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Glycolysis inhibition for anticancer treatment
TLDR
The increased dependence of cancer cells on glycolytic pathway for ATP generation provides a biochemical basis for the design of therapeutic strategies to preferentially kill cancer cells by pharmacological inhibition of Glycolysis. Expand
High-dose 5-fluorouracil with delayed uridine "rescue" in mice.
TLDR
Examination of the effect of uridine Rescue on the incorporation of FUra into RNA and the subsequent recovery from inhibition of DNA synthesis in bone marrow versus tumor revealed that the uridine rescue schedule resulted in relatively faster clearance of F Ura from RNA of both tissues but a striking enhancement of the rate of recovery ofDNA synthesis only in the bone marrow. Expand
Combination clinical trials with thymidine and fluorouracil: A phase I and clinical pharmacologic evaluation
TLDR
Plasma analyses for TdR and FU and their metabolic products by high pressure liquid chromatography have demonstrated a marked elevation and prolongation of FU levels. Expand
ATP depletion + pyrimidine depletion can markedly enhance cancer therapy: fresh insight for a new approach.
TLDR
In the 1980s, necrosis was considered the mode of cell death induced by DNA-damaging anticancer agents because of the activity of PARP, which cleaves the glycolytic coenzyme, NAD+, leading to formation of poly(ADP-ribose). Expand
AZD7545, a novel inhibitor of pyruvate dehydrogenase kinase 2 (PDHK2), activates pyruvate dehydrogenase in vivo and improves blood glucose control in obese (fa/fa) Zucker rats.
TLDR
AZD7545 (10 mg/kg) twice daily for 7 days markedly improved the 24-h glucose profile, by eliminating the postprandial elevation in blood glucose, suggesting that PDHK inhibitors may be beneficial agents for improving glucose control in the treatment of type 2 diabetes. Expand
Improving the anti-tumor activity of 5-fluorouracil by increasing its incorporation into RNA via metabolic modulation.
TLDR
Kinetic analysis reveals that, although the injection of 5FUra leads to an immediate cessation of thymidylate synthetase activity, DNA synthesis continues at a lower rate for 12 hr and then ceases completely, and that this event is paralleled by a striking icrease in anti-tumor activity. Expand
An overview of thymidine
TLDR
In vivo effects of TdR employed as an agent for cancer therapy are reviewed, and metabolic modulation with still other metabolites and a hormone was demonstrated to protect from host toxicity due to certain anti‐cancer agents without offsetting anti‐tumor activity. Expand
Potentiation of the anti‐tumor activity of 5FU by thymidine and its correlation with the formation of (5FU) RNA
TLDR
The thesis that the antitumor activity of 5‐fluorouracil (FU) is achieved solely by the inhibition of thymidylate synthetase by the derivative, fluorodeoxymonophosphate (FdUMP), is questioned. Expand
Plasma levels of a viral protein as a diagnostic signal for the presence of tumor : the murine mammary tumor model.
TLDR
Plasma gp52 is a potentially useful and specific systemic indicator of the presence and extent of murine mammary neoplasia and is suggested to be a responsive parameter of disease status. Expand
Phase I and clinical pharmacological evaluation of biochemical modulation of 5-fluorouracil with N-(phosphonacetyl)-L-aspartic acid.
TLDR
It was determined that PALA (250 mg/sq m) is effective in inhibiting total-body pyrimidine synthesis, and the toxicity observed using that combination of doses was mild to moderate myelosuppression, mucositis, diarrhea, nausea, and vomiting. Expand
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