Eskandari Ebrahim, Dahmardeh Tayebeh, Dahmardeh Fatemeh, Pahlevani Elham, Metanat Malihe
Genetic of Non-Communicable Disease Research Center, Zahedan University of Medical Sciences, Zahedan, Islamic Republic of Iran.
Department of Clinical Biochemistry, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Islamic Republic of Iran.
Virusdisease. 2017 Sep;28(3):289-294. doi: 10.1007/s13337-017-0391-7. Epub 2017 Aug 22.
TP53 and phosphate and tension homolog (PTEN) are two tumor suppressor genes that regulate cell proliferation, migration, and death. P53 and PTEN deficiency has been associated with hepatic fibrosis, a prominent pathological feature associated with chronic hepatitis B (CHB). The present study is aimed to assess the association of PTEN 32-bp Ins/Del (rs34421660) and TP53 16-bp Ins/Del polymorphisms with CHB infection susceptibility. A total of 411 subjects were recruited in this case-control study of 213 patients with CHB infection and 198 healthy individuals as controls. PTEN and TP53 deletions were detected by polymerase chain reaction method. We found no significant association between PTEN 32-bp Ins/Del polymorphism and the risk for CHB using either of codominant (Ins/Del vs. Ins/Ins: = 0.427; Del/Del vs. Ins/Ins: = 0.235), dominant (Ins/Del + Del/Del vs. Ins/Ins = 0.343) or recessive genetic model (Del/Del vs. Ins/Ins + Ins/Del: = 0.516). At allelic level although the PTEN Del variant allele was more common in CHB patients compared to controls (55 vs. 51), but the difference did not reach the statistical significant range (OR 0.87, = 0.327). Similarly, no association was observed between TP53 16-bp Ins/Del and the risk for CHB infection at both genotype and allele levels ( > 0.05). In summary, our study demonstrated that the PTEN 32-bp and TP53 16-bp Ins/Del polymorphisms did not affect the risk of CHB infection in the Iranian population.
TP53基因和磷酸酶及张力蛋白同源物（PTEN）是两个调控细胞增殖、迁移和死亡的抑癌基因。P53和PTEN基因缺陷与肝纤维化有关，肝纤维化是慢性乙型肝炎（CHB）的一个突出病理特征。本研究旨在评估PTEN基因32bp插入/缺失（rs34421660）和TP53基因16bp插入/缺失多态性与CHB感染易感性的关联。在这项病例对照研究中，共招募了411名受试者，其中213例为CHB感染患者，198名健康个体作为对照。采用聚合酶链反应法检测PTEN和TP53基因的缺失情况。我们发现，无论是共显性遗传模型（插入/缺失vs.插入/插入：P = 0.427；缺失/缺失vs.插入/插入：P = 0.235）、显性遗传模型（插入/缺失 + 缺失/缺失vs.插入/插入：P = 0.343）还是隐性遗传模型（缺失/缺失vs.插入/插入 + 插入/缺失：P = 0.516），PTEN基因32bp插入/缺失多态性与CHB感染风险之间均无显著关联。在等位基因水平上，尽管CHB患者中PTEN基因缺失变异等位基因比对照组更常见（55%对51%），但差异未达到统计学显著范围（比值比0.87，P = 0.327）。同样，在基因型和等位基因水平上，均未观察到TP53基因16bp插入/缺失与CHB感染风险之间存在关联（P>0.05）。总之，我们的研究表明，PTEN基因32bp和TP53基因16bp插入/缺失多态性不影响伊朗人群CHB感染风险。
