ReviewCancer science2005
p73, a sophisticated p53 family member in the cancer world.
Review in Cancer science, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis 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
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.
- Association betweenThe Journal of international medical research · 2022Pooled it
- A combination of artemisinin, moxidectin, and doxorubicin drugs can selectively and efficiently induce apoptosis in acute lymphoblastic and chronic myeloid leukemia cells in vitro and ex vivo.Medical oncology (Northwood, London, England) · 2026Article
- Clinicopathological Significance of Transcription Factor p73 in Breast Cancers: Protein Expression and Transcriptomic Study.Biomedicines · 2025Article
- Oncostatin M orchestrates collective epithelial migration via HIF1A activation.bioRxiv : the preprint server for biology · 2025Article
- Transcription Factor p73 Is a Predictor of Platinum Resistance and Promotes Aggressive Epithelial Ovarian Cancers.International journal of molecular sciences · 2025Article
- RNF144A and RNF144B: Important molecules for health.Open life sciences · 2025Review
- The Proteasome Inhibitor CEP-18770 Induces Cell Death in Medulloblastoma.Pharmaceutics · 2024Article
- Isoform-specific disruption of theeLife · 2023Article
- Epigenetic Abnormalities in Chondrosarcoma.International journal of molecular sciences · 2023Review
- Review
- Protein adduction causes non-mutational inhibition of p53 tumor suppressor.Cell reports · 2023Article
- STAT3 promotes RNA polymerase III-directed transcription by controlling the miR-106a-5p/TP73 axis.eLife · 2023Article
- Research progress of Bub3 gene in malignant tumors.Cell biology international · 2022Review
- Article
- Review
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- Targeting Post-Translational Modifications of the p73 Protein: A Promising Therapeutic Strategy for Tumors.Cancers · 2021Review
- Long noncoding RNA CASC7 inhibits the proliferation and migration of papillary thyroid cancer cells by inhibiting miR-34a-5p.The journal of physiological sciences : JPS · 2021Article
- The role of Aurora-A in human cancers and future therapeutics.American journal of cancer research · 2020Review
- RNA-Binding Motif Protein 38 as a Potential Biomarker and Therapeutic Target in Cancer.OncoTargets and therapy · 2020Review
8 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
p73 belongs to a family of p53-related nuclear transcription factors that includes p53, p73 and p63. The overall structure and sequence homology indicates that a p63/p73-like protogene is the ancestral gene, whereas p53 evolved later in higher organisms. In accordance with their structural similarity, p73 functions in a manner analogous to p53 by inducing tumor cell apoptosis and participating in the cell cycle checkpoint control through transactivating an overlapping set of p53/p73-target genes. In sharp contrast to p53, however, p73 is expressed as two NH(2)-terminally distinct isoforms including transcriptionally active (TA) and transcriptionally inactive (DeltaN) forms. DeltaNp73, which has oncogenic potential, acts in a dominant negative manner against TAp73 as well as p53. p73 is induced to be stabilized in response to a subset of DNA-damaging agents in a way that is distinct from that of p53, and exerts its pro-apoptotic activity. Several lines of evidence suggest that p73 can induce tumor cell apoptosis in a p53-dependent and p53-independent manner. Some tumors exhibit resistance to the p53-dependent apoptotic program, therefore p73, which can induce apoptotic cell death by p53-independent mechanisms, is particularly useful. In this review, we discuss the regulatory mechanisms of p73 activity, and also the functional significance of p73 in the regulation of cellular processes including tumorigenesis, apoptosis and neurogenesis.
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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.