ArticleCell2013
A polymorphic p53 response element in KIT ligand influences cancer risk and has undergone natural selection.
Article in Cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 3 of them syntheses that pooled it.
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Who cites it
78 citing papers in PubMed, 3 syntheses or guidelines pooled it, 121 citations in OpenAlex.
- Germline and Somatic Genetic Variants in the p53 Pathway Interact to Affect Cancer Risk, Progression, and Drug Response.Cancer research · 2021Pooled it
- Association between KITLG Gene Polymorphisms and Testicular Germ Cell Tumors: A Systematic Review and Meta-analysis.Current medical science · 2019Pooled it
- Identification of 19 new risk loci and potential regulatory mechanisms influencing susceptibility to testicular germ cell tumor.Nature genetics · 2017Pooled it
- Epigenetic modulation of prostate cancer disparities in men with African ancestry.Nature reviews. Urology · 2026Review
- Exploring the Role of CDO1 in Breast Cancer: Insights into Tumor Biology and Therapeutic Potential.Annals of surgical oncology · 2025Article
- p53motifDB: integration of genomic information and tumour suppressor p53 binding motifs.Database : the journal of biological databases and curation · 2025Article
- Determinants of p53 DNA binding, gene regulation, and cell fate decisions.Cell death and differentiation · 2024Review
- Predicting and overcoming resistance to CDK9 inhibitors for cancer therapy.Acta pharmaceutica Sinica. B · 2023Article
- Shared gene targets of the ATF4 and p53 transcriptional networks.bioRxiv : the preprint server for biology · 2023Article
- Shared Gene Targets of the ATF4 and p53 Transcriptional Networks.Molecular and cellular biology · 2023Article
- 27-year trends in incidence rates for testis cancer across a large statewide registry.American journal of clinical and experimental urology · 2023Article
- Structural Basis of Mutation-Dependent p53 Tetramerization Deficiency.International journal of molecular sciences · 2022Article
- Cross-continental admixture in the Kho population from northwest Pakistan.European journal of human genetics : EJHG · 2022Article
- The genotypes and phenotypes of missense mutations in the proline domain of the p53 protein.Cell death and differentiation · 2022Review
- p53-dependent induction of P2X7 on hematopoietic stem and progenitor cells regulates hematopoietic response to genotoxic stress.Cell death & disease · 2021Article
- Article
- Causal inference multiple imputation investigation of the impact of cannabinoids and other substances on ethnic differentials in US testicular cancer incidence.BMC pharmacology & toxicology · 2021Article
- Human population dynamics andScience advances · 2021Article
- Evolutionary selection of alleles in the melanophilin gene that impacts on prostate organ function and cancer risk.Evolution, medicine, and public health · 2021Article
- Tumor suppressor p53: from engaging DNA to target gene regulation.Nucleic acids research · 2020Article
18 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 7 institutions in 3 countries.
Funding
Abstract
The ability of p53 to regulate transcription is crucial for tumor suppression and implies that inherited polymorphisms in functional p53-binding sites could influence cancer. Here, we identify a polymorphic p53 responsive element and demonstrate its influence on cancer risk using genome-wide data sets of cancer susceptibility loci, genetic variation, p53 occupancy, and p53-binding sites. We uncover a single-nucleotide polymorphism (SNP) in a functional p53-binding site and establish its influence on the ability of p53 to bind to and regulate transcription of the KITLG gene. The SNP resides in KITLG and associates with one of the largest risks identified among cancer genome-wide association studies. We establish that the SNP has undergone positive selection throughout evolution, signifying a selective benefit, but go on to show that similar SNPs are rare in the genome due to negative selection, indicating that polymorphisms in p53-binding sites are primarily detrimental to humans.
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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.