ArticleInternational journal of oncology2013
DFMO/eflornithine inhibits migration and invasion downstream of MYCN and involves p27Kip1 activity in neuroblastoma.
Article in International journal of oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 56 citations in OpenAlex.
- Maintenance DFMO Increases Survival in High Risk Neuroblastoma.Scientific reports · 2018Trial
- Cysteine Restriction Induces Ferroptosis Depending on theGastro hep advances · 2026Article
- Novel Compounds Target Aberrant Calcium Signaling in the Treatment of Relapsed High-Risk Neuroblastoma.International journal of molecular sciences · 2025Article
- Antitumor potential of polyamines in cancer.Acta biochimica et biophysica Sinica · 2025Review
- Molecular regulation and therapeutic targeting ofFrontiers in cell and developmental biology · 2025Review
- Microbiota-derived metabolites in tumorigenesis: mechanistic insights and therapeutic implications.Frontiers in pharmacology · 2025Review
- Polyamine Derived Photosensitizer: A Novel Approach for Photodynamic Therapy of Cancer.Molecules (Basel, Switzerland) · 2024Article
- US Food and Drug Administration Approval Summary: Eflornithine for High-Risk Neuroblastoma After Prior Multiagent, Multimodality Therapy.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024Article
- Bachmann-Bupp syndrome and treatment.Developmental medicine and child neurology · 2024Review
- Polyamines: their significance for maintaining health and contributing to diseases.Cell communication and signaling : CCS · 2023Review
- A newAmino acids · 2023Article
- Review
- Deregulation of the cyclin-dependent kinase inhibitor p27 as a putative candidate for transformation inAIMS microbiology · 2023Article
- Probenecid increases renal retention and antitumor activity of DFMO in neuroblastoma.Cancer chemotherapy and pharmacology · 2021Article
- Design, Synthesis, and Biological Evaluation of Benzo[cd]indol-2(1H)-ones Derivatives as a Lysosome-Targeted Anti-metastatic Agent.Frontiers in oncology · 2021Article
- Article
- Review
- The involvement of polyamine uptake and synthesis pathways in the proliferation of neonatal astrocytes.Amino acids · 2020Article
- Regulation of cancer cell metabolism: oncogenic MYC in the driver's seat.Signal transduction and targeted therapy · 2020Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Neuroblastoma (NB) is the most common extracranial pediatric tumor. NB patients over 18 months of age at the time of diagnosis are often in the later stages of the disease, present with widespread dissemination, and often possess MYCN tumor gene amplification. MYCN is a transcription factor that regulates the expression of a number of genes including ornithine decarboxylase (ODC), a rate-limiting enzyme in the biosynthesis of polyamines. Inhibiting ODC in NB cells produces many deleterious effects including G(1) cell cycle arrest, inhibition of cell proliferation, and decreased tumor growth, making ODC a promising target for drug interference. DFMO treatment leads to the accumulation of the cyclin-dependent kinase inhibitor p27(Kip1) protein and causes p27(Kip1)/Rb-coupled G(1) cell cycle arrest in MYCN-amplified NB tumor cells through a process that involves p27(Kip1) phosphorylation at residues Ser10 and Thr198. While p27(Kip1) is well known for its role as a cyclin-dependent kinase inhibitor, recent studies have revealed a novel function of p27(Kip1) as a regulator of cell migration and invasion. In the present study we found that p27(Kip1) regulates the migration and invasion in NB and that these events are dependent on the state of phosphorylation of p27(Kip1). DFMO treatments induced MYCN protein downregulation and phosphorylation of Akt/PKB (Ser473) and GSK3-β (Ser9), and polyamine supplementation alleviated the DFMO-induced effects. Importantly, we provide strong evidence that p27(Kip1) mRNA correlates with clinical features and the survival probability of NB patients.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.