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 accumulation of bone-seeking radiopharmaceuticals in extraosseous lesions has been reported in patients with myocardial infarctions, cerebral infarctions, and some soft-tissue tumors. While the precise mechanisms involved remain uncertain, the spectrum of abnormalities exhibiting such accumulation increases. In our laboratory, 99mTc-diphosphonate concentrated in four hepatic tumors (one cholangiocarcinoma and three metastases from colon carcinoma). This property of phosphate-related radiopharmaceuticals has not been reported previously. Awareness of the possibility of focal diphosphonate accumulation in the liver should help avoid confusion with right lower rib-cage metastasis or pleural effusion.
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PMID:Accumulation of 99mTc-diphosphonate in four patients with hepatic neoplasm: case reports. 18 68

The relative distribution of T- and B-lymphocytes in the blood and in pleural or abdominal effusions was compared among 24 patients with fluid accumulation due to metastatic cancer and 8 patients without evidence of cancer. The data obtained indicated that the mean percentage of T-lymphocytes in malignant effusions was significantly greater than that in the peripheral blood of the same patients. At the same time, the mean eprcentage of B-lymphocytes was decreased in malignant effusions when compared with peripheral blood. Neither of these differences was observed when effusions and blood of patients with nonmalignant effusions were compared. In addition, patients with both types of effusions had fewer total lymphocytes in their blood than did normal control patients, whereas those with cancer-associated effusions had an increased proportion of active T-lymphocytes in their blood.
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PMID:Distribution of T-lymphocytes and B-lymphocytes in peripheral blood and effusions of patients with cancer. 30 1

This report summarizes our experience during a four-year period with the repair of 8 thoracic cage and 3 diaphragmatic defects requiring reinforcement with prosthetic material. Defects as large as the entire left hemidiaphragm or the right anterior chest wall including ribs two through six from the midsternum to the midaxillary line were adequately repaired. The technical approach utilized to obtain a secure, nonmobile thoracic cage involved the placement of sutures through drill holes or around ribs, rather than through the periosteum or pericostal soft tissues. Successful diaphragmatic repair was dependent on proper anchoring of the medial border of the prosthesis, placing sutures in the pericardium as necessary. Skin coverage for thoracic cage defects was achieved with widely undermined and advanced local tissue or previously delayed pedicle flaps. All patients had good evidence of chest wall stabilization after operation, and all were removed from mechanical ventilation within three days. One patient died of myocardial infarction twenty days after operation, and a second patient died later of metastatic disease. On the basis of our experience, we conclude that the range of chest wall lesions that can be surgically corrected or palliated is increased by the use of prosthetics implanted with techniques described here.
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PMID:Repair of chest wall defects with prosthetic material. 45 17

Rarity of placental metastasis is only apparent, for only few placentas of cancerous mothers have been examined histologically. However, it may show biological and immunological conditions which are characteristics of foeto-placental unit. During metastatic spread of solid tumors or hematologic malignancies in the mother, tumor emboli may be localized in intervillous spaces, without being real placental metastasis. Rarely tumor emboli are able to invade the struma of chorionic villi and produce true placental metastases: twelve such observations have been published, seven of which were malignant melanomas. It is even more exceptional that metastatic spread reaches the foetus. In most of the cases, it is thus protected against maternal cancer. This historical observation holds true. The fear of transplacental graft to the foetus is not an argument favorable of terminating a cancer associated pregnancy and foetal metastasis of maternal origin are not among the causes of congenital cancers in children.
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PMID:[Placental metastasis (author's transl)]. 46 47

Bone imaging studies of 1650 patients with known or strongly suspected extraosseous malignancies were reviewed to determine whether a completely negative posterior view was sufficient to exclude metastatic disease. Of 708 negative posterior images, 27 (3.4%) were positive for metastasis on anterior views. All of the anterior lesions were in the sternium, sternoclavicular joints and first four ribs. When the posterior view is positive, further views may be unnecessary. Negative or equivocal posterior images necessitate anterior views of the thoracic cage.
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PMID:Is the anterior bone scan necessary in the diagnosis of osseous metastases? 65 74

Bone scans with 99mtechnetium diphosphonate were performed on 2 patients with gynecomastia induced by diethylstilbestrol therapy for adenocarcinoma of the prostate. Neither patient had evidence of bone metastases but both scans revealed increased isotope concentration over the anterior rib cage at the lateral margin of the chest wall, corresponding in location to the hypertrophic breasts. This observation may be related to similar radionuclide uptake in normal and abnormal female breasts. One should not mistake the finding of gynecomastia for metastases of the ribs.
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PMID:Gynecomastia demonstrated on the bone scan. 87 1

The purpose of this study was to develop an animal model of rectal cancer. Three murine-derived cell lines, B16 melanoma, CT26 and MCA38 colon carcinoma, as well as the human colon cancer cell line LS174T were injected into the submucosa of the mouse rectum. Subcutaneous CT26 anbd B16 tumours and intra-caecal CT26 tumours served as controls for tumourigenicity of the cell lines. B16 melanoma produced a locally aggressive rectal tumour as well as skin and para-aortic lymph node metastases. CT26 produced local tumour when injected intra-rectally and colon tumours and liver metastases when injected into the caecum. MCA38 and LS174T intra-rectal injections resulted in large rectal carcinomas without metastases. We believe that growth of a colon cancer cell line in the rectum approximates the human disease more closely than other models of colorectal cancer. We would expect that the model could similarly be utilized to assess the effects of novel adjuvant treatments for rectal cancer as well as in the study of the tumour biology of rectal cancer.
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PMID:Intra-rectal injection of tumour cells: a novel animal model of rectal cancer. 134 Dec 58

The development of new and effective marker substances has optimized tumor-marker-guided follow-up programs to monitor generalization of disease and to assess the therapeutic outcome. Isoferritins of placental origin were first determined in the serum of patients with lymphoproliferative disease by way of the recently developed monoclonal antibody CMH-9. We have set up an Austro-Israeli working group and analysed 64 patients in terms of the sensitivity of placental ferritin (PLF) compared with the standard markers carcinoembryonic antigen (CEA) and mucinous-like cancer-associated antigen (MCA) in patients with metastatic breast cancer. We have additionally evaluated the importance of combined marker determination. Analysis of the data in view of site of metastatic spread yielded satisfying results both for PLF (sensitivity 70.4%) as well as MCA (sensitivity 76.9%) for visceral metastases; a combination of these two markers revealed a striking sensitivity of 88.4%, which, however, could not be improved by adding the third marker (CEA). With regard to non-visceral metastases, CEA and MCA were clearly superior.
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PMID:Placental isoferritin (PLF) in comparison with MCA and CEA in advanced breast cancer--first data from a pilot study. 177 47

A series of 61 consecutive procedures of chest wall resection and reconstruction in 58 patients during the period between August, 1986 and December, 1990 is reported. The ages ranged between 6-77 years. The chest wall resection was indicated for malignant affections in 54 cases. Among these, there were 24 patients with bronchial carcinoma invading the chest wall, 17 patients with primary or metastatic sarcoma, 11 patients with recurrent breast cancer and 3 with cancer metastases of varying origin. Pulmonary resection included pneumonectomy in 8 cases, lobectomy in 19, segmental and wedge resections in 26. In the majority of resections, the reconstruction was accomplished without implants. In cases with full thickness removal of the chest wall, the plane of the rib cage and/or the sternum was reconstructed using Vicryl mesh (n = 7), PTFE soft tissue patch (n = 11), marlex-mesh (n = 1), or methyl-methacrylate (n = 3). There was one case of hospital mortality, 6 weeks postoperatively, due to neurological failure from an independent preoperatively undiagnosed brain tumor. There were 4 reoperations: one early and one late (4 months) infection, one case of limited superficial necrosis of a flap and one with chronic lymphous drainage from a large myocutaneous flap. In no instance was primary postoperative ventilation therapy necessary. Mechanical ventilation was instituted only on day 8 in the patient who accounts for the mortality in this series. In the presence of primary infection, the greater omentum was used for the restoration of the integument.
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PMID:Reconstruction of chest wall defects. 180 37

Recent studies have revealed a role for platelets and the platelet-adhesive proteins, fibronectin and von Willebrand factor (vWF) in platelet-tumor cell interaction in vitro and metastasis in vivo. The present report documents the effect of thrombin treatment of platelets on this interaction in vitro and in vivo. In vitro, thrombin at 100-1,000 mU/ml maximally stimulated the adhesion of six different tumor cell lines from three different species two- to fivefold. As little as 1-10 mU/ml was effective. The effect of thrombin was specific (inhibitable by hirudin, dansyl-arginine N-(3-ethyl-1,5 pentanediyl) amide and unreactive with the inactive thrombin analogue N-P-tosyl-L-phenylchloromethylketone-thrombin and D-phenylalanyl-L-propyl-L-arginine chloromethylketone-thrombin (PPACK-thrombin), and required high-affinity thrombin receptors (competition with PPACK-thrombin but not with N-P-tosyl-L-lysine-chloromethyl-ketone-thrombin). Functionally active thrombin was required on the platelet surface. Binding of tumor cells to thrombin-activated platelets was inhibitable by agents known to interfere with the platelet GPIIb-GPIIIa integrin: monoclonal antibody 10E5, tetrapeptide RGDS and gamma chain fibrinogen decapeptide LGGAKQAGDV, as well as polyclonal antibodies against the platelet adhesive ligands, fibronectin and vWF. In vivo, thrombin at 250-500 mU per animal increased murine pulmonary metastases fourfold with CT26 colon carcinoma cells and 68-413-fold with B16 amelanotic melanoma cells. Thus, thrombin amplifies tumor-platelet adhesion in vitro two- to fivefold via occupancy of high-affinity platelet thrombin receptors, and modulation of GPIIb-GPIIIa adhesion via an RGD-dependent mechanism. In vivo, thrombin enhances tumor metastases 4-413-fold with two different tumor cell lines.
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PMID:Thrombin stimulates tumor-platelet adhesion in vitro and metastasis in vivo. 184 69


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