ReviewSub-cellular biochemistry2014
Alterations of p63 and p73 in human cancers.
Review in Sub-cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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.
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Who cites it
38 citing papers in PubMed, 58 citations in OpenAlex.
- WT1 gene: a potential therapeutic target for multiple cancer treatment strategies.Clinical and experimental medicine · 2025Review
- TAp73 and ΔTAp73 isoforms show cell-type specific distributions and alterations in cancer.Scientific reports · 2024Article
- Review
- p53 amyloid pathology is correlated with higher cancer grade irrespective of the mutant or wild-type form.Journal of cell science · 2023Article
- Disease-related p63 DBD mutations impair DNA binding by distinct mechanisms and varying degree.Cell death & disease · 2023Article
- Phylogenetic analysis of the MCL1 BH3 binding groove and rBH3 sequence motifs in the p53 and INK4 protein families.PloS one · 2023Article
- Pramlintide: A Novel Therapeutic Approach for Osteosarcoma through Metabolic Reprogramming.Cancers · 2022Article
- Delineating functional mechanisms of the p53/p63/p73 family of transcription factors through identification of protein-protein interactions using interface mimicry.Molecular carcinogenesis · 2022Article
- Should mutant TP53 be targeted for cancer therapy?Cell death and differentiation · 2022Review
- Review
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- Differential p53-Mediated Cellular Responses to DNA-Damaging Therapeutic Agents.International journal of molecular sciences · 2021Review
- p73 as a Tissue Architect.Frontiers in cell and developmental biology · 2021Review
- The p53 Signalling Pathway in Cutaneous Basal Cell Carcinoma: An Immunohistochemical Description.Acta dermato-venereologica · 2020Article
- Review
- RNA-Binding Motif Protein 38 as a Potential Biomarker and Therapeutic Target in Cancer.OncoTargets and therapy · 2020Review
- The Diverse Functions of Mutant 53, Its Family Members and Isoforms in Cancer.International journal of molecular sciences · 2019Review
- DMPK is a New Candidate Mediator of Tumor Suppressor p53-Dependent Cell Death.Molecules (Basel, Switzerland) · 2019Article
- Expression and clinical significance of p73 in Wilms tumor in children.Oncology letters · 2019Article
- c-MYB and DMTF1 in Cancer.Cancer investigation · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
p53 and its related genes, p63 and p73 constitute the p53 gene family. While p53 is the most frequently mutated gene in human tumors, p63 and p73 are rarely mutated or deleted in cancers. Many studies have reported p63/p73 overexpression in human cancers while others showed that a loss of p63/p73 is associated with tumor progression and metastasis. Thus, whether p63 or p73 is a tumor suppressor gene or an oncogene has been a matter of debate. This controversy has been attributed to the existence of multiple splicing isoforms with distinct functions; the full-length TA isoform of p63 has structural and functional similarity to wild-type p53, whereas the ΔNp63 acts primarily in dominant-negative fashion against all family members of p53. Differential activities of TA and ΔN isoforms have been shown in vivo by creating isform-specific gene knockout mice. All p53, p63, p73 proteins bind to and activate target genes with p53-response elements; p63 also binds to distinct p63-response elements and regulate expression of specific target genes involved in skin, limb, and craniofacial development. Interestingly, several studies have shown that both p63 and p73 are involved in cellular response to cancer therapy and others have indicated that both of these molecules are required for p53-induced apoptosis, suggesting functional interplay among p53 family proteins. Consistent with these findings, aberrant splicing that result in ΔNp63 or ΔNp73 overexpression are frequently found in human cancers, and is associated with poor clinical outcomes of patients in the latter. Thus immunohistochemical staining of tumor specimen with ΔNp73-specific antibody might have diagnostic values in cancer clinics.
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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.