukin-2 was seen to induce a lytic reaction against tumor cells through the activation of a cytolytic system of natural killer cells. If administered to man in heavy doses, it causes a clinical response in the treatment of metastases from melanoma and renal cell carcinoma in 20-40% of cases. However, the clinical use of the drug, in therapeutic doses, is prevented by the occurrence of several side-effects, the major one being increased permeability of alveolar vessels with capillary leak and interstitial pulmonary edema (Vascular Leak Syndrome in the English literature). Thus, this work was aimed at evaluating chest radiographs during interleukin-2 treatment to detect, in the pulmonary district, the early stages of the vascular leak syndrome--i.e., pulmonary edema, pleural and pericardial effusions. Forty-three patients had been treated for metastases from renal cell carcinoma and melanoma November 1989 through September 1991: standard chest radiographs demonstrated 26 cases (60%) of pulmonary edema, 14 cases (32%) of bilateral pleural effusions and 12 cases (27%) of pericardial effusions. Daily chest films of the patients undergoing interleukin-2 therapy allowed the early stage of the vascular leak syndrome to be depicted, thus enabling the physician to use the highest tolerated doses and eventually to stop infusion before marked respiratory distress develops.
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PMID:[Radiologic characteristics of the thorax during therapy with interleukin-2]. 145 17

The chest roentgenograms of 54 patients receiving high dose interleukin-2 with or without lymphokine-activated killer cell therapy for advanced cancer were retrospectively reviewed. Thirty-nine patients (72 percent) developed chest roentgenographic abnormalities consisting of pleural effusions, 28 (52 percent); diffuse infiltrates (pulmonary edema), 22 (41 percent); and focal infiltrates, 12 (22 percent). These abnormalities resolved in 30 of 39 (77 percent) patients by four weeks after therapy. Simple pleural effusions were the only residual roentgenographic abnormalities seen and were present primarily in patients receiving IL-2 by bolus intravenous injection (8 of 28) (29 percent) as compared to continuous intravenous infusion (1 of 24) (4 percent) (p = 0.03). Only roentgenographic evidence of pulmonary edema appeared to correlate with the degree of clinical pulmonary toxicity (p = 0.001). The development of chest roentgenographic abnormalities correlated with the administration of IL-2 solely by bolus intravenous injection (p = 0.04), a pretreatment FEV1 of less than 3 L (p = 0.04), and treatment associated bacteremia (p = 0.09), but not with prior therapy, the presence of pulmonary metastases or the degree of systemic capillary leak as measured by percentage of weight gain during therapy. Although the roentgenographic abnormalities did not relate to the number of LAK cells received, two patients developed sudden onset of dyspnea and chest roentgenographic evidence of pulmonary edema shortly after the first LAK cell administration, implying that a direct cause-and-effect relationship exists in some patients. Possible mechanisms for these IL-2 related chest roentgenographic abnormalities and pulmonary toxicity in general are discussed.
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PMID:Chest roentgenographic abnormalities in IL-2 recipients. Incidence and correlation with clinical parameters. 154 Nov 42

Seventeen patients with chemotherapy-resistant metastatic sarcoma were treated with whole body hyperthermia (WBH) combined simultaneously with 1-3-Bis(2-chloroethyl)-1-nitrosourea (BCNU). All of the patients had chemotherapy resistant metastases to major organ sites. Patients were heated to 41.8-42.0 degrees C for 2 h using an insulated blanket heating technique. Two patients (12%) experienced partial responses (PR). In addition, four objective tumour responses (OR) lasting more than 4 months were documented. One patient with previously rapidly growing chondrosarcoma pulmonary metastases experienced stable disease (SD) for 38 months from the onset of treatment. Median survival of seven patients with responding tumours (PR, OR and SD) compared with 10 patients with progressive disease was 15 versus 2 months, respectively. Cumulative thrombocytopenia was a therapy-limiting toxicity of the combined treatment, and occurred in six of seven patients. Acute toxicities attributable to WBH alone included transient thrombocytopenia in all patients, non-cardiogenic pulmonary oedema in two patients, and mild hypotension in five patients. Acute granulocytosis was observed in all patients. No treatment related deaths occurred. These data suggest that WBH combined with chemotherapy is associated with disease response in patients with chemotherapy-resistant, widely disseminated sarcoma metastases.
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PMID:Chemotherapy resistant sarcoma treated with whole body hyperthermia (WBH) combined with 1-3-bis(2-chloroethyl)-1-nitrosourea (BCNU). 160 34

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

To evaluate the radiographic manifestations of the response of intrathoracic metastases to and the toxicity of interleukin-2 (IL-2) therapy, the chest radiographs and computed tomographic scans of 43 patients receiving 103 cycles of IL-2 treatment and lymphokine-activated killer cells for advanced renal cell carcinoma were reviewed. Among these 43 patients, 31 could be assessed for response of metastatic disease: Complete response was seen in one (3%), partial response in 11 (36%), mixed response in nine (29%), progressive disease in five (16%), and stable disease in five (16%). In 103 treatment cycles radiographic evidence of toxicity included pleural effusions (45.6%), pulmonary edema (21.4%), increased cardiothoracic ratio (16.5%), increased azygos vein diameter (9.7%), pericardial effusion (5.8%), and hilar lymphadenopathy (1.0%). These toxic effects could be distinguished from metastatic disease by a temporal relationship to treatment cycles. A favorable response to IL-2 therapy was significantly correlated (P less than .001) with the presence of pleural effusions.
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PMID:Interleukin-2 therapy for advanced renal cell carcinoma: radiographic evaluation of response and complications. 239 11

The administration of interleukin-2 (IL-2) and lymphokine activated killer (LAK) cells to patients with advanced metastatic cancer has yielded encouraging results. The purported ability of LAK cells to be discriminatively tumoricidal, thus sparing normal host tissue, represents a major advance over conventional chemotherapy. However, IL-2 adoptive immunotherapy results in dose-limiting toxicity characterized by weight gain, dyspnea, ascites, and peripheral-pulmonary edema suggestive of a vascular leak syndrome. It is unclear whether the observed toxicity is directly related to IL-2 and/or LAK cells. The authors examined the cytolytic nature of human LAK cells against human endothelial, epithelial, and fibroblast cell lines. Bovine endothelial cells also were studied. Using a 51Cr release assay, the cytolytic potential, time course, and effect of reactive oxygen intermediate inhibitors were studied. LAK cells were uniformly toxic against all cell lines, in contrast to high dose rIL-2 and excipient. Significant cytolysis was observed within 30 minutes and increased over the first 2 hours of LAK cells coming in contact with target cells. Reactive oxygen intermediate inhibitors did not reduce cytolytic activity. The authors thus found human LAK cells to be rapidly cytolytic against a variety of human and bovine cell lines. This cytolysis was independent of reactive oxygen intermediates.
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PMID:Nonspecific cytotoxicity of recombinant interleukin-2 activated lymphocytes. 266 84

The patient was a 70-year-old male with complaint of macrohematuria at the first visit to our clinic on June 10, 1986. At that time, cystoscopy revealed a thumb sized papillary tumor and a rice sized non papillary tumor, and the biopsy specimen was pathologically diagnosed as undifferentiated carcinoma. But, he refused admission. On January 30, 1987, he came back to our clinic with complaints of dyspnea, general fatigue and weight loss. Moderate lt. gynecomastia was found and the level of serum hCG-beta was detected as high as 101 ng/ml. Excretory urogram and enhanced CT revealed a large mass in the bladder. In the seventeenth day after admission, he died of lung edema and heart failure. The findings of autopsy showed a large light greenish to light brownish tumor of 10 X 10 X 3 cm in the bladder. Distant metastases were observed in internal, common iliac and paraaortic lymph nodes, but without other distant metastasis. In histological and immunohistochemical studies, the final diagnosis is choriocarcinoma of the bladder, containing syncytiotrophoblastic giant cells with hCG-beta granules as an undifferentiated carcinoma. To our knowledge this case is the eighth described in Japan. Herein we report a new case of primary choriocarcinoma of the bladder and make a brief review of the literatures.
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PMID:[Primary choriocarcinoma of the bladder: a case report of autopsy]. 267 66

Radiographic identification of pulmonary metastases has proved to be a challenging problem. We applied high resolution CT (HRCT) to 180 post-mortem lung specimens prepared by a method that allows for direct one-to-one pathologic-radiologic correlation. Of the 180 lungs, 32 had pulmonary metastases. The location, number, size, and interstitial changes were evaluated in 32 cases with pulmonary metastases. The pulmonary metastases were peripheral lesions in 94% of these 32 patients, and multiple tumors were found in 91% of these cases. The metastases were less than 1 cm in diameter in 78%. Twenty-two of the 32 cases (69%) had obvious interstitial changes. In 19 of these 22 cases the interstitial change was characterized by the appearance of a "beaded septum" on HRCT. This beaded septal change corresponded directly to tumor growth in pulmonary capillaries and lymphatics and the septal interstitium. This sign was not noted in any of the specimens with pulmonary edema or fibrosis or in normal lungs. We believe that detection of the beaded septum sign on HRCT is highly suggestive of pulmonary metastases.
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PMID:Computed tomography of inflation-fixed lungs: the beaded septum sign of pulmonary metastases. 272 71


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