a model established on the gene dosage effect , which likely results of these chromosome imbalances , may be proposed : ( 1 ) increase of thymidine kinase activity ( chromosome 17q ) and thus of the salvage pathway of thymidine synthesis ( 2 ) decrease of thymidine de novo pathways by decreased of thymidylate synthase ( chromosome 18 ) and of dihydrofolate reductase ( chromosome 5q ) and thus accumulation of 2'-deoxyuridine-5'-p , which saves 2'-deoxycytidine 5'-p ( 3 ) decrease of cytidylate ( or uridylate ) kinase ( chromosome 1p ) and thus accumulation of 2-deoxycytidine-5-pp and of uridine-5-p ( ump ) decreasing the metabolisation of orotidine-5'-p , precursor of 2-deoxycytidine-5-pp , which ( 4 ) saves -d-5-ribosyl-pp ( prpp ) or even conversion of orotidine-5'-p in prpp .
C0008633
chromosome
C0796347
chromosome 5q