Allelic Frequency of p53 Gene Codon 72 Polymorphism in Urologic Cancers

Wu, Wen‐Jeng; Kakehi, Yoshiyuki; Habuchi, Tomonori; Kinoshita, Hidefumi; Ogawa, Osamu; Terachi, Toshiro; Huang, Chun‐Hsiung; Chiang, Chin-Pei; Yoshida, Osamu

doi:10.1111/j.1349-7006.1995.tb02461.x

Cited by 57 publications

(40 citation statements)

References 28 publications

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“…1). Whereas the core domain binds DNA in a sequence-specific fashion, the C-terminal domain of p53 interacts with DNA in a manner independent of the sequence (2)(3)(4) and is subject to multiple acetylations and phosphorylations that activate p53. How the two DNA-binding domains coordinate their actions and influence dynamics of p53 has been a subject of great interest and controversy.…”

Section: Recognition | Response Element | Transcription Factormentioning

confidence: 99%

A single-molecule characterization of p53 search on DNA

Tafvizi

Huang

Fersht

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

226

301

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The tumor suppressor p53 slides along DNA while searching for its cognate site. Central to this process is the basic C-terminal domain, whose regulatory role and its coordination with the core DNAbinding domain is highly debated. Here we use single-molecule techniques to characterize the search process and disentangle the roles played by these two DNA-binding domains in the search process. We demonstrate that the C-terminal domain is capable of rapid translocation, while the core domain is unable to slide and instead hops along DNA. These findings are integrated into a model, in which the C-terminal domain mediates fast sliding of p53, while the core domain samples DNA by frequent dissociation and reassociation, allowing for rapid scanning of long DNA regions. The model further proposes how modifications of the C-terminal domain can activate "latent" p53 and reconciles seemingly contradictory data on the action of different domains and their coordination.recognition | response element | transcription factor

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Section: Recognition | Response Element | Transcription Factormentioning

confidence: 99%

A single-molecule characterization of p53 search on DNA

Tafvizi

Huang

Fersht

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

226

301

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“…Genomic DNA was extracted from frozen tissue by proteinase-K digestion and phenol:chloroform extraction, according to methods reported previously [13]. DNA from normal tissues or peripheral blood mononuclear cells was also extracted as a matching normal control.…”

Section: Dna Extraction and Analysismentioning

confidence: 99%

Genetic alterations of the p16 gene in urothelial carcinoma in Taiwanese patients

Wu¹,

Kakehi

Chang

et al. 2000

BJU International

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Objective To measure changes in the p16 gene (MTS1, a negative regulator of cell-cycle progression at the G1 checkpoint, and a tumour suppressor gene) in urothelial carcinomas (including upper tract urothelial and bladder tumours), and to correlate these measurements with the clinical status of such patients in Taiwan, where renal pelvic tumours comprise 47% of all kidney tumours and are more common than the average worldwide. Materials and methods Thirty-®ve upper tract urothelial and 61 bladder tumours were examined for changes in p16. Deletion of the gene was assessed by Southern blot analysis and mutation analysed using polymerase chain reaction-single strand conformation polymorphism, followed by direct sequencing. Results Of the 61 bladder carcinomas, homozygous deletion of p16 was detected in 12 (20%). However, a homozygous deletion was detected in 11 of 35 (31%) upper tract urothelial carcinomas, a higher frequency than that reported for transitional cell bladder carcinomas. Deletion was detected as frequently in stage I tumours as in late-stage tumours, suggesting that p16 deletion is a relatively early event in urothelial tumorigenesis. No point mutations were noted for p16 in any of the primary urothelial tumours. Most multiple and recurrent tumours and metastatic nodules in individual patients contained identical p16 genetic lesions, con®rming that the tumours were probably monoclonal. In addition, there was a high gene dose of p16 in bladder carcinomas from patients with lymph node metastasis. Conclusion Deletion of p16 appears to be a common event in urothelial carcinomas, especially in upper tract urothelial tumours. High levels of p16 were detected in tumours with lymph node metastasis. It seems likely that a high p16 level is associated with carcinomas of advanced stage and grade, and with poor prognosis in patients with such cancers.

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“…The tumor suppressor protein, p53, can mediate multiple cellular functions, such as tumor suppression, gene transcription, DNA synthesis and repair, angiogenesis, differentiation, cell cycle regulation, and cell senescence and apoptosis [Vousden and Lane 2007]. The P53 protein is present in human, mouse, and rat testes [Almon et al 1993], located on chromosome 17p13 [Wu et al 1995]. In general, during spermatogenesis TP53 regulates apoptosis to control germ cell quality [Zauberman et al 1995].…”

Section: Introductionmentioning

confidence: 99%

No association ofTP53 codon 72 SNP with male infertility: a study in a Chinese population and a meta-analysis

Chan

Jiang

et al. 2015

Systems Biology in Reproductive Medicine

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Genetic polymorphisms may affect human male fertility. Even though TP53 plays a role in spermatogenesis we know little about the association of the functional polymorphism at codon 72 of TP53 with respect to susceptibility to male infertility. We conducted a case-control study to investigate this association in a Chinese population and performed a meta-analysis in different populations to clarify this association. The single nucleotide polymorphism (SNP) of TP53 codon 72 (rs1042522 G4C) was genotyped by PCR-RFLP in 83 Chinese male infertility patients and 401 healthy controls. Meta-analysis was performed using the data from four currently available studies. The data from our study were overlayed using the v.9.0 STATA software package. We observed no association between the TP53 codon 72 polymorphism and male infertility (p ¼ 0.84, OR ¼ 1.04, 95% CI, 0.74-1.45). Meta-analysis confirmed the casecontrol result that there was no significant association between the codon 72 polymorphism of Abbreviations: Arg: arginine allele; CI: confidence interval; HWE Hardy-Weinberg equilibrium; OR: odds ratio; PCR-RFLP: polymerase chain reaction-estriction fragment length polymorphism; Pro: proline allele; SNP: single nucleotide polymorphism; TP53: tumor protein 53.

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Allelic Frequency of p53 Gene Codon 72 Polymorphism in Urologic Cancers

Cited by 57 publications

References 28 publications

A single-molecule characterization of p53 search on DNA

A single-molecule characterization of p53 search on DNA

Genetic alterations of the p16 gene in urothelial carcinoma in Taiwanese patients

No association ofTP53 codon 72 SNP with male infertility: a study in a Chinese population and a meta-analysis

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