Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Antifolates targeting purine synthesis allow entry of tumor cells into S phase regardless of p53 function.

Cancer research - 15 Sept 2002

Bronder Julie L, Moran Richard G

Abstract excerpt

The class of folate antimetabolites typified by (6R)-dideazatetrahydrofolate (lometrexol, DDATHF) are specific inhibitors of de novo purine synthesis because of potent inhibition of glycinamide ribonucleotide formyltransferase (GART) but do not induce detectable levels of DNA strand breaks. As such, they are a test case of the concept that ribonucleotide depletion can be sensed by p53, resulting in a G(1) cell...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Folic Acid Antagonists
Share to G1 Phase
Share to Glutamates

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hydroxymethyl and Formyl Transferases

Share to Leukemia L1210

Share to Purines

Share to S Phase

Share to Tetrahydrofolates

Source

Identifiers

PMID: 12234990

Genes

GART

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Antifolates targeting purine synthesis allow entry of tumor cells into S phase regardless of p53 function.PMID 12234990Read ↗

A Defect in the p53 Response Pathway Induced by de Novo Purine Synthesis InhibitionSemantic proximity Read ↗

Disruption of p53 in human cancer cells alters the responses to therapeutic agentsSemantic proximity Read ↗

Activation of the p53 DNA damage response pathway after inhibition of DNA methyltransferase by 5-aza-2'-deoxycytidine.Semantic proximity Read ↗

DNA mismatch repair (MMR)‐dependent 5‐fluorouracil cytotoxicity and the potential for new therapeutic targetsSemantic proximity Read ↗

Loss of Uracil DNA Glycosylase Selectively Resensitizes p53-Mutant and -Deficient Cells to 5-FdU.Semantic proximity Read ↗

Differences in the Induction of DNA Damage, Cell Cycle Arrest, and Cell Death by 5-Fluorouracil and AntifolatesSemantic proximity Read ↗

5‐Fluorouracil and its active metabolite FdUMP cause DNA damage in human SW620 colon adenocarcinoma cell lineSemantic proximity Read ↗

Prevention of fluorodeoxyuridine-induced cytotoxicity and DNA damage in HT29 colon carcinoma cells by conditional expression of wild-type p53 phenotype.Semantic proximity Read ↗

Inactivation of p53 in normal human cells increases G2/M arrest and sensitivity to DNA-damaging agents.Semantic proximity Read ↗

Thymidylate synthase inhibition triggers apoptosis via caspases-8 and -9 in both wild-type and mutant p53 colon cancer cell lines.Semantic proximity Read ↗

Gene Amplification in a p53-Deficient Cell Line Requires Cell Cycle Progression under Conditions That Generate DNA BreakageSemantic proximity Read ↗

Effects of perturbations of pools of deoxyribonucleoside triphosphates on expression of ribonucleotide reductase, a G1/S transition state enzyme, in p53-mutated cells.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.