ReviewCancer2020
What 20 years of research has taught us about the TP53 p.R337H mutation.
Review in Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 51 citations in OpenAlex.
- Clinical and surveillance outcomes of the TP53 c.1000G > C (p.Gly334Arg) variant.Familial cancer · 2026Article
- Article
- Performance of LFSPRO prediction in TP53 mutation status for prospectively collected probands.American journal of human genetics · 2026Article
- Genome Sequencing of Undiagnosed European Patients Suspected of Hereditary Cancer: Diagnostic Yield and Identification of Candidate Causative Variants.JCO precision oncology · 2026Article
- Reconstructing the Origin and Demographic Expansion of the TP53 p.R337H Founder Variant in Brazil.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026Article
- A quantitative, Bayesian-informed approach to gene-specific variant classification: Updated Expert Panel recommendations improve classification of TP53 germline variants for Li-Fraumeni syndrome.Genome medicine · 2025Review
- Characteristics predicting reduced penetrance variants in the high-risk cancer predisposition gene TP53.HGG advances · 2025Article
- TP53 p.R181H is enriched in the Swedish cohort (SWEP53) and associated with a distinct breast and prostate phenotype.Scientific reports · 2025Article
- Deciphering dual clinical entities associated with TP53 pathogenic variants: Insights from 53,085 HBOC panel analyses in French laboratories.International journal of cancer · 2025Article
- The TP53 tumor suppressor gene: From molecular biology to clinical investigations.Journal of internal medicine · 2025Review
- TP53 missense allele predisposing to high risk of breast cancer but not pediatric cancers.Journal of the National Cancer Institute · 2025Article
- Somatic mutational profiling and clinical impact of driver genes in Latin-Iberian medulloblastomas: Towards precision medicine.Neuropathology : official journal of the Japanese Society of Neuropathology · 2025Article
- Personalized screening strategies forLancet regional health. Americas · 2025Article
- Germline p.R181H variant in TP53 in a family exemplifying the genotype-phenotype correlations in Li-Fraumeni syndrome.Familial cancer · 2024Article
- Clinical and genetic characteristics of carriers of the TP53 c.541C > T, p.Arg181Cys pathogenic variant causing hereditary cancer in patients of Arab-Muslim descent.Familial cancer · 2024Article
- Current insights and future directions of Li-Fraumeni syndrome.Discover oncology · 2024Review
- Article
- Germline mutations in cancer predisposition genes among pediatric patients with cancer and congenital anomalies.Pediatric research · 2024Article
- Translating p53-based therapies for cancer into the clinic.Nature reviews. Cancer · 2024Review
- The Ashkenazi-Centric G334R Variant ofMolecular and cellular biology · 2024Article
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
Abstract
The p53 tumor suppressor transcriptionally regulates a myriad of genes involved in cell cycle control, DNA repair, cell survival, and cell metabolism and represents one of the most well-studied inhibitors of tumorigenesis. Since the discovery of TP53 in 1979, somatic mutations have been shown to be extremely common; more than 50% of human cancers carry loss-of-function mutations in TP53. Inherited or germline TP53 mutations are rare and are involved in complex hereditary cancer predisposition disorders, and affected family members can develop diverse tumor types and multiple primary cancers at young ages. In Brazil, a fascinating history of p53 and cancer predisposition began in the year 2000 with identification of the TP53 p.R337H mutation in close association with the development of adrenocortical tumors. In these past 20 years, much has been learned about the genetics and biochemistry of this mutation, which is widespread in Brazil because of a founder effect. This review highlights the contributions of TP53 p.R337H research over the last 20 years, the findings of which have sparked passionate debate among researchers worldwide, to understanding cancer predisposition in Brazilian individuals and families.
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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.