ArticleNeoplasia (New York, N.Y.)2008
Chemotherapy-induced apoptosis in a transgenic model of neuroblastoma proceeds through p53 induction.
Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 65 citations in OpenAlex.
- In silico models in oncology, neurology, and epidemiology: systems-level and multiscale perspectives.NPJ systems biology and applications · 2026Review
- Extrachromosomal DNA-Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in MYCN-Amplified Cancers.Cancer discovery · 2025Article
- Trajectory analysis reveals an uncommitted neuroblastic state in MYCN-driven neuroblastoma development.Neuro-oncology · 2025Article
- Three-Dimensional Culture Systems in Neuroblastoma Research.Organoids · 2025Article
- Comparison ofHeliyon · 2024Article
- Mathematical Model of Clonal Evolution Proposes a Personalised Multi-Modal Therapy for High-Risk Neuroblastoma.Cancers · 2023Article
- Article
- Molecular Iodine/Cyclophosphamide Synergism on Chemoresistant Neuroblastoma Models.International journal of molecular sciences · 2021Article
- The enigmatic helicase DHX9 and its association with the hallmarks of cancer.Future science OA · 2020Review
- Neuroblastoma patient-derived cultures are enriched for a mesenchymal gene signature and reflect individual drug response.Cancer science · 2020Article
- Targeting anaplastic lymphoma kinase in neuroblastoma.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2019Review
- The HDAC6 inhibitor C1A modulates autophagy substrates in diverse cancer cells and induces cell death.British journal of cancer · 2018Article
- miR-10a rejuvenates aged human mesenchymal stem cells and improves heart function after myocardial infarction through KLF4.Stem cell research & therapy · 2018Article
- RLIP76 Inhibition: A Promising Developmental Therapy for Neuroblastoma.Pharmaceutical research · 2017Review
- Exosomal miR-10a derived from amniotic fluid stem cells preserves ovarian follicles after chemotherapy.Scientific reports · 2016Article
- Downregulation of MYCN through PI3K Inhibition in Mouse Models of Pediatric Neural Cancer.Frontiers in oncology · 2015Article
- Glial progenitors as targets for transformation in glioma.Advances in cancer research · 2014Review
- Neuroblastoma and MYCN.Cold Spring Harbor perspectives in medicine · 2013Review
- Apoptotic cell death in neuroblastoma.Cells · 2013Article
- Oncolytic adenovirus armed with shRNA targeting MYCN gene inhibits neuroblastoma cell proliferation and in vivo xenograft tumor growth.Journal of cancer research and clinical oncology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Chemoresistance in neuroblastoma is a significant issue complicating treatment of this common pediatric solid tumor. MYCN-amplified neuroblastomas are infrequently mutated at p53 and are chemosensitive at diagnosis but acquire p53 mutations and chemoresistance with relapse. Paradoxically, Myc-driven transformation is thought to require apoptotic blockade. We used the TH-MYCN transgenic murine model to examine the role of p53-driven apoptosis on neuroblastoma tumorigenesis and the response to chemotherapy. Tumors formed with high penetrance and low latency in p53-haploinsufficient TH-MYCN mice. Cyclophosphamide (CPM) induced a complete remission in p53 wild type TH-MYCN tumors, mirroring the sensitivity of childhood neuroblastoma to this agent. Treated tumors showed a prominent proliferation block, induction of p53 protein, and massive apoptosis proceeding through induction of the Bcl-2 homology domain-3-only proteins PUMA and Bim, leading to the activation of Bax and cleavage of caspase-3 and -9. Apoptosis induced by CPM was reduced in p53-haploinsufficient tumors. Treatment of MYCN-expressing human neuroblastoma cell lines with CPM induced apoptosis that was suppressible by siRNA to p53. Taken together, the results indicate that the p53 pathway plays a significant role in opposing MYCN-driven oncogenesis in a mouse model of neuroblastoma and that basal inactivation of the pathway is achieved in progressing tumors. This, in part, explains the striking sensitivity of such tumors to chemotoxic agents that induce p53-dependent apoptosis and is consistent with clinical observations that therapy-associated mutations in p53 are a likely contributor to the biology of tumors at relapse and secondarily mediate resistance to therapy.
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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.