Abstract:PIN1 is one member of the parvulin PPIase family. By controlling Pro-directed phosphorylation, PIN1 plays an important role in cell transformation and oncogenesis. There are many polymorphisms in the PIN1 gene, including rs2233678 and rs2233679 affecting the PIN1 promoter. Recently, a number of case-control studies were conducted to investigate the association between PIN1 gene rs2233678 and rs2233679 polymorphism and cancer risk. However, published data are still conflicting. In this paper, we summarized data… Show more
“…For example, the SNP rs2233679 (NO. 3) was identified as the −667CC homogeneous genotype in the promoter of PIN1 gene, but the influences of −667C and −667T on Pin1 expression and relevant diseases are still not very identical, necessitating further clinical investigations especially in different ethnic groups [ [16] , [17] , [18] , [19] ]. Fig.…”
Objective
A novel genetic and molecular basis of nonalcoholic fatty liver disease (NAFLD) was explored.
Study design
A 38-year-old male, who has no bad living and dietary habits, was diagnosed as NAFLD. The potential pathogenic role of Pin1 was evaluated by enzyme-linked immunosorbent (ELISA) assay and single nucleotide polymorphism (SNP) sequencing.
Results
ELISA determined a six-time higher concentration of plasma Pin1 compared to our previous data. Nine
PIN1
SNPs were sequenced and classified according to their NAFLD-pathogenic risks, suggesting that rs2233678 and rs2287839 may be the most important genotypes that result in Pin1 overexpression and NAFLD development.
Conclusion
In summary, this work explores a novel basis for early-onset NAFLD and highlights that elevated plasma Pin1 may predict NAFLD risk at early stage. Hypothetically, inhibiting Pin1 may benefit NAFLD prevention in the future.
“…For example, the SNP rs2233679 (NO. 3) was identified as the −667CC homogeneous genotype in the promoter of PIN1 gene, but the influences of −667C and −667T on Pin1 expression and relevant diseases are still not very identical, necessitating further clinical investigations especially in different ethnic groups [ [16] , [17] , [18] , [19] ]. Fig.…”
Objective
A novel genetic and molecular basis of nonalcoholic fatty liver disease (NAFLD) was explored.
Study design
A 38-year-old male, who has no bad living and dietary habits, was diagnosed as NAFLD. The potential pathogenic role of Pin1 was evaluated by enzyme-linked immunosorbent (ELISA) assay and single nucleotide polymorphism (SNP) sequencing.
Results
ELISA determined a six-time higher concentration of plasma Pin1 compared to our previous data. Nine
PIN1
SNPs were sequenced and classified according to their NAFLD-pathogenic risks, suggesting that rs2233678 and rs2287839 may be the most important genotypes that result in Pin1 overexpression and NAFLD development.
Conclusion
In summary, this work explores a novel basis for early-onset NAFLD and highlights that elevated plasma Pin1 may predict NAFLD risk at early stage. Hypothetically, inhibiting Pin1 may benefit NAFLD prevention in the future.
“…The optimal therapy for chest wall tumors is surgical resection, in which local resection can be performed on benign or malignant tumors (Afsharfard et al, 2013;Alipour et al, 2014;Fouladi et al, 2014;Hu et al, 2013;Sedighi et al, 2013;Talaiezadeh et al, 2013;Zhu et al, 2013;Hu et al, 2014;Jia et al, 2014;Ozkan-Gurdal et al, 2014). However, the resection range should be properly enlarged to such tumors as desmoids, chondroma and osteoclastoma, or be resolved as in malignant tumors, though with benign pathological examinations (Errani et al, 2010;Nieuwenhuis et al, 2011).…”
“…Various Polymorphisms have been studied to elucidate the association with the risk of lung cancer Zhu et al, 2013;Bayram, 2014). CYP1A2 is located on chromosome 15q in opposite orientation and separated by 23.3 kb, it is a major drug-metabolizing enzyme, with a wide range of substrates (Eaton et al, 1995).…”
Background: Previous published data on the association between CYP1A2 rs762551, rs2069514, rs2069526, and rs2470890 polymorphisms and lung cancer risk have not allowed a definite conclusion. The present metaanalysis of the literature was performed to derive a more precise estimation of the relationship. Materials and Methods: 8 publications covering 23 studies were selected for this meta-analysis, including 1,665 cases and 2,383 controls for CYP1A2 rs762551 (from 8 studies), 1,456 cases and 1,792 controls for CYP1A2 rs2069514 (from 7 studies), 657 cases and 984 controls for CYP1A2 rs2069526 (from 5 studies) and 691 cases and 968 controls for CYP1A2 rs2470890 (from 3 studies). Results: When all the eligible studies were pooled into the meta-analysis for the CYP1A2 rs762551 polymorphism, significantly increased lung cancer risk was observed in the dominant model (OR=1.21, 95 % CI=1.00-1.46). In the subgroup analysis by ethnicity, significantly increased risk of lung cancer was observed in Caucasians (dominant model: OR=1.29, 95%CI=1.11-1.51; recessive model: OR=1.33, 95%CI=1.01-1.75; additive model: OR=1.49, 95%CI=1.12-1.98). There was no evidence of significant association between lung cancer risk and CYP1A2 rs2069514, s2470890, and rs2069526 polymorphisms. Conclusions: In summary, this meta-analysis indicates that the CYP1A2 rs762551 polymorphism is linked to an increased lung cancer risk in Caucasians. Moreover, our work also points out the importance of new studies for rs2069514 associations in lung cancer, where at least some of the covariates responsible for heterogeneity could be controlled, to obtain a more conclusive understanding about the function of the rs2069514 polymorphism in lung cancer development.
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