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 cellular origin of estrogen-induced kidney tumors in male Syrian hamsters has been repeatedly the subject of controversy. Several authors have proposed that the tumors arise from proximal tubules, from a combination of tubular and interstitial stromal cells, or solely from interstitial cells. Because of the model character of this tumor for hormone-associated cancer, it was further investigated in this study with respect to morphology, enzyme and intermediate filament pattern, the expression of alpha-smooth muscle actin and the extracellular matrix proteins fibronectin and tenascin. These analyses were carried out with early and late tumors as well as metastases to determine possible changes in expression of biochemical parameters during the development and progression of this neoplasm. The enzyme histochemical and intermediate filament patterns were usually the same as those described previously for proliferative foci and early tumors, i.e. highly elevated activities of glucose-6-phosphate dehydrogenase, adenylate cyclase and alkaline phosphatase, a lack of glucose-6-phosphatase and gamma-glutamyltransferase and coexpression of vimentin and desmin, alpha-smooth muscle actin could not be detected in early lesions. In five of 24 advanced tumors inclusions of kidney tubules were found which showed various degrees of alteration in their morphology and enzyme histochemical pattern, but were often directly connected with tubular segments of normal appearance outside the tumor. Like the normal tubules, the enclosed tubular segments were strongly positive for cytokeratin but never expressed vimentin or desmin. Among the 24 tumors studied, two contained cysts which expressed cytokeratin and sometimes also vimentin but not desmin. The enzyme histochemistry of the cells lining the cysts was similar to that of the surrounding tumor mass, except adenylate cyclase was lacking and alkaline phosphatase was not uniformly distributed. In tumors containing cytokeratin-positive cysts, there often were cytokeratin-positive, vimentin-negative and desmin-negative tumor formations in close contact to these cysts. With the exception of cyst formation, the pattern of metastases were identical to that of the primary tumors. All large tumors and the main component of the metastases expressed vimentin, desmin and fibronectin. Mesothelia surrounding metastatic tumor complexes were positive for vimentin, desmin, alpha-smooth muscle actin, fibronectin, cytokeratin and tenascin. It was concluded from these and previous observations on early stages of tumor development that the estrogen-induced hamster kidney tumor originates from mesenchymal interstitial cells (probably pericytes) which may rarely acquire an epithelial phenotype by metaplastic transformation during tumor progression.
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PMID:Changes in the cellular phenotype and extracellular matrix during progression of estrogen-induced mesenchymal kidney tumors in Syrian hamsters. 171 81

The systemic administration of interleukin-2 (IL-2) can lead to significant antitumor responses in some patients with metastatic cancer in whom standard therapy has failed. A limitation of this immunotherapy is the toxicity associated with IL-2 infusion. To assess toxicity, we determined aspartate aminotransferase (AST; EC 2.6.1.1), alanine aminotransferase (ALT; EC 2.6.1.2), gamma-glutamyltransferase (GGT; EC 2.3.2.2), lactate dehydrogenase (LD; EC 1.1.1.27), alkaline phosphatase (ALP; EC 3.1.3.1), creatine kinase (CK; EC 2.7.3.2), total bilirubin (TBI), direct bilirubin (DBI), creatinine, urea nitrogen, and C-reactive protein in serum from 21 patients before and during five consecutive days of IL-2 treatment. Ten patients were followed for an additional five days after the end of IL-2 therapy. The IL-2 infusion caused liver toxicity and prerenal azotemia, as evidenced by significant increases (P less than 0.05) of all analytes except CK by day 1. There was a progressive increase in the results (except CK) for these tests until IL-2 treatment was stopped. Seven tests related to liver function (AST, ALT, GGT, LD, ALP, DBI, and TBI) showed increases, but the test results indicated significant improvement and moved toward the baseline value five days after the end of IL-2 therapy. Concentrations of creatinine and urea nitrogen in serum were normal three days after the cessation of IL-2 therapy.
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PMID:Changes in laboratory results for cancer patients treated with interleukin-2. 231 Dec 9

Urinary excretion of alpha-glucosidase (AGL), gamma-glutamyltransferase (GGT) and ribonuclease (RNase), and serum amylase and immunoreactive trypsin (IRT) were determined in 38 control subjects, 48 patients with pancreatic cancer, 77 with chronic pancreatitis and 47 with extrapancreatic diseases in order to ascertain the presence of a renal tubular damage and to investigate its etiology. A significantly increased frequency of pathological results for all urinary enzymes was documented in the various groups of patients as compared to controls. Significant correlations were detected among AGL, GGT and RNase. Considering the subjects as a whole, GGT and RNase excretions correlated with serum IRT and amylase; the two urinary enzymes were found to be higher when jaundice was present. In chronic pancreatic disease enzymuria was related to increased serum pancreatic enzymes; in extrapancreatic diseases it was associated to hyperbilirubinemia. The vast majority of patients with pancreatic cancer and elevated urinary enzymes presented hepatic metastases and/or jaundice. We can conclude that an anatomical and functional tubular impairment is detectable in some patients with chronic pancreatic and extrapancreatic diseases. Tubular damage seems to least in part to be related to pancreatic inflammation and necrosis in chronic pancreatic disease, while jaundice may be found to play an important role in diseases of the hepatobiliary tract. In pancreatic cancer, liver dysfunction (presence of liver metastases and/or extrahepatic cholestasis) also appears to be involved in altering tubular cells.
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PMID:Renal tubular dysfunction in pancreatic cancer and chronic pancreatitis. 256 74

In 1983 we initiated a prospective nonrandomized study of the value of preoperative chemotherapy in previously untreated patients with stages III and IV squamous cell carcinoma of the head and neck. In 1983 and 1984, 50 patients were entered in the study. Prior to therapy all patients were evaluated by a representative from the Medical Oncology, Radiation Therapy, and Head and Neck Surgery Divisions, University of Utah School of Medicine, Salt Lake City. In addition to the standard preoperative evaluation, pretreatment computed tomographic scans were performed on all patients. Follow-up computed tomographic scans were performed after the second cycle of chemotherapy and at the completion of treatment. Initial therapy in all patients consisted of induction chemotherapy with cisplatin (day 1, 100 mg/m2) and fluorouracil (days 1 through 5, 1000 mg/m2). Several factors were examined for their utility in predicting response to therapy and survival. Factors evaluated included: (1) extent and timing of chemotherapeutic response; (2) computed tomographic quantitated primary tumor size; (3) size of computed tomographic quantitated regional (neck) metastases; (4) performance status; (5) cancer stage; (6) total lymphocyte count; and (7) serum liver function tests. The factor found to be most useful in predicting improved survival was the extent of response to chemotherapy. The remaining factors, performance status, regional lymph node status, serum gamma-glutamyltransferase levels, and cancer stage, were also found to correlate with length of survival but were much less important than the response to chemotherapy.
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PMID:Prognostic indicators in head and neck cancer patients receiving combined therapy. 257 81

Serum concentrations of lipids and apolipoprotein A-I, A-II and B were determined in patients with hepatic metastases of colorectal cancer, with primary liver cancer and with cirrhosis. In all three liver diseases, the HDL fraction and apolipoproteins A-I and A-II showed significantly low values, while apolipoprotein B was only increased in hepatic metastases. The decrease of apolipoprotein A-II levels was more prominent in cirrhosis, thereby enhancing the A-I/A-II ratio. This ratio is decreased in metastasis and normal in hepatomas. In patients with hepatic metastases a correlation was observed between alkaline phosphatase and apolipoprotein A-II (p less than 0.05), and between gamma-glutamyltransferase and the A-I/A-II ratio (p less than 0.05). The present work suggests that determination of apolipoproteins and lipids of the HDL fraction offers a new approach to the study of liver diseases.
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PMID:Serum apolipoproteins A-I, A-II and B in hepatic metastases. Comparison with other liver diseases: hepatomas and cirrhosis. 287 62

Enzymes of glutathione metabolism, particularly gamma-glutamyltransferase (GGT) and glutathione S-transferase (GST), play a role in multistage hepatocarcinogenesis. The enhanced expression of these enzymes in preneoplastic altered hepatic foci, nodules, and hepatocellular carcinomas has been demonstrated after treatment with a variety of initiating and promoting agents. Glutathione is necessary for the detoxification of xenobiotics and carcinogens and for cell replication. Induction of GGT in altered hepatocytes may permit these cells to utilize extracellular glutathione to preserve their internal glutathione levels. GST induction allows glutathione utilization for the protection of the altered hepatocyte in an environment of exposure to xenobiotics, such as promoting agents. Thus, the combined effects of GGT and GST, in a toxic environment, may provide for the enhanced proliferation observed in preneoplastic hepatocytes. New clinical and research opportunities may involve the use of GGT and the placental isozyme of GST (PGST) as markers of preneoplasia and neoplasia in humans. Many factors, such as hormones, diet, and exposure to initiating and promoting agents, influence GGT and GST expression. The recent cloning of cDNAs to GGT and PGST offers opportunities for the study of factors involved in the genetic expression of these two enzymes. Coupled with the use of hepatocyte culture and transplantation, the factors involved at the molecular level in the creation of hepatocellular neoplasia may be discovered.
Cancer Metastasis Rev 1987
PMID:Enzymes of glutathione metabolism as biochemical markers during hepatocarcinogenesis. 288 99

The usefulness and specificity of the main tumor markers (carcinoembryonic antigen, CEA; gastrointestinal cancer-associated antigen, GICA; tissue polypeptide antigen, TPA; fibrinopeptide A, FpA; gamma-glutamyltransferase, gamma-GT) have been investigated in the diagnosis and follow-up of the circumscribed and disseminated gastric cancers (GCs). The comprehensive evaluation of all of these markers has given the most reliable results. For the diagnosis and follow-up of GCs, the present study has shown that the sensitivity and specificity of the above markers have the following decreasing order: FpA, TPA, GICA, CEA, gamma-GT. However gamma-GT has proved to be a reliable index of the presence of hepatic metastases.
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PMID:Specificity of carcinoembryonic antigen, gastrointestinal cancer-associated antigen, tissue polypeptide antigen, fibrinopeptide A and gamma-glutamyltransferase in the diagnosis and follow-up of gastric cancer. 289 1

An 8-year-old Holstein cow was referred with a history of weight loss, poor milk production, and hyperfibrinoginemia. Laboratory evaluation showed high gamma-glutamyltransferase activity, prolonged sulfobromophthalein clearance half-time, and prolonged prothrombin and partial thromboplastin times. Multiple firm nodules with histologic evidence of bile ductule carcinoma were found on exploratory laparotomy and liver biopsy. Pulmonary and lymph node tumor metastases were extensive. Tumor development in this case could not be associated with any of the known contributing factors in ruminants. This case demonstrates the extensive metastatic potential of this tumor and nonspecific signs with which bovine hepatic disease can be manifested.
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PMID:Metastasis of bile ductule carcinoma in a cow. 403 Apr 54

We describe a simple, rapid, and reproducible ion exchange mini-column chromatographic method for the quantitative measurement of biliary alkaline phosphatase in plasma. We have used this method to evaluate a cellulose acetate electrophoretic method, which was used to assess the value of measuring biliary alkaline phosphatase in 85 patients with breast cancer investigated for possible hepatic metastases. Biliary alkaline phosphatase activity was abnormal in 19 of 24 patients (79%) with liver metastases, but abnormalities were also found in 12 of 61 patients (20%) without hepatic metastases; in only 37% of patients with positive test results was this a consequence of liver metastases. For the identification of liver metastases, therefore, the method has useful sensitivity but limited specificity. Neither sensitivity nor specificity was significantly better than that of plasma gamma-glutamyltransferase activity, which was measured concomitantly.
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PMID:Measurement of biliary alkaline phosphatase by mini-column chromatography and by electrophoresis and its application to the detection of liver metastases in patients with breast cancer. 614 Nov 85

In 430 stage I-II breast cancer patients the cost-benefit of investigations during follow-up have been studied. Median follow-up time was 8 years and 128 patients had relapsed, 91 with metastatic disease. High costs of routine chest X-ray, limited skeletal X-ray and bone scan examinations were associated with low incidence of diagnosed relapses not suspected otherwise. In the eight blood analyses examined, increases of more than 10 mm/h in erythrocyte sedimentation rate (ESR), 20 U/l in gamma-glutamyltransferase (GT) or 60 U/l in alkaline phosphatase (ALP) resulted in a combined sensitivity of 55% and specificity of 91% for relapses with distant metastases. Elevation of at least two blood tests gave a combined sensitivity of 31% and a specificity of 98%. The importance of using individual reference values in screening for recurrences is emphasised. Symptomatic relapse or relapse detected at interval visits were not independent prognostic factors. The blood tests ALP, ESR and GT were strong predictors of survival measured from relapse which increase their legitimacy in follow-up. A more frequent follow-up for patients with 4+ involved nodes is proposed: three visits annually the first 5 years vs. two visits annually for the others. We conclude that history, clinical examination, ALP, ESR and GT are sufficient as a baseline screening for relapse in breast cancer patients.
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PMID:Follow-up of breast cancer patients stage I-II: a baseline strategy. 849 40


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