Abstract
Children suffering from acute lymphoblastic leukemia (ALL) possess an increased concentration of cytidine triphosphate (CTP) in their lymphoblasts compared to resting lymphocytes.1 This might be due to either an enhanced flux through the pyrimidine “de novo” and/or uridine salvage pathway or to an increased flux through the cytidine salvage pathway. By studying ribonucleotide fluxes in a MOLT-3 lymphoblastic cell line it has been shown that the increased CTP concentration is the result of an enhanced activity of CTP synthetase (CTPS).2 We now analyzed the “in vitro” CTPS activity in lymphoblasts of children with ALL. If increased, CTPS might be inhibited by drugs like cyclopentenylcytosine (CPEC).
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
