Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The following hematological and biochemical reference values were determined in 150 hares: hematocrit, blood count and leucocytic formula, Na, K, Cl, P, Ca, Mg, Cu, Zn, glucose, urea, creatinine, uric acid, cholesterol, bilirubin, triglycerides, proteins and fractions, PAL, PAC, TGO, TGP, amylase, GGT, LDH. Once the effects of sex and age have been established, the references defined here will be used as a base for interpreting disturbances linked either to pathology or nutrition.
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PMID:[Contribution to the definition of reference values in the hare: hematology -- blood biochemistry (author's transl)]. 57 73

Effects in vitro of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) on alkaline phosphatase (PAL), gamma-glutamyltransferase (gamma-GT) and acid phosphatase (PAC) activities were investigated on renal cortex from hypophysectomized rats. In these animals the biosynthesis of 1,25-(OH)2D3 and the specific activities of kidney PAL and gamma-GT were decreased. The course of these effects was determined from 45 min to 8 h. In the presence of 1,25-(OH)2D3 (2 x 10(-6) M) a delayed (5h) but simultaneous stimulation of the three enzymes was observed. It reached a maximum at 6h and disappeared at 8h. The dose-response relation was studied at 6h. In the presence of 1,25-(OH)2D3 (5 x 10(-7) M), the three enzymes were activated. The effect was maximal at 10(-6) M; it was +22% for PAL, +17% and +15% respectively for gamma-GT and PAC compared with controls. Cycloheximide suppressed the induction of PAL but not of gamma-GT activity. The effects of the secosteroid on renal enzymes seems to be a pharmacological more than a physiological one.
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PMID:[In vitro effects of 1,25-dihydroxycholecalciferol on alkaline phosphatase and gamma-glutamyltransferase activity in hypophysectomized rats]. 169 95

The effects of 24R,25-dihydroxyvitamin D3 (24,25-(OH)2D3 on alkaline phosphatase (PAL), gamma-glutamyltransferase (GGT) and acid phosphatase (PAC) activities were investigated on renal cortex slices of hypophysectomized rats. Indeed after hypophysectomy renal 24,25-(OH)2D3 production was increased and renal PAL and GGT activities were decreased. After 5h incubation with physiological concentrations (0.1-10 nM) of 24,25-(OH)2D3 significant increases of PAL and GGT activities were produced. The maximum stimulation obtained with 1 nM was +23% for PAL and +26% for GGT as compared to controls. PAC was not modified. The time course of these effects was studied from 45 min to 8 h. In the presence of 24,25-(OH)2D3 (1 nM), delayed (3h) stimulation of PAL and GGT appeared. It reached the maximal value after 6h, +37% for PAL and +30% for GGT and persisted again at 8h. Cycloheximide added to incubation medium with steroid inhibited the stimulating effect on PAL only. Actinomycin D suppressed the induction of both enzymes, indicating that the observed actions of 24,25-(OH)2D3 depend on protein synthesis whose responsible mechanisms were different. These protein synthesis inhibitors did not modified enzymatic activities. Physiological significance of these renal effects is to be clarified.
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PMID:[In vitro effects of 24R,25-dihydroxyvitamin D3 on alkaline phosphatase and gamma-glutamyltransferase in the kidney of hypophysectomized rats]. 171 64

Anticancer chemotherapy with cisplatin (CDD) as the main drug (combined with adriamycin (ADM) and cyclophosphamide (CPM), PAC therapy) was performed on patients with ovarian cancer. Urinastatin (US) was concurrently administered to assess its effectiveness in preventing CDDP-induced nephrotoxicity. Twenty-two patients with gynecological malignant tumor were treated with PAC therapy, and of these, twelve concurrently received US. The ten who did not receive US served as the control. As a rule, one course of PAC therapy consisted of 50mg/m2 CDDP, 50mg/m2 ADM and 500mg/m2 CPM. Before the administration of CDDP, US 100,000 units was administered by I.V. drip infusion and after the administration, US 400,000 units was again administered by I.V. drip infusion at a speed of 100,000 to 200,000 units/hour. A total of approximately 3,500ml of fluids was administered I.V.. Each course of PAC therapy took 7 to 14 hours to complete. The control group underwent PAC therapy in a regimen not including US. As indexes of nephrotoxicity, serum levels of BUN, creatinine (Cr), and creatinine clearance (Ccr), and N-acetyl-beta-glucosaminidase (NAG), gamma-glutamyl transpeptidase (gamma-GTP), and arylamidase (AA) activity in the urine was determined before treatment and at days 1, 2, 3, 7, 14, and 21 after the initiation of PAC therapy. Changes in serum BUN, Cr, and Ccr levels after CDDP administration in the group with and the group without concurrent US were similar. Urinary gamma-GTP, AA, and NAG activity remained unchanged after CDDP administration in the group with concurrent US. In contrast, in the group without US, this urinary enzyme activity was transiently increased after CDDP administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Preventive effect of urinastatin on cisplatin-induced nephrotoxicity]. 259 19

Cis-dichlorodiammine platinum (CDDP) has recently been introduced for the treatment of human malignancies. CDDP belongs to the group of heavy metals and has nephrotoxicity, whose side effects limit the dose that can be used in patients. The urinary excretion of lactate dehydrogenase (LDH), gamma-glutamyl transpeptidase (gamma-GTP), alkaline phosphatase (ALP), arylamidase (AA) activity and beta 2-microglobulin was determined in ovarian cancer patients receiving sequential combination chemotherapy with CDDP, adriamycin (ADM) and cyclophosphamide (CPA) (PAC chemotherapy) to evaluate the sensitivity of these indices for acute renal tubular damage and compared with the change in serum BUN, Cr and Ccr values. Increases in enzyme excretion after PAC chemotherapy were more often noticed and the urinary enzyme activity varied up to the 10.4-fold of the control, while serum BUN, Cr and Ccr values remained almost within normal limits. Enzyme excretion returned almost to the normal value in one week. A comparison between the urinary enzyme excretion especially AA value and serum BUN, Cr and Ccr values indicated that the serial determination of the urinary AA excretion pattern is more useful in detecting CDDP-induced nephrotoxicity than that of serum BUN, Cr and Ccr values.
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PMID:[Cisplatin and ovarian carcinoma--early detection of cisplatin-induced nephrotoxicity]. 404 May 42

It is currently accepted that colorectal tumorigenesis results from accumulation of multiple mutations in certain genes. This concept prompted us to search for possible mutations in the APC, k-ras, and p53 genes in an advanced cancer coexisting with a large villous adenoma of the rectum in a 54-year-old patient with no family history of colorectal cancer. Genomic DNA extracted from multiple subregions of the tumor and surrounding normal mucosa was studied by polymerase chain reaction (PCR) followed by single-strand conformation polymorphism (SSCP) analysis and direct sequencing. Both the adenoma and carcinoma had abnormal PCR-SSCP for APC (exon 11) and k-ras, irrespective of the location within the tumors. However, p53 abnormality (exon 7) was detected only in samples taken from the carcinoma. Subsequent sequencing revealed a TTG to TAG mutation at codon 479 of APC, a GGT to GAT mutation at codon 12 of k-ras in both the adenoma and carcinoma, and a CGG to TGG mutation at codon 248 of p53 (exon 7) in the carcinoma. These findings were in accord with the current concept of colorectal tumor progression whereby genetic alteration of APC and k-ras occurs relatively early while that of p53 is rather late and is possibly a decisive event in relation to malignancy.
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PMID:A very large villous adenoma with an adjacent cancer of the rectum: an informative case for testing the proposed molecular basis of colorectal tumorigenesis. 889 82

To elucidate early molecular events related to colon carcinogenesis, we examined alterations in the expression of colon cancer-related genes such as cyclooxygenase (COX)-2, APC and c-Myc, cell proliferation and apoptosis in the background colon mucosa, and K-ras mutation at aberrant crypt foci (ACF) in the colons of azoxymethane (AOM)-treated rats 4 weeks after the first exposure to AOM. About 40 ACF/colon were induced in the colons of rats treated with AOM (Group 1); however, rats not treated with AOM (Group 2) showed no ACF formation in the colon. The level of AgNORs in the colonic mucosa was significantly higher in Group 1 than in Group 2 (P<0.01). The colonic mucosa in Group 1 looked macroscopically and histologically normal, but the proliferative activity of the mucosa of rats treated with AOM was clearly elevated. COX-2 mRNA expression was not detected in normal colonic mucosa in Group 2, but 3 out of 10 rats in Group 1 showed COX-2 mRNA expression in their colons by reverse transcription (RT)-polymerase chain reaction (PCR). There was a tendency toward an increased expression level of COX-2 in the AOM-treated group. The level of APC mRNA expression in Group 1 was significantly lower than that in Group 2 (P<0.01). Moreover, the level of c-Myc mRNA expression in Group 1 was significantly higher than that in Group 2 (P<0.01). An average of 0.034+/-0.006% apoptosis in colonic mucosa was detected in Group 1; the incidence of apoptosis in Group 2 was 0.021+/-0.005%. The difference between Groups 1 and 2 was significant (P<0.01). These results indicate that apoptosis was possibly induced to eliminate cells damaged by AOM administration. Six out of 22 (27%) ACF with 4 or more crypts showed K-ras mutations at codon 12; all mutations were G to A transitions (GGT to GAT). ACF with 1-3 crypts showed no mutations in the K-ras gene. In conclusion, AOM caused an increase in COX-2 and c-Myc mRNA expression, a decrease in APC mRNA expression, induction of apoptosis in normal-appearing colonic mucosa, and a K-ras mutation in ACF with 4 or more crypts. These findings may help to identify key targets in the early steps of colon carcinogenesis, against which drugs that would be broadly effective for chemoprevention of colon cancer could be developed.
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PMID:Molecular changes in the early stage of colon carcinogenesis in rats treated with azoxymethane. 1214 79