ReviewOncogene2003
P53 and radiation responses.
Review in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 174 papers, 2 of them syntheses that pooled it.
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
174 citing papers in PubMed, 2 syntheses or guidelines pooled it, 500 citations in OpenAlex.
- The Radiosensitizing Potentials of Silymarin/Silibinin in Cancer: A Systematic Review.Current medicinal chemistry · 2024Pooled it
- P53 abnormalities and outcomes in colorectal cancer: a systematic review.British journal of cancer · 2005Pooled it
- Endogenous inhibitors of PP2A activate oncogenic and DNA damage response kinases in glioblastoma.Cancer letters · 2026Article
- Cellular senescence in lung cancer immune microenvironment and senotherapeutic opportunities.iScience · 2026Review
- Understanding Cancer Health Disparities.Cancers · 2026Review
- In vitro determination of patient-specific variation challenges the universal RBE gold standard for proton radiation therapy.Clinical and translational radiation oncology · 2026Article
- Potential targets for boron transport in boron neutron capture therapy.Frontiers in oncology · 2026Review
- Carbon ion combined photon radiotherapy induces ferroptosis via NCOA4-mediated ferritinophagy in glioblastoma.Redox biology · 2025Article
- Radiation dose escalation in locally advanced oesophageal cancer: a systematic review and hierarchical Bayesian meta-analysis.EClinicalMedicine · 2025Article
- DNA-damage orchestrates self-renewal and differentiation via reciprocal p53 family and Hippo/Wnt/TGF-β pathway activation in embryonic stem cells.Cellular and molecular life sciences : CMLS · 2025Article
- Ferroptosis: a double-edged sword that enhances radiation sensitivity and facilitates radiation-induced injury in tumors.Frontiers in immunology · 2025Review
- Senescence and senolysis in cancer: The latest findings.Cancer science · 2024Review
- APR-246 as a radiosensitization strategy for mutant p53 cancers treated with alpha-particles-based radiotherapy.Cell death & disease · 2024Article
- Dynamic role of CUL4B in radiation-induced intestinal injury-regeneration.Scientific reports · 2024Article
- Cell fate regulation governed by p53: Friends or reversible foes in cancer therapy.Cancer communications (London, England) · 2024Review
- Somatic gene mutations involved in DNA damage response/Fanconi anemia signaling are tissue- and cell-type specific in human solid tumors.Frontiers in medicine · 2024Article
- Multimodality local ablative therapy of 23 lung metastases with surgical resection and percutaneous cryoablation in a patient with Li-Fraumeni Syndrome: A case report.Radiology case reports · 2023Article
- Article
- Signaling Network Response to α-Particle-Targeted Therapy with theJournal of nuclear medicine : official publication, Society of Nuclear Medicine · 2023Article
- Article
114 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells have evolved elaborate mechanisms (checkpoints) to monitor genomic integrity in order to ensure the high-fidelity transmission of genetic information. Cells harboring defects in checkpoint pathways respond to DNA damage improperly, which in turn may enhance the rate of cancer development. Ionizing radiation (IR) primarily leads to double-strand DNA breaks (DSBs), which activate DNA damage checkpoints to initiate signals ultimately leading to a binary decision between cell death and cell survival. TP53 has been recognized as an important checkpoint protein, functioning mainly through transcriptional control of target genes that influence multiple response pathways and leading to the diversity of responses to IR in mammalian cells. We review how the tumor suppressor P53 is involved in the complex response to IR to enforce the cell's fate to live by inducing the growth arrest coupled to DNA damage repair or to die by inducing irreversible growth arrest or apoptosis. Moreover, recent insights have emerged in our understanding of how P53 modulates radiosensitivity in tissues following IR as well as its role in sensitizing cells to chemo- and radiotherapy. The P53 pathway remains an attractive target for exploitation in the war on cancer.
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.