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- Sanyal, S, et al.
(författare)
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Polymorphisms in NQO1 and the clinical course of urinary bladder neoplasms
- 2007
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Ingår i: Scandinavian Journal of Urology and Nephrology. - : Informa UK Limited. - 0036-5599 .- 1651-2065. ; 41:3, s. 182-190
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Tidskriftsartikel (refereegranskat)abstract
- Objective. Urinary bladder neoplasms differ considerably in biological potential, and tumor morphology alone cannot predict their clinical behaviors. Polymorphisms in xenobiotic metabolic genes reportedly modulate susceptibility to bladder neoplasms and may affect the clinical course and outcomes of the disease. This study was conducted to determine the effect of polymorphisms in the xenobiotic metabolic genes on the disease course and clinical outcomes of urinary bladder neoplasms. Material and methods. Patients with urinary bladder neoplasms who had been followed up for a 5-year period were genotyped for NQO1 (R139W, P187S), NAT (rapid/slow), GSTP1 (I105V), GSTT1 and GSTM1 (non-null/null) and MTHFR (A222V, E429A) polymorphisms. Results. Variant allele carriers of the NQO1 (P187S) polymorphism showed a higher risk for high-stage disease than non-carriers at diagnosis [relative risk (RR)=1.4; 95% CI 1.0-1.8). A higher risk for highly malignant disease (T2+) was also observed in variant allele carriers than non-carriers of the GSTP1 (I105V) polymorphism (RR=1.6; 95% CI 1.1-2.5). NQO1 (R139W) variant allele carrier patients with intermediate malignant disease (TaG3+T1) had shorter disease-free survival than non-carriers (p=0.05). In contrast, carriers of the variant allele for the MTHFR (A222V) polymorphism had significantly longer disease-free survival than non-carriers (p=0.02). Conclusions. Our data are consistent with the notion that NQO1 polymorphisms influence the course and clinical outcomes of urinary bladder neoplasms. However, our results need to be confirmed in a large study as most of the associations detected were only of marginal statistical significance, and would be lost on correction for multiple comparisons.
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- Adermark, Louise, 1974, et al.
(författare)
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Prospective association between use of electronic cigarettes and use of conventional cigarettes: a systematic review and meta-analysis
- 2021
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Ingår i: Erj Open Research. - Sheffield : European Respiratory Society (ERS). - 2312-0541. ; 7:3
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Tidskriftsartikel (refereegranskat)abstract
- Objective The aim of this systematic review and meta-analysis was to assess the association between e-cigarette use and subsequent initiation or recurrence of cigarette smoking. Data sources A systematic literature search was finalised on 11 November 2019 using PubMed (including MEDLINE), EMBASE, Cochrane Library, Scopus, PubMed Health, NICE Evidence Search, PROSPERO, CRD and PsycInfo. Study selection Studies were included if meeting the following criteria: reporting empirical results; longitudinal observational design with a minimum of 3 months of follow-up; including general population samples; allowing for the comparison between users and nonusers of e-cigarettes. Studies rated as having high risk of bias were excluded. Studies were independently assessed by at least two authors. The procedures described by PRISMA were followed, and the quality of evidence was rated using GRADE. Data synthesis 30 longitudinal studies from 22 different cohorts assessing e-cigarette use among nonsmokers or never-smokers at baseline, and subsequent use of cigarette smoking at follow-up, were included in this review. A random-effects meta-analysis based on 89076 participants showed a pooled unadjusted odds ratio (OR) of cigarette smoking among baseline nonsmoker e-cigarette users compared with nonusers of 4.68 (CI 3.64-6.02), while the adjusted OR was 3.37 (CI 2.68-4.24). These results were consistent irrespective of whether the outcome was measured as ever-smoking or as past 30-day smoking. The evidence was graded as moderate. Conclusions Use of e-cigarettes may predict the initiation or recurrence of cigarette smoking.
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- Ryk, C., et al.
(författare)
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Influence of GSTM1, GSTT1, GSTP1 and NAT2 genotypes on the p53 mutational spectrum in bladder tumours
- 2005
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Ingår i: Int J Cancer. - 0020-7136. ; 113:5, s. 761-8
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Tidskriftsartikel (refereegranskat)abstract
- Genetic polymorphisms affecting expression or activity of the corresponding enzymes can influence the risk of acquiring gene mutations and various cancers. We have studied 327 bladder cancer patients with regard to the functionally related polymorphisms of GSTM1, GSTT1, GSTP1 and NAT2 and analysed the p53 mutational status of their tumours. Fifty p53 mutations, 26% transversions and 74% transitions, were detected in 44 patients. P53 mutation frequency was significantly higher in higher-grade tumours than in low-grade tumours (OR = 2.09, 95% CI 1.44-3.02, adjusted for age and sex). Also, a significant association was found between tumour stage (Tis and T2+ vs. Ta and T1) and presence of the GSTP1 val allele (adjusted OR = 2.00, CI 1.14-3.52). Overall, there was no significant difference in frequency of p53 mutation among patients with different genotypes. Among patients with p53 mutation, transversions were significantly more frequent in GSTM1-negative as compared to GSTM1-positive individuals (OR = 5.18, CI 1.07-25.02, adjusted for age, sex and tumour stage). With one exception, all tumours with the most common type of transversion, G:C-C:G, occurred in GSTM1-negative patients. Among smokers, all transversions (3 of 3), but only 2 of 13 transitions, were found among carriers of the GSTP1 variant allele, and samples carrying at least 1 variant GSTP1 allele had more transitions at CpG sites than wild-type samples (adjusted OR = 4.61, CI 0.82-26.04). No significant associations were found for the NAT2 gene. Our results suggest that impaired glutathione conjugation may affect the mutation spectrum in critical target genes.
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- Ryk, C., et al.
(författare)
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Influence of polymorphism in DNA repair and defence genes on p53 mutations in bladder tumours
- 2006
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Ingår i: Cancer Lett. - : Elsevier BV. - 0304-3835 .- 1872-7980. ; 241:1, s. 142-9
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Tidskriftsartikel (refereegranskat)abstract
- We studied the effects of polymorphisms in nine genes involved in DNA repair and detoxification on occurrence and type of p53 mutation in 327 bladder cancer patients. The included polymorphisms are XPC(Lys939Gln), XPD(Lys751Gln), XPG(Asp1104His), XRCC1(Arg3999Gln), XRCC3(Thr241Met), NBS1(Glu185Gln), cyclin D1(Pro241Pro), MTHFR(Ala222Val and Glu429Ala) and NQO1(Arg139Trp and Pro187Ser). We found increased risk for p53 mutation among cyclin D1 variant allele homozygotes (OR 2.4 CI 0.8-6.7). Among non-smokers, 75% (3/4) with p53 mutation but only 12.5% (3/24) without p53 mutations were XRCC3 241Met homozygotes (P=0.03). Among smokers, all p53 transversions (3/3), but only 41.7% (5/12) of p53 transitions were found among carriers of the XPC 939Gln allele. Individuals carrying the NQO1 187Ser allele showed increased risk for p53 transversions (OR 4.7, CI 0.9-26.1). All (2/2) NQO1 139Trp allele carriers but only 17.5% (7/40) of the Arg139 homozygotes had p53 transversions. Our findings suggest that altered repair and detoxification due to genetic polymorphism may influence the occurrence of p53 mutations in bladder cancer.
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- Ryk, C., et al.
(författare)
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The (CCTTT)n microsatellite polymorphism in the NOS2 gene may influence lung cancer risk and long-term survival, especially in non-smokers
- 2014
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Ingår i: Tumor Biology. - : Kluwer Academic Publishers. - 1010-4283 .- 1423-0380. ; 35:5, s. 4425-4434
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Tidskriftsartikel (refereegranskat)abstract
- We analyzed the associations of the NOS2 (CCTTT)n promoter polymorphism to lung cancer risk and tumor histology in smokers and non-smokers. We also investigated lung cancer long-term survival in relation to the polymorphism, smoking data, histology, age at diagnosis, and gender. One hundred eighty-five lung-cancer patients and 164 matched controls, where non-smokers were enriched among the lung cancer cases, were genotyped by fragment analysis and sequencing. Genotypes were combined with information on histology, patient smoking status, and cancer-specific death, using a 20-year follow-up. We divided the (CCTTT)n alleles into short (n≤10), intermediate (n=11-12), and long (n≥13). Patients homozygous for short repeats had significantly increased risk of lung cancer (p=0.030) compared to carriers of two long alleles (LL). Lack of long allele was associated with a significantly increased lung cancer risk overall (p=0.011), especially among non-smokers (p=0.001). A significantly higher lung cancer survival was seen in non-smokers compared to smokers (p=0.046) and in low-dose smokers compared to high-dose smokers at the time of diagnosis (p=0.028). Moreover, non-smoking patients with squamous cell carcinoma (p=0.015) or adenocarcinoma (p=0.024) showed a significantly lower survival compared to other lung carcinomas. Nitric oxide can induce proliferation as well as apoptosis depending on cellular context. Our results suggest that the (CCTTT)n NOS2 microsatellite may influence the risk of developing lung cancer, especially in non-smokers, possibly by affecting intracellular nitric oxide levels. Our results also give additional information about the yet poorly understood etiological and prognostic differences between lung cancer in non-smokers and smokers. © International Society of Oncology and BioMarkers (ISOBM) 2014.
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