Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CSF beta-glucuronidase, polyamines and carcinoembryonic antigen (CEA) were analyzed in 16 patients with meningeal carcinomatosis from solid tumor in systemic organs, 27 with benign brain lesions, 18 with primary brain tumors, 14 with metastatic brain tumors and 5 with leptomeningeal dissemination of other malignant diseases. Beta-glucuronidase levels in all cases of meningeal carcinomatosis, meningeal gliomatosis and meningeal lymphoma were higher than 100 micrograms/dl/hr; on the other hand, levels in all cases of benign brain lesions were below 100 micrograms/dl/hr. Levels of beta-glucuronidase and polyamines were not high in the cases with positive cytology after tumor resection. Polyamine levels were below 0.05 nmol/ml in all cases after resection of the metastatic brain tumor. Cystic fluid of malignant tumors showed high levels of beta-glucuronidase and polyamines. On the other hand, the levels of polyamines in the cystic fluid of benign tumor were low, although the levels of beta-glucuronidase were high. Some cases of meningeal carcinomatosis with high levels of serum CEA did not show high levels of CSF CEA. For metastatic brain tumors, the cases with intraparenchymal tumors, especially with dural attachment showed high levels of beta-glucuronidase and CEA preoperatively, but they returned to normal after surgery. In cases of meningeal carcinomatosis treated by intrathecal chemotherapy with methotrexate (MTX) and cytosine arabinoside (Ara-C), CSF beta-glucuronidase reflected the neurological status better than the cell count decreased rapidly following chemotherapy and beta-glucuronidase was considered as a useful CSF marker in cases of meningeal carcinomatosis to monitor the course of the disease. The same situation was observed in CSF CEA and CEA was also considered as a useful marker when CEA levels in CSF are higher than those in serum.
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PMID:Measurements of CSF biochemical tumor markers in patients with meningeal carcinomatosis and brain tumors. 156 Feb 55

We have assessed the diagnostic value of the determination of cerebrospinal fluid lactate dehydrogenase, carcinoembryonic antigen, beta 2-microglobulin, beta-glucuronidase and total protein, using linear discriminant analysis, in detecting central nervous system metastases from extracranial malignancies. We conclude that, using these tests, it is impossible to differentiate between control individuals and patients with brain or epidural metastases. Leptomeningeal dissemination from either solid tumours or non-Hodgkin lymphoma could be differentiated from control individuals and patients with brain or epidural metastases. In this differentiation it is essential that bacterial, fungal or tuberculous meningitis be excluded from the differential diagnosis by other diagnostic procedures. The combination of beta-glucuronidase and beta 2-microglobulin provides almost the same diagnostic information as the combination of all parameters.
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PMID:Tumour markers in the cerebrospinal fluid of patients with central nervous system metastases from extracranial malignancies. 340 30

The concentration of carcinoembryonic antigen (CEA) in cerebrospinal fluid (CSF) was determined by using an enzyme immunoassay for 204 patients with various nonneoplastic neurologic disorders, 8 patients with systemic infectious diseases, 19 patients with systemic neoplastic diseases without involvement of the nervous system, and 35 patients with neoplastic neurologic disorders. The highest CEA level in CSF among patients without neoplastic neurologic disorders was 0.6 ng/ml. Of 35 patients with neoplastic neurologic disorders, 10 had CEA levels in CSF that exceeded 0.6 ng/ml, the highest level being 70.5 ng/ml. All 10 patients had carcinomas. Among 14 patients with neoplastic meningitis, 5 of 8 patients with meningeal carcinomatosis had elevated CEA concentrations. Although the efficacy of the assay for CEA in CSF must be compared with that of other laboratory tests such as cytologic examination and the assay for beta-glucuronidase--and any potentially false-positive results should be ruled out by determination of the serum CEA level--the CEA concentration in CSF can be used as an adjunctive diagnostic procedure for detection of meningeal carcinomatosis.
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PMID:Elevation of carcinoembryonic antigen in cerebrospinal fluid among patients with meningeal carcinomatosis. 351 Mar 43

The clinical efficacy of four laboratory tests in detecting leptomeningeal metastases in 57 patients with breast carcinoma was assessed. The sensitivity and specificity of beta-glucuronidase, beta 2-microglobulin, carcinoembryonic antigen and lactate dehydrogenase in cerebrospinal fluid were determined. As a single test beta-glucuronidase was the most sensitive (93%) and specific (93%) for discriminating between leptomeningeal metastases and other CNS metastases from breast cancer. Lactate dehydrogenase was the next most useful marker. Both beta 2-microglobulin and carcinoembryonic antigen had a sensitivity of 60%. More specific results were achieved by combining beta-glucuronidase and lactate dehydrogenase. CSF beta-glucuronidase may be useful by itself and in combination with lactate dehydrogenase in the detection of leptomeningeal metastases from breast carcinoma.
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PMID:Sensitivity and specificity of single and combined tumour markers in the diagnosis of leptomeningeal metastasis from breast cancer. 972 63

The clinical findings and response to treatment of leptomeningeal metastases from solid tumors are analyzed in 90 patients treated at Memorial Sloan-Kettering Cancer Center during the period from January 1975 to February 1980. Patients included those who had either typical clinical findings of leptomeningeal tumor or conclusive laboratory evidence supporting the diagnosis. Carcinoma of the breast (46 patients), lung (23 patients) and melanoma (11 patients) were the common primary tumors. Symptoms of leptomeningeal metastasis occurred as the presenting sign in five patients and as late as ten years after the primary tumor was diagnosed in four other patients. Most patients had active systemic disease outside the nervous system. Signs and symptoms could be classified as involving either the brain, cranial nerves, or spinal nerves. Most patients had either symptoms or signs in more than one area at the time the diagnosis was established. The initial spinal fluid examination was abnormal in all but three patients, but only 49 had cytologic evidence of leptomeningeal metastases. Repeated spinal fluid assay yielded a positive cytology in 82 patients. Measurement of biochemical markers, including beta-glucuronidase, carcinoembryonic antigen and lactic dehydrogenase, assisted in the diagnosis. Approximately half of the patients treated by intraventricular methotrexate experienced improvement or stabilization of neurological symptoms for more than a month; median survival was 5.8 months after diagnosis, with a range of 1--29 months. In 18 patients disease was limited to the nervous system, and median survival was eight months, with four patients surviving one year and two patients for two years. Side effects of therapy were, for the most part, minor. We conclude that vigorous treatment of leptomeningeal metastases with intrathecal chemotherapeutic agents improves symptomatology in some patients, and at times prolongs survival.
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PMID:Diagnosis and treatment of leptomeningeal metastases from solid tumors: experience with 90 patients. 689 13

beta-Glucuronidase and carcinoembryonic antigen (CEA) were measured in the cerebrospinal fluid of patients with cancer. Both substances were found to reliably detect the presence of leptomeningeal infiltration by carcinoma. Neither substance was reliable in the detection of leptomeningeal infiltration by lymphoma or of metastases to the brain parenchyma or spinal epidural space. beta-Glucuronidase was moderately elevated in chronic infectious meningitis, whereas CEA was not. Both markers approached control levels with favorable treatment of the leptomeningeal metastases, reflecting the effectiveness of treatment. Both beta-glucuronidase and CEA hold promise as indicators of early metastatic involvement of the leptomeninges by carcinoma.
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PMID:Cerebrospinal fluid biochemical markers of central nervous system metastases. 721 47

A two component system, consisting of a fusion protein and an appropriate prodrug, suited to perform selective tumor therapy in vivo, is presented. The fusion protein, owing to its humanized carcinoembryonic antigen (CEA)-specific variable region, specifically binds to CEA-expressing tumors and has an enzymatic activity comparable to human beta-glucuronidase. The prodrug is a nontoxic glucuronide-spacer-derivative of doxorubicin decomposing to doxorubicin by enzymatic deglucuronidation. In vivo studies in nude mice bearing human CEA-expressing tumor xenografts revealed that 7 d after injection of 20 mg/kg fusion protein, a high specificity ratio (> 100:1) was obtained between tumor and plasma. Injection of 250 mg/kg of prodrug at d 7 resulted in tumor therapeutic effects superior to conventional chemotherapy without any detectable toxicity. These superior therapeutic effects that were observed using established human tumor xenografts can be explained by the approx 10-fold higher drug concentrations found in tumors of mice treated with fusion protein and prodrug than in those treated with the maximal tolerable dose of drug alone.
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PMID:Fusion protein mediated prodrug activation (FMPA) in vivo. 773 40

A two component system, consisting of a fusion protein and an appropriate prodrug, suited to perform selective tumor therapy in vivo is presented. The fusion protein, due to its humanized carcinoembryonic antigen-specific variable region, specifically binds to carcinoembryonic antigen-expressing tumors and has an enzymatic activity comparable to that of human beta-glucuronidase. The prodrug is a nontoxic glucuronide-spacer derivative of doxorubicin decomposing to doxorubicin by enzymatic deglucuronidation. In vivo studies in nude mice bearing human carcinoembryonic antigen-expressing tumor xenografts revealed that 7 days after injection of 20 mg/kg fusion protein a high specificity ratio (> 100:1) was obtained between tumor and plasma or tumor and normal tissues. Injection of 250 mg/kg of prodrug at day 7 resulted in tumor therapeutic effects superior to those of conventional chemotherapy without any detectable toxicity. These superior therapeutic effects which were observed using established human tumor xenografts can be explained by the approximately 4-12-fold higher doxorubicin concentrations found in tumors of mice treated with fusion protein and prodrug than in those treated with the maximal tolerable dose of drug alone. The nondetectable toxicity in the animals treated with fusion protein and prodrug is probably caused by up to 5-fold lower drug concentrations in normal tissues compared to the animals treated with doxorubicin. Thus, a more tumor-selective therapy, resulting in stronger therapeutic effects and reduced toxicity seems to be possible by the appropriate use of the humanized nontoxic fusion protein and the nontoxic prodrug.
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PMID:Tumor-selective prodrug activation by fusion protein-mediated catalysis. 817 22

Activity of beta-glucuronidase (GL), placentar izoenzyme of alkaline phosphatase (PLAP), cathepsin B (CB) and concentrations of carcinoembryonic antigen (CEA) were determined in serums and bile of pigs with experimental cholangiocarcinoma and in control animals. No differences in serum GL, PLAP, CB activities or CEA were observed. The same was found in bile for GL, PLAP and CEA. However, in bile the situation was different for CB. In all the tumour bearing animals we were able to demonstrate in the course of tumour development a stricking progression in CB activity. Very impressive was namely an elevation of CB alkaline-stable form, generated (according also to the chromatographic studies of the bile) from primary cholangiocarcinoma tissue.
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PMID:[Cathepsin B-like substance in the monitoring of chemically induced primary cholangiocarcinoma in swine]. 896 25