Related Experiment Video
Updated: Jun 17, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
Study on TP53 codon 72 polymorphisms with oral carcinoma susceptibility
Xian-Lu Zhuo1, Qi Li, Yan Zhou
1Department of Otolaryngology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Background And Aims:
Previous published data have implicated TP53 codon 72 polymorphisms as risk factors for various cancers. Growing bodies of studies have been conducted on the association of TP53 codon 72 polymorphisms with susceptibility to oral carcinoma and have yielded inconclusive results. The aim of the present study was to derive a more precise estimation of this relationship.
Methods:
We conducted a search in the relevant databases without a language limitation, covering all papers published until May 2009. The associated literature was acquired through deliberate searching and selected based on the established inclusion criteria for publications.
Results:
Nine studies including 1990 cases and 2074 controls were selected. Data were extracted and further analyzed using systematic meta-analyses. Results showed that no significant differences of oral cancer risk were found between individuals carrying homozygote Arg/Arg genotype and those carrying Pro/Pro genotype (OR: 0.96, 95% CI: 0.78-1.19). Likewise, no evidence indicated that individuals with Arg/Arg genotype have a significant risk of oral cancer compared with those with a combined Pro genotype (Arg/Pro+Pro/Pro) (OR: 0.98, 95% CI: 0.85-1.12). Similarly, individuals with a combined Arg genotype (Arg/Pro+Arg/Arg) do not have a marked increased or decreased susceptibility to oral cancer relative to those with homozygote Pro/Pro genotype (OR: 1.00, 95% CI: 0.83-1.21). Moreover, when stratifying for race, results were similar among Asians or Caucasians. In addition, TP53 codon 72 polymorphisms may not associate with oral cancer risks in smokers and HPV infection status.
Conclusions:
No evidence suggests that TP53 codon 72 polymorphisms may be a risk factor for oral carcinoma.
More Related Videos
11:20Simple and Rapid Method to Obtain High-quality Tumor DNA from Clinical-pathological Specimens Using Touch Imprint Cytology
Published on: March 21, 2018
07:00Identification of OTX1 and OTX2 As Two Possible Molecular Markers for Sinonasal Carcinomas and Olfactory Neuroblastomas
Published on: February 28, 2019
Related Concept Videos
Single Nucleotide Polymorphisms-SNPs
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
Abnormal Proliferation
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase
Loss of Tumor Suppressor Gene Functions
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...