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Background: The DNA repair gene XPD, an important caretaker of the overall genome stability, is thought to play a major role in the development of human malignancy. Polymorphic variants of XPD, at codon 312, 751, and other sites, have been associated with cancer susceptibility, but few studies have investigated their effect on prostate cancer risk., Patients and Methods: In this hospital-based case-control study, the association of XPD codon 312, 751 and promoter-114 polymorphisms with prostate cancer risk in a Taiwanese population were investigated. In total, 123 patients with prostate cancer and 479 healthy controls recruited from the China Medical Hospital in Central Taiwan were genotyped., Results: We found a significant difference in the frequency of the XPD codon 312 genotype, but not the XPD codon 751 or promoter-114 genotypes, between the prostate cancer and control groups. Those who had GIA or A/A at XPD codon 312 showed a 1.81-fold (95% confidence interval=1.21-2.69) increased risk of prostate cancer compared to those with GIG. As for XPD codon 312 or promoter-114, there was no difference in distribution between the prostate cancer and control groups., Conclusion: Our findings suggest that the heterozygous and homozygous A allele of the XPD codon 312 may be associated with the development of prostate cancer and may be a useful marker for primary prevention and anticancer intervention.

Background: The tumor suppressor gene p53 and its downstream effector p21(CDKN1A/WAF1/CIP1) are thought to play major roles in the development of human malignancy. Polymorphic variants of p53, at codon 72, and CDKN1A, at codon 31, have been associated with cancer susceptibility, but few studies have investigated their effect on oral cancer risk., Materials and Methods: In this hospital-based case-control study, the association of p53 codon 72 and CDKN1A codon 31 polymorphisms with oral cancer risk in a Taiwanese population were investigated. In total, 137 patients with oral cancer and 105 age-matched controls recruited from the Chinese Medical Hospital in Central Taiwan were genotyped., Results: We found a significant difference in the frequency of the p53 genotype, but not the CDKN1A genotype, between the oral cancer and control groups. Those who had Arg/Arg at p53 codon 72 showed a 2.68-fold (95% confidence interval = 1.19-6.01) increased risk of oral cancer compared to those with Pro/Pro. The distribution of the combination of p53 codon 72 and CDKN1A codon 31 was different in the oral cancer and control groups. The percentages of three subgroups with the p53 GG homozygote were all higher in the oral cancer group, and the risky double homozygote, p53/CDKN1A GG/CC form, was almost 9-fold higher than the control group., Conclusion: Our findings suggest that the homozygous Arg allele of the p53 codon 72 may be associated with the development of oral cancer and be a useful marker for primary prevention and anticancer intervention.

The possibility that a family history of asthma may have a role in susceptibility to bronchopulmonary dysplasia (BPD) had been raised in several reports, and there was evidence of a strong association between transporter associated with antigen processing (TAP1) polymorphism and asthma in Taiwanese population. To test whether TAP polymorphism has a role in the BPD, we investigated the association between TAP1 polymorphism and BPD by analyzing the results of genotype distribution. The study included 224 ventilated preterm infants (<30 weeks) who had respiratory distress syndrome (RDS) and needed intermittent mandatory ventilation (IMV) during Jan. 1999 to July 2003. The typing of TAP1 polymorphism was performed by polymerase chain reaction (PCR)-based restriction analysis. The demography between two groups of these ventilated preterm infants was not different. We observed no significant differences in genotype distribution or allele frequency of the TAPI polymorphisms between BPD and their respective control infants. There was also no significant difference in genotype distribution of the TAP1 polymorphism with duration of IMV. Therefor, we conclude that TAP1 polymorphism is not a useful marker for predicting the susceptibility or severity to BPD for Taiwanese.

Interleukin 4 (IL-4) stimulates and amplifies the inflammatory response, stimulates collagen synthesis in fibroblasts, promotes the progression to fibrosis and has been shown to inhibit the production of several inflammatory cytokines in the development of bronchopulmonary dysplasia (BPD) and airway hyperreactivity. We aimed to investigate whether IL-4 polymorphisms in ventilated preterm infants were associated with BPD. BPD was defined as infants who remained dependent on active respiratory support or oxygen supplementation at 36 weeks postconceptional age. A case-control study of 224 preterm infants (<30 weeks) who had respiratory distress syndrome and needed intermittent mandatory ventilation (IMV) were undertaken between January 1999 and December 2003. The typing of each genetic polymorphism was performed by polymerase-chain-reaction-based restriction analysis. Genotype distribution and allelic frequencies were compared between ventilated preterm infants who developed BPD and those who did not and the duration of IMV. The demography of these ventilated BPD and non-BPD preterm infants was not different. We observed no significant differences in genotype distribution or allelic frequency of the IL-4 intron 3 or IL-4 promoter polymorphisms between ventilated preterm infants who developed BPD and who did not. There was no significant association of the genotype or allelic frequency of IL-4 polymorphism with duration of IMV. We conclude that neither IL-4 intron 3 nor the 590 promoter polymorphism is a useful marker for predicting the susceptibility to BPD in ventilated Taiwanese preterm infants., (Copyright (c) 2005 S. Karger AG, Basel.)

Pathological findings pertaining to bronchopulmonary dysplasia (BPD) are consistent with a process of prolonged lung inflammation and impaired healing. The balance of the competing activities of coagulation and fibrinolysis may contribute to the premature lung's response to acute injury. We investigated the association of the urokinase gene polymorphism with BPD in ventilated preterm infants whose gestational age was below 30 weeks. BPD is defined as infants remaining dependent upon active respiratory support and/or oxygen supplementation and featuring characteristic radiographic changes in the lung fields on the 28th postnatal day (BPD-28d) and at a corrected age of 36 weeks of gestation (BPD-36w). Two hundred and four ventilated preterm infants were enrolled in the study. The typing of each specific genotype polymorphism was performed by polymerase chain reaction (PCR) and restriction analysis. Perinatal risk factors for BPD, genotype distribution, and allelic frequencies were compared between infants suffering from BPD (28-d), BPD (36-w) and their respective ventilated preterm infants who did not develop BPD infants. The genotype proportions of the urokinase 3'-UTR polymorphism for BPD (28-d), BPD (36-w) and their respective ventilated preterm infants who did not develop BPD did not differ significantly. There was no difference in allelic frequency for the urokinase 3'-UTR polymorphism between BPD (28-d), BPD (36-w) and their respective ventilated preterm infants who did not develop BPD infants. We concluded that urokinase gene 3'-UTR C/T polymorphism is not a suitable marker for predicting susceptibility and severity to BPD for preterm infants of Taiwanese.