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Prostate cancer is one of the most commonly diagnosed malignancies among males worldwide. It has been shown that MMP-7 gene is closely correlated with prostate carcinogenesis. However, the role of the MMP-7 genotypes has been seldom examined among prostate cancer patients. Therefore, the purpose of the study was to evaluate the contribution of MMP-7 promoter genotypes A-181G (rs11568818) and C-153T (rs11568819) to prostate cancer risk in Taiwan.Two hundred and eighteen prostate cancer patients and 436 sex- and age-matched healthy controls were genotyped for MMP-7 rs11568818 and rs11568819 by polymerase chain reaction-restriction fragment length polymorphism and direct sequencing methodologies.The percentages of wild-type AA, and variant AG and GG genotypes on MMP-7 rs11568818 were 85.3, 13.5, and 1.2% among the prostate cancer cases and 87.6, 10.1, and 2.3% among the healthy controls, respectively (p for trend=0.2557). Interestingly, no MMP-7 rs11568819 genotypes were identified among Taiwanese. The allelic frequency distribution also showed that the variant G allele of MMP-7 rs11568818 seemed not to be a determinant of prostate cancer risk (p=0.7977). There was no joint effect between the genotypes of MMP-7 rs11568818 and age and smoking status on prostate cancer risk.rs11568818 and rs11568819 at MMP-7 promoter region, played no role in determining personal susceptibility to prostate cancer in Taiwan.

Prostate cancer is one of the most commonly diagnosed malignancies among males, especially in Western populations. Matrix metalloproteinase-2 (MMP-2) plays a critical role in extracellular regulation and metastasis. However, its genotypes have seldom been examined among patients with prostate cancer (PCa). Therefore, the purpose of the study was to evaluate the association of genotypes at MMP-2 promoter -1306 (rs243865) and -735 (rs2285053) with PCa risk in a Taiwanese cohort.The profiles of MMP-2 rs243865 and rs2285053 genotypes were examined among 218 PCa patients and 436 healthy controls by polymerase chain reaction-restriction fragment length polymorphism methodologies.The percentages of wild-type CC, and variant CT and TT genotypes on MMP-2 rs243865 were 88.5, 10.6, and 0.9% in the PCa case group and 85.6, 13.5, and 0.9% in the control group, respectively (p for trend=0.5544). The allelic frequency distribution showed that the variant T allele at MMP-2 rs24386 5 was not associated with PCa risk (p=0.3250). As for MMP-2 rs2285053, the results were also non-significant. In addition, there was no association between the genotypes of MMP-2 rs243865 or rs2285053 with age or smoking status on PCa risk.rs11568818 and rs11568819 at MMP-2 promoter region played minor roles in determining individual PCa risk.

We aimed to examine the associations of the genotypes for mir146a and mir196a with bladder cancer (BLCA) risk in Taiwan. Mir146a rs2910164 and mir196a rs11614913 genotypes among 375 bladder cancer patients and 375 healthy subjects were determined using the typical PCR-RFLP methodology, and their associations and interactions with age, gender, smoking and alcohol drinking status on BLCA risk were evaluated. Simultaneously, the serum expression level of mir146a was measured using quantitative RT-PCR. The results showed that the partitions of CC, CG and GG of mir146a genotypes were 31.7, 45.6 and 22.7% in the control group and 21.9, 44.3 and 33.8% in the case group, respectively. In logistic regression analysis, the heterozygous variant genotype CG carriers were at a bolder line significantly increased BLCA risk (OR = 1.41, 95% CI = 0.99–2.01) and the homozygous variant GG carriers were at a 2.17-fold increased BLCA risk (OR = 2.17, 95%CI = 1.46–3.21). Moreover, the GG/CG genotype carriers have significantly higher serum levels of mir146a than the CC genotype (p mir196a rs11614913 SNP were not associated with BLCA risk. In conclusion, genotypes of mir146a rs2910164 may serve as a risk prediction marker for BLCA.

Aim There is very little literature reporting the association of matrix metalloproteinase-1 (MMP1) with personal susceptibility to bladder cancer. In the current study, we carried out the first examination of the contribution of MMP1 rs1799750 to bladder cancer risk in Taiwanese. Materials and methods A total of 375 bladder cancer cases and 375 healthy controls were genotyped for MMP1 rs1799750 via polymerase chain reaction-restriction fragment length polymorphism methodology and this was evaluated for association with clinicopathological factors. Results The frequencies of MMP1 rs1799750 2G/2G, 1G/2G, and 1G/1G genotypes were 35.7%, 44.8% and 19.5% in the group with bladder cancer and 32.5%, 46.4%, and 21.1% in the healthy control group (p for trend=0.6362). The odds ratios (ORs) for bladder cancer risk after adjusting for age and gender for those carrying 1G/2G and 1G/1G genotypes at MMP1 rs1799750 were 0.88 (95% CI=0.62-1.24, p=0.4357) and 0.83 (95% CI=0.61-1.26, p=0.3990), respectively, compared with the wild-type 2G/2G genotype. In allelic frequency analysis, the adjusted OR for those carrying the 1G allele at MMP1 rs1799750 was 0.87 (95% CI=0.71-1.23, p=0.3479) compared to those people carrying a 2G allele. Conclusion Our findings indicated that the genotypes at MMP1 rs1799750 appear to play little role in determining personal susceptibility to bladder cancer for Taiwanese.

Background/Aim: In literature, few studies have examined the diagnostic or prognostic potential of matrix metalloproteinases (MMP) in pterygium, whose formation and progression are closely related to imbalance in the extracellular microenvironment. In this study, we investigated the contribution of MMP7 promoter (A-181G and C-153T) polymorphic genotypes to pterygium risk. Materials and Methods: A total of 134 cases and 268 controls were collected and their MMP7 genotypes at A-181G and C-153T were examined by polymerase chain reaction-restriction fragment length polymorphism methodology. Results: The AA, AG and GG genotypes at MMP7 promoter A-181G were non-significantly differentially distributed between the two groups at 85.8, 11.2 and 3.0%, respectively, in pterygium cases and 88.4, 9.7 and 1.9% in controls, respectively (p for trend=0.6822). There was no polymorphic genotype for MMP7 C-153T among our Taiwanese cohort. Conclusion: A-181G and C-153T genotypes at MMP7 do not have a direct role in determining Taiwanese susceptibility to pterygium.

Shang-Rong Zhong,1 Han-Hsuan Yang,1– 3 Cheng-Hsi Liao,4– 7 Deng-Ho Yang,5,6,8,9 Shih-Kai Tu,1,5 Chia-Lien Hung,6 Chun-Cheng Liao1,5,6 1Department of Family Medicine, Taichung Armed Forces General Hospital, Taichung, Taiwan; 2Department of Occupational Medicine, Taichung Veterans General Hospital, Taichung, Taiwan; 3School of Professional Education and Continuing Studies, National Taiwan University, Taipei, Taiwan; 4Division of Urology, Department of Surgery, Taichung Armed Forces General Hospital, Taichung, Taiwan; 5School of Medicine, National Defense Medical Center, Taipei, Taiwan; 6Department of Medical Education and Research, Taichung Armed Forces General Hospital, Taichung, Taiwan; 7Graduate Institute of Biomedical Science, China Medical University, Taichung, Taiwan; 8Division of Rheumatology/Immunology/Allergy, Department of Internal Medicine, Taichung Armed Forces General Hospital, Taichung, Taiwan; 9Department of Medical Laboratory Science and Biotechnology, Central Taiwan University of Science and Technology, Taichung, TaiwanCorrespondence: Chun-Cheng Liao Email milkbottle97@yahoo.com.twPurpose: To assess the association between serum testosterone (T) and metabolic syndrome (MS) in different age groups in Taiwanese men.Materials and Methods: Male participants, regardless of age or any underlying disease, were identified from MJ Health Screening Center in Taiwan from 2007 to 2016 for this cross-sectional study. They were divided into three groups according to age, and further classified according to MS diagnosis. Basic patient characteristics with relevant parameters were obtained. One-way ANOVA of mean T values between different numbers of measures that exceeds the cut-off values of MS components was performed to assess the relationship of T and MS. Logistic regression analysis was also used to estimate the risk for MS with each increment in T, age, and BMI.Results: A total of 4,931 men were included. The MS group had significantly lower serum T levels compared to the non-MS group in each age group. The one-way ANOVA found the mean value of T was significantly higher in patients without MS component (6.19± 2.12 ng/mL) than those with 1– 5 MS components (with one MS component: 5.48± 2.13 ng/mL, two MS components: 4.93± 2.03 ng/mL, three MS components: 4.37± 1.60 ng/mL, four MS components: 4.13± 2.89 ng/mL, five MS components: 3.74± 1.27 ng/mL, and P< 0.001). There was no significant difference between the patients with three components and the patients with four or five components. Logistic regression models with age stratification showed T with lower odds ratio (OR) for MS after adjusting for BMI in those ≥ 65 years old (OR=0.693; 95% CI=0.559– 0.858; P< 0.001); 50– 64 years old (OR=0.868; 95% CI=0.802– 0.940; P< 0.001) and < 50 years old (OR=0.810; 95% CI=0.758– 0.865; P< 0.001).Conclusion: Lower serum T was strongly associated with MS, with the predictive value increasing with age in Taiwanese men.Keywords: testosterone, metabolic syndrome, hypogonadism, insulin resistance

Background/Aim: Interleukin-16 has been reported to exhibit tumoricidal effects, however, the contribution of IL-16 genotypes to lung cancer is still largely unrevealed. This study aimed at investigating whether IL-16 genotypes contribute to lung cancer susceptibility. Materials and Methods: IL-16 rs4778889, rs11556218, and rs4072111 genotypic characteristics were determined among 358 lung cancer patients and 716 controls via the polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) methodology. Results: The highlight finding is that the distributions of genotypic (p=8.6E-10) and allelic (p=0.0001) frequencies of IL-16 rs11556218 was significantly different between cases and controls. In detail, the frequencies of IL-16 rs11556218 heterozygous variant TG and homozygous variant GG were 36.6 and 7.3% among the lung cancer patients, significantly higher than those among the controls (22.5% and 2.6%). On the other way, no difference was observed regarding IL-16 rs4778889 or IL-16 rs4072111. Conclusion: The present study indicates IL-16 rs11556218 G allele is significantly associated with increased Taiwan lung cancer risk.

The DNA repair capacity plays a critical role in maintaining the genomic stability and gatekeeping for individual cancer risk. In this study, we aim at evaluation the role of the Asp148Glu (rs1130409) variant at apurinic/apyrimidinic endonuclease (APE) gene in renal cell carcinoma (RCC) risk and the contribution of different genotypes to its transcriptional mRNA levels. In the case-control study, 92 RCC patients and 580 cancer-free patients matched by age and gender were recruited. The apurinic/APE genotyping work was conducted with typical restriction fragment length polymorphism methodology after polymerase chain reaction. At the meanwhile, thirty renal tissue samples with variant genotypes were examined for their apurinic/APE mRNA and protein expressions by real-time quantitative reverse transcription method and Western blotting. The results showed that compared with the wild-type TT genotype, the people with TG and GG genotypes of apurinic/APE Asp148Glu had 0.88- and 1.09-fold risk of RCC, respectively. We have also examined the in vivo transcriptional (RNA) and translational (protein) levels with renal tissues of various apurinic/APE Asp148Glu genotypes, revealing that the apurinic/APE mRNA and protein were of similar levels among people of TT, TG, or GG genotypes. There was no joint gene-environment effect of apurinic/APE Asp148Glu genotype and smoking habit on RCC risk. The evidence indicated that apurinic/APE Asp148Glu genotypic variants did not alter its mRNA and protein expression among RCC patients. The genotype of apurinic/APE Asp148Glu may not serve as a proper predictive marker for RCC risk in Taiwan.

BACKGROUND/AIM Lung cancer is the leading cause of cancer-related death and a better marker for advanced personalized therapeutic approaches, such as immunotherapies, is in urgent need. Interleukin-12 (IL-12) is a cytokine that has been reported to exhibit potent tumoricidal effects, however, the contribution of IL-12 genotypes to lung cancer is still largely unrevealed. The aim of this study was to investigate whether single nucleotide polymorphisms (SNPs) in IL-12A and IL-12B are associated with lung cancer in a Taiwanese population. MATERIALS AND METHODS Genotypes of 358 lung cancer patients and 716 controls were determined by the polymerase chain reaction-restriction fragment length polymorphism method. RESULTS The distributions of genotypic (p=0.0036) and allelic (p=0.0005) frequencies of IL-12A rs568408 demonstrated significant differences between cases and controls. In detail, the AA genotype of IL-12A rs568408 was associated with a significantly elevated risk of lung cancer compared with the GG genotype (odds ratio(OR)=2.41, 95% confidence interval(CI)=1.36-4.29, p=0.0021). No difference was observed regarding IL-12A rs2243115 and IL-12B rs3212227 genotypes between the case and control groups. In addition, the results of interaction analysis showed that the AA genotype of IL-12A rs568408 was associated with elevated lung cancer risk, especially among those with smoking habits (p=0.0043). CONCLUSION IL-12A rs568404 AA genotype may contribute to the etiology and serve as a genomic determinant of lung cancer in Taiwanese, especially smokers.

Background/Aim: The breakage of matrix metalloproteinases (MMPs) has been reported to be one of the mechanisms required for tumor invasion, and the expression of MMP-7 in serum is correlated with poor prognosis of urinary bladder cancer patients. However, the role of the MMP-7 genotypes has been seldom examined among bladder cancer patients. Therefore, this study aimed at examining the promoter polymorphic MMP-7 genotypes A-181G and C-153T among Taiwanese bladder cancer patients and evaluate the contribution of the genotypic variants of MMP-7 to bladder cancer risk in Taiwan. Materials and Methods: Three hundred and seventy-five bladder cancer patients and the same number of gender- and age-matched healthy controls were genotyped for A-181G and C-153T in the promoter of MMP-7 via polymerase chain reaction-restriction fragment length polymorphism methodology. Results: The frequencies of AA, AG and GG at A-181G of the promoter of MMP-7 were 89.1, 8.8 and 2.1% in the bladder cancer patient group and 87.5, 10.9 and 1.6% in the matched healthy control group, respectively (p for trend=0.5475). There was no polymorphic genotype for MMP-7 C-153T among the Taiwanese population. The comparisons in allelic frequency distribution also support the findings that the G allele may not be the determinant allele for bladder cancer in Taiwan. In addition, the results showed that there is no significant association of the bladder risk with the MMP-7 A-181G genotype, even after adjustment for the possible confounding factors. Furthermore, there is no interaction of the genotypes of MMP-7 with age, gender, smoking and alcohol consumption on bladder cancer risk. Conclusion: The results of this study suggest that the two MMP-7 polymorphisms, - A-181G and C-153T, do not play a major role in determining personal susceptibility to bladder cancer in Taiwan.

Background/aim Mounting evidence has suggested that polymorphisms in the promoters of matrix metalloproteinase (MMP) genes are associated with the risk of many types of cancer, but no study has ever explored these polymorphisms as biomarkers for renal cell cancer (RCC). Recently, it was suggested that serum MMP-7 levels have both diagnostic and prognostic potential for RCC. In this study, we focused on the contribution of two functional polymorphisms in the promoter region of MMP-7 (A-181G and C-153T) to RCC. Materials and methods These two polymorphisms were genotyped in 92 patients with RCC and 580 controls by PRC-RFLP analysis. Results The results showed that there is no significant association of the RCC risk with the MMP-7 A-181G genotype, even after adjusted for the possible confounding factors. The MMP-7 C-153T polymorphism was not identified among the subjects investigated. Conclusion Our findings suggest that the two MMP-7 polymorphisms A-181G and C-153T do not play a major role in determining personal susceptibility to RCC in Taiwan.

AIM Bladder cancer is the sixth most common cancer worldwide and its incidence is particularly high in many developed regions including southwestern Taiwan. However, the genetic contribution to the etiology of bladder cancer is not well-understood. The aim of this study was to evaluate the association of the enhancer of zeste homolog 2 (EZH2) genotypes with Taiwan bladder cancer risk. MATERIALS AND METHODS Three polymorphic variants of EZH2 were analyzed regarding their association with bladder cancer risk, and three hundred and seventy-five patients with bladder cancer and same number of age- and gender-matched healthy controls recruited were genotyped by the PCR-RFLP method. RESULTS Among the three polymorphic sites examined, the genotypes of EZH2 rs887569 (C to T), but not rs41277434 (A to C) or rs3757441 (T to C), were positively associated with bladder cancer risk (p for trend =0.0146). Individuals with the EZH2 rs887569 TT genotypes were associated with decreased cancer risk than those with wild-type CC genotype. The stratified analyses showed that EZH2 rs887569 TT genotypes had protective effects on non-smokers but obviously not on smokers. CONCLUSION Our findings provide evidence that the T allele of EZH2 rs887569 may be associated with the lower risk of bladder cancer development, especially among non-smokers.

BACKGROUND/AIM The family of matrix metalloproteinases (MMPs) is responsible for the maintenance of extracellular matrix component homeostasis and the association of MMP-1 genetic polymorphisms with personal susceptibility to prostate cancer has only been investigated in Turkish and Japan populations and never in Taiwan. In the current study, we aimed to examine the contribution of a polymorphism in the promoter region of MMP-1 to Taiwan prostate cancer. MATERIALS AND METHODS The MMP-1 rs1799705 polymorphic genotypes were genotyped among 218 prostate cancer patients and 436 healthy controls by the typical polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methodology. RESULTS The percentages of 2G/2G, 1G/2G, and 1G/1G for MMP-1 -1607 genotypes were 36.2, 40.4 and 23.4% in the prostate cancer group and 33.7, 44.3, and 22.0% in the healthy control group (p trend=0.6362), respectively. The odds ratios (ORs) after adjusting for age and smoking status for those carrying 1G/2G and 1G/1G genotypes at MMP-1 -1607 were 0.84 (95%CI=0.55-1.21, p=0.3862) and 0.94 (95%CI=0.67-1.53, p=0.9586), respectively, compared to those carrying the wild-type 2G/2G genotype. Supporting these findings, the adjusted OR for those carrying the 1G allele at MMP-1 -1607 was 1.03 (95%CI=0.71-1.45, p=0.6910), compared to those carrying the wild-type 2G allele. CONCLUSION Our findings suggest that the polymorphic genotypes at MMP-1 promoter -1607 may play a major role in determining personal cancer susceptibility for prostate cancer in Taiwan.

Background/Aim: Pterygium is composed of proliferating fibrovascular tissue, and its formation and progression are closely related to the homeostasis of the extracellular microenvironment. However, few studies have examined the contribution of matrix metalloproteinases (MMP) to either diagnostic or prognostic potential in pterygium. In this study, we investigated the contribution of a polymorphism in the promoter region of MMP-8 (-799C/T) and two non-synonymous polymorphisms (Val436Ala and Lys460Thr) to pterygium. Materials and Methods: In this study, 134 patients with pterygium and 268 non-cancer controls patients were collected and the MMP-8 -799C/T, Val436Ala and Lys460Thr polymorphic genotypes of each subject were examined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results: The results showed that the three polymorphisms investigated were not significantly associated with risk of pterygium. In addition, the stratified analysis showed that there was no interaction between MMP-8 genotype with age or gender on pterygium risk determination. Conclusion: Polymorphisms at MMP-8 -799C/T, Val436Ala and Lys460Thr may not mainly contribute to determining personal susceptibility to pterygium in the Taiwanese examined.

Few studies discussed the link between benign prostatic hyperplasia (BPH) and bladder cancer. We performed this cohort study to investigate whether there is an association between BPH and subsequent risk of bladder cancer. We identified 35,092 study subjects including 17546 BPH patients and 17546 comparisons from the National Health Insurance database. The comparison cohort was frequency matched with age and index-year. We measured subsequent bladder cancer rates (per 1000 person-years) in two cohorts. Attributable risks (ARs) was calculated based on the bladder cancer rates in two cohorts. The hazard ratios (HRs) and 95% confidence intervals (CIs) for bladder cancer were estimated via Cox proportional hazard regression. BPH patients had a higher bladder cancer rate than comparisons (AR = 0.81 per 1000 person-years) and exhibited 4.69- and 4.11-fold increases in bladder cancer risk in the crude and adjusted Cox models, respectively (95% CIs = 4.15–6.99 and 2.70–6.26). The AR was highest in patients aged 65–74 years old (AR = 1.33). BPH patients with chronic kidney disease were at an elevated bladder cancer risk. Regarding the association between bladder cancer and transurethral prostatectomy (TURP), BPH patients who underwent TURP were at a higher risk of bladder cancer (AR = 1.69; HR = 6.17, 95% CI = 3.68–10.3) than those who did not (AR = 0.69; HR = 3.73, 95% CI = 2.43–5.74). In this study, BPH patients were found to have an increased risk of subsequent bladder cancer. Based on the limitations of retrospective nature, further studies are needed.

Ultraviolet B (UVB), with a wavelength of 280-320 nm, represents one of the most important environmental factors for skin disorders, including sunburn, hyperpigmentation, solar keratosis, solar elastosis and skin cancer. Therefore, protection against excessive UVA-induced damage is useful for prevention of sunburn and other human diseases. Baicalin, a major component of traditional Chinese medicine Scutellaria baicalensis, has been reported to possess antioxidant and cytostatic capacities. In this study, we examined whether baicalin is also capable of protecting human keratinocytes from UVB irradiation. The results showed that baicalin effectively scavenged reactive oxygen species (ROS) elevated within 4 h after UVB radiation and reversed the UVB-suppressed cell viability and UVB-induced apoptosis after 24 h. Our results demonstrated the utility of baicalin to complement the contributions of traditional Chinese medicine in UVB-induced damage to skin and suggested their potential application as pharmaceutical agents in long-term sun-shining injury prevention.

Renal cell carcinoma (RCC) accounts for approximately 3% of all cancer-related mortalities worldwide and the risk factors for the development of RCC have not yet been fully elucidated. Mounting proteomic evidence suggests that inflammatory process plays a role in RCC etiology and interleukin-10 (IL-10) is an important immunosuppressive cytokine. However, little is known on the contribution of IL-10 genotypes to RCC. This study aimed at evaluating the contribution of IL-10 promoter A-1082G (rs1800896), T-819C (rs3021097), A-592C (rs1800872) genetic polymorphisms to the risk of RCC in Taiwan.Associations of the three IL-10 polymorphic genotypes with the risk of RCC were examined among 92 RCC patients and 580 age- and gender-matched cancer-free controls by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methodology.The pilot results showed that the percentages of TT and TC for IL-10 T-819C genotypes were significantly higher in the RCC patient group than those in the healthy control group. The CC genotype carriers were of lower risk for RCC (odds ratio (OR)=0.33, 95% confidence interval (CI)=0.12-0.93, p=0.0369). There is no difference in the distribution of A-1082G or A-592C genotype between the RCC and control groups.The CC genotype of IL-10 T-819C genotype may have a protective effect on RCC risk in Taiwan. Further investigation with larger sample size in addition to genotype-phenotype correlation and intracellular mechanisms are our future work.

The DNA-repair gene X-ray repair cross-complementing group 3 (XRCC3) is important in DNA double-strand break repair and plays a critical part in initiation of carcinogenesis. Triple-negative breast cancer (TNBC) is the most difficult breast cancer subtype with no existing gene-targeting drugs and little knowledge on its genetic etiology. This study aimed to investigate the contribution of the XRCC3 genotype to individual TNBC susceptibility.A total of 2,464 Taiwan citizens consisting of 1,232 breast cancer cases and 1,232 controls were enrolled in this case-control study, and genotyping of XRCC3 rs1799794, rs45603942, rs861530, rs3212057, rs1799796, rs861539 and rs28903081 were performed with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). We also conducted risk-stratified sub-group analyses to determine the association between the genotype and age- and hormone-related characteristics of breast cancer sub-groups.There was no significant difference between breast cancer and control groups in the distributions of the genotypic or allelic frequencies as for the XRCC3 rs1799794 (p=0.5195 and 0.9545), rs45603942 (p=0.3478 and 0.1449), rs861530 (p=0.4567 and 0.5081), rs3212057 (p=1.0000 and 1.0000), rs1799796 (p=0.8487 and 0.7315) and rs28903081 (p=1.0000 and 1.0000), respectively. However, the XRCC3 rs861539 TT genotype was more prevalent in patients with breast cancer [odds ratio (OR)=2.99, 95% confidence interval (CI)=1.62-5.55; p=0.0002], and especially among those who were younger than 55 years (OR=2.61, 95% CI=1.82-3.73; p=0.0001), with first menarche earlier than 12.2 years (OR=2.47, 95% CI=1.74-3.52; p=0.0001), with menopause at 49.0 years old or later (OR=2.53, 95% CI=1.76-3.62; p=0.0001), or with TNBC (OR=2.05, 95% CI=1.46-4.28; p=4.63*10(-4)).XRCC3 rs861539 TT is a potential predictive marker for TNBC in Taiwanese women and investigations in other populations are warranted for further universal application in cancer detection and prediction.

The present study aimed at investigating whether X-ray repair cross complementing protein 3 (XRCC3) genotype may serve as a useful marker for detecting leiomyoma and predicting risk.A total of 640 women (166 patients with leiomyoma and 474 healthy controls) were examined for their XRCC3 rs1799794, rs45603942, rs861530, rs3212057, rs1799796, rs861539, rs28903081 genotype. The distributions of genotypic and allelic frequencies between the two groups were compared.The results showed that the CT and TT genotypes of XRCC3 rs861539 were associated with increased leiomyoma risk (odds ratio=2.19, 95% confidence interval=1.23-3.90; odds ratio=3.72, 95% confidence interval=1.23-11.26, respectively). On allelic frequency analysis, we found a significant difference in the distribution of the T allelic frequency of the XRCC3 rs861539 (p=5.88 × 10(-5)). None of the other six single nucleotide polymorphisms were associated with altered leiomyoma susceptibility.The T allele (CT and TT genotypes) of XRCC3 rs861539 contributes to increased risk of leiomyoma among Taiwanese women and may serve as a early detection and predictive marker.

Reliable biomarkers are in urgent need for diagnosis, outcome prediction and treatment-effect monitoring for upper tract urothelial carcinomas (UTUC). Although up-regulation of cyclo-oxygenase 2 (COX2) is found in stroma and tumor cells in more than half of the patients with UTUC investigated, the genomic contribution of COX2 to UTUC has not been studied. The study aimed to evaluate the association of six polymorphic genotypes of COX2 with UTUC within a Taiwanese population.A total of 218 patients with UTUC and 580 healthy controls were genotyped for six COX2 polymorphisms, namely A-1195G, G-765C, T+8473C, intron 1, intron 5 and intron 6, and examined for their association with UTUC risk.The distribution of genotypes of COX2 G-765C and intron 5 were significantly different between patient and control groups (p=0.0001 and 0.0016, respectively), while others were not (p0.05). The haplotype analysis showed that compared to the GG/TT haplotype of COX2 G-765C/intron 5, those carrying GG/AT variants have a significantly increased risk of UTUC (odds ratio=4.83, 95% confidence interval=1.79-13.06), while those carrying CG/TT variants have a decreased risk (odds ratio=0.26, 95% confidence interval=0.14-0.49).Our results suggest that individual and combined COX2 G-765C/intron 5 genotypes play a role in controlling COX2 expression and UTUC development.

Renal cell carcinoma (RCC) accounts for about 3% of all cancer-related mortalities worldwide and the risk factors for the development of RCC have not yet been fully elucidated. Mounting evidence shows that overexpression of cyclo-oxygenase 2 (COX2) is commonly found in malignant tumors, including RCC. However, the contribution of genotypic variations of COX2 to RCC has not been studied. We hypothesized that variants of the COX2 gene are associated with risk of susceptibility to RCC in Taiwan. In this hospital-based case-control study, 92 patients with RCC and 580 age- and gender-matched cancer-free controls were recruited and the associations of COX2 A-1195G, G-765C, T+8473C, intron 1, intron 5, and intron 6 polymorphisms with RCC risk were examined in this Taiwanese population. The results showed that compared to the wild-type GG genotype, the CG genotype for COX2 G-765C was significantly associated with a lower risk of RCC (odds ratio=0.34, 95% confidence interval=0.15-0.80, p=0.0082). For other polymorphic sites, no obvious associations were found. There was also an obvious association of COX2 G765C genotype with reduced RCC risk among those without family cancer history (p=0.0331). These evidence indicated that COX2 G-765C genotype involved in the etiology of RCC and may serve as a novel genetic marker for susceptibility of RCC.

Gastric cancer is one of the most common malignant tumors worldwide. Due to the complex initiation and intricate progression mechanisms, early detection and effective treatment of gastric cancer are both difficult to achieve. The genetic polymorphisms encoding critical protein cyclin D1 (CCND1) to regulate cell cycle transition from G1 phase to S phase may determine the susceptibility of individuals to gastric cancer. The study aimed to examine the contribution of CCND1 genotypes to gastric cancer risk in Taiwan.The genotypes of CCND1 A870G (rs9344) and G1722C (rs678653) were determined by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis among 358 gastric patients and 358 cancer-free controls, and the distribution of genotypic and allelic frequencies among the two groups were compared.The results showed that there were significant differences between gastric cancer and control groups in the distribution of the genotypes (p=6.86×10(-4)) and allelic frequency (p=0.0016) in the CCND1 A870G genotype. In addition, individuals who carried the AG or GG genotype had 0.55- and 0.51-fold of odds ratios of developing gastric cancer compared to those who carried the AA genotype (95% confidence intervals [CI]=0.39-0.76 and 0.32-0.81, respectively). There was no such association of CCND1 G1722C with gastric cancer. Furthermore, there was an obvious interaction of the CCND1 A870G genotype with personal smoking habit on gastric cancer risk (p=0.0005).Cell-cycle regulation may play a role in gastric cancer initiation and development and the CCND1 A870G genotype maybe a useful biomarker for detection of early gastric cancer.

Gastric cancer is the second cause of death from cancer worldwide and its prevalence and mortality rates are still very high in developed countries. Interleukin-10 (IL10) is a pleiotropic cytokine produced by macrophages which can suppress and stimulate the immune response in tumorigenesis signaling. However, the contribution of IL10 genomic variants to gastric cancer is still largely unknown. In the present study, we aimed at investigating the role of IL10 genotypes in gastric cancer risk. The promoter single nucleotide polymorphisms on IL10, A-1082G (rs1800896), T-819C (rs3021097) and A-592C (rs1800872), were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method among 716 Taiwanese people (358 patients gastric cancer and 358 cancer-free controls). The results showed that there was a significant difference between the patient and control groups in the genotypic frequency distribution of IL10 A-1082G genotypes (p=0.0004). In addition, those carrying the G allele were found to have a higher risk for gastric cancer compared with those with the A allele (p=3.19×10(-5)). Furthermore, personal cigarrete smoking habits enhanced the gastric cancer risk for those IL10 A-1082G AG and GG carriers. In conclusion, AG and GG genotype at IL10 A-1082G, together with smoking, synergistically contribute to individual susceptibility for gastric cancer in Taiwan.