Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P47989 (xanthine oxidase)
 8,633 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In cancer cells, a marked imbalance in the enzymic pattern of purine metabolism is linked with transformation and/or progression. In chemically-induced, transplantable hepatomas in rat, the specific activities of the anabolic enzymes, IMP dehydrogenase, GMP synthetase, adenylosuccinate synthetase, adenylosuccinase, AMP deaminase and amidophosphoribosyltransferase, increased to 13.5-, 3.7-, 3.1-, 1.8-, 5.5- and 2.8-fold, respectively, of those in normal liver. Activities of the catabolic enzymes, inosine phosphorylase, xanthine oxidase and uricase, decreased to 19, 10 and 4%, respectively. This enzymic imbalance was specific to hepatic neoplasia, since no similar pattern was observed in differentiating or regenerating liver. Most enzymic alterations were present also in chemically- and virus-induced animal tumors, in human kidney, liver and colon carcinomas, and in human colon carcinoma xenografts. The molecular correlation concept applies to purine biochemistry and an important segment of neoplastic gene expression was identified in the behavior of key purine-metabolizing enzymes.
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PMID:Enzymes of purine metabolism in cancer. 686 38

The molecular and biochemical aspects of purine nucleotide biosynthesis through de novo and salvage pathways, the production of uric acid, and their regulation mechanisms are reviewed for further understanding of hyperuricemia and gout. The metabolic rate of purine nucleotide biosynthesis is chiefly determined by the regulation of the de novo pathway, especially amidophosphoribosyltransferase and PRPP synthetase, and the accumulation of uric acid results from the acceleration of de novo biosynthesis and catabolism of purine nucleotide or the decrease in urinary excretion of uric acid. Moreover, several enzyme mutations of purine nucleotide metabolism are also clinically important including gout with hyperactive HPRT and the deficiency of HPRT (Lesch-Nyhan syndrome), adenylosuccinate lyase, xanthine oxidase, APRT, PNP, or ADA (SCID) with gene therapy.
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PMID:[Metabolism of purine nucleotides and the production of uric acid]. 897 90