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this study proposes that A/A genotype at position -607 in @GENE$ gene can be used as a new genetic maker in Thai population for predicting @DISEASE$ development.
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Common polymorphisms in the genes @GENE$ and LOC387715 are independently related to @DISEASE$ progression after adjustment for other known AMD risk factors.
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Results do not support any overall association of the Ala-9Val @GENE$ polymorphism to the development of @DISEASE$.
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@GENE$ methylation occurs frequently in human colonic @DISEASE$ and cancers and is closely associated with K-ras mutations.
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In conclusion, @GENE$ 8092C > A polymorphism may modify the associations between cumulative cigarette smoking and @DISEASE$ risk.
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Allele A in @GENE$ gene +252 site can significantly increase the relative risk of @DISEASE$ in women in Guangdong, among which TNF-beta AA genotype might be one of the genetic susceptible factors for endometriosis.
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Our data indicate that the -160 single nucleotide polymorphism in @GENE$ is a low-penetrant @DISEASE$ susceptibility gene that might explain a proportion of familial and notably hereditary prostate cancer.
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These results suggest that the @GENE$/-159 polymorphism is an important marker for the @DISEASE$ of IgAN and may modulate the level of the inflammatory responses.
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there is no evidence for an association of @GENE$ alleles with @DISEASE$ in our study groups.
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The association between the @GENE$ G allele and early RA is largely explained by individuals with @DISEASE$ who have coexisting autoimmune endocrinopathies.
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The results suggest that the presence of alleles @GENE$*0104, DRB1*07/06, HCMV sequences and the fetal inheritance of maternal G*0104, should be considered as conditioning factors for the development of @DISEASE$.
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These results suggest that the @GENE$ -93G-->A polymorphism could be used as a marker of genetic susceptibility to @DISEASE$ of the lung.
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In patients with @DISEASE$, the possession of the 298Asp and -786C variants of the @GENE$ gene are a risk factor for coronary in-stent restenosis, demonstrating the importance of the nitric oxide system in restenosis.
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We conclude that the @GENE$ and AGT polymorphisms do not contribute to the genetic susceptibility to @DISEASE$ and retinopathy in a caucasian Mediterranean population.
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There are no statistically significant differences in the frequencies of the Rad52 mutations between the control group and sporadic @DISEASE$ patients and between the control groups and familial breast/ovarian cancer patients, indicating that these two mutations of the @GENE$ do not play a major role in the initiation of sporadic ovarian carcinoma and familial breast/ovarian cancer.
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These results implicate @GENE$ in susceptibility to Crohn's disease, and suggest a link between an @DISEASE$ to bacterial components and development of disease.
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Thus, our analyses of the genetic variations of the @GENE$ gene suggest that, at least in French Caucasians, they do not represent a major cause of @DISEASE$.
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Variants in the regulatory region shared by PARK2 and @GENE$ therefore act as common risk factors for @DISEASE$.
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These results suggested that the @GENE$ gene might be involved in the susceptibility to RA in the Chinese Han population and both +49 and CT60 of CTLA-4 gene might be the causal variants in @DISEASE$ disease.
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A large @DISEASE$ of exons 9 and 10 of @GENE$ confers an increased risk of prostate cancer in Polish men.
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By analysis of a large number of subjects and a more specific patient selection, we showed the first genetic evidence that @GENE$ C677T, MS A2756G and MTRR A66G genotypes were independently associated with @DISEASE$.
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Our findings argue against an association between @GENE$ polymorphism and @DISEASE$ and support the hypothesis for a different pathogenesis of GH in respect to EH.
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No evidence was obtained that the studied polymorphism in @GENE$ is a determinant of the coumarin-associated @DISEASE$.
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These findings, coupled with similar findings in Utah Caucasians, suggest that sequence variation in @GENE$ may influence risk of @DISEASE$.
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The CD154 3'@GENE$ microsatellite is associated with @DISEASE$, and the most represented alleles in patients were accompanied by a more prolonged protein expression in activated lymphocytes from controls.
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These data suggest that CYP1A1*4, NAT1 and @GENE$ variants are involved in the susceptibility to @DISEASE$ by modifying the impact of exogenous and/or endogenous exposures.
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We conclude that the human @GENE$ gene is rather involved in the development of @DISEASE$ and changes in total IgE levels than contributing to the pathogenesis of asthma.
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The prevalence of the Arg allele of the Trp64Arg polymorphism in the @GENE$-adrenergic receptor gene may contribute to the susceptibility to @DISEASE$ among obese/overweight individuals.
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Together, our findings suggest that @GENE$ gene polymorphisms do not influence the susceptibility to MS or the clinical characteristics of @DISEASE$ in Japanese patients.
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The results do not provide evidence that the @GENE$ gene is involved in biological vulnerability to @DISEASE$.
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Our results indicate that the intron 2 CYP46 C/C genotype may predispose to @DISEASE$, and this association is independent of the @GENE$ genotype.
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Abnormal @GENE$ gene copy numbers are a genetic risk factor in @DISEASE$.
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We conclude that the effect of the -308G > A polymorphism on the development of @DISEASE$ is, if any, weak and the majority of Japanese schizophrenics are unrelated to the -308G > A polymorphism of the @GENE$ gene.
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These data did not provide evidence for a contribution of the 102T/C SNP of @GENE$ gene to susceptibility to the southern Han Chinese @DISEASE$.
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Our findings show that the probability of having the @GENE$ 1083TT genotype decreases as habitual caffeine @DISEASE$ increases.
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In conclusion, our data suggest that genetic variation in the @GENE$ gene may have a @DISEASE$ effect on visceral and sc visfatin mRNA expression profiles but does not play a major role in the development of obesity or T2DM.
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These data strongly suggest that @GENE$ is not a significant susceptibility allele for @DISEASE$.
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Combined with staging, direct monitoring of @GENE$ @DISEASE$ improves prognostic accuracy for colorectal cancer.
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This study provides further evidence to support the role of @GENE$ in the pathogenesis of @DISEASE$, and indicates that the MMP9 C-1562T functional polymorphism may represent a genetic component contributing to susceptibility to this vascular disease.
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As DKK family members have previously been found to show altered expression in @DISEASE$ brain and to bind to neuregulin, this finding suggests that @GENE$ may play a role in schizophrenia pathogenesis.
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The presence of 894T allele on @GENE$ gene is associated with @DISEASE$ endothelial function and higher levels of von Willebrand factor in relatively young patients with myocardial infarction.
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These results do not suggest that @GENE$ or PsPRODH contribute to the aetiology of @DISEASE$, and that the putative schizophrenia susceptibility gene in 22q11 remains unknown.
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mtDNA @GENE$ is a rapid and reliable high-throughput method for mutations detection, and T3 394C @DISEASE$ in ND1 gene might contribute to the pathogenesis of mitochondrial diabetes.
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The prothrombotic Pl(@GENE$) allele of platelet fibrinogen receptor GPIIb/IIIa increased the risk of @DISEASE$ in RCC in men.
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The majority of the Colombian @DISEASE$ cases, predominantly late-onset, were negative for PSEN and @GENE$ mutations.
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The interaction of @GENE$ and ADD3 gene variants in humans is statistically associated with variation in @DISEASE$ pressure, suggesting the presence of epistatic effects among these loci.
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The observed association suggests that individuals with @GENE$-251TT and interleukin-10-819TT, a combination presumably causing mild inflammation, have a higher probability of the continuing @DISEASE$, especially among current smokers.
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Sequence variation in @GENE$ is not the major cause of radiotherapy @DISEASE$ in women with breast cancer.
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The @GENE$ gene significantly influences the risk of @DISEASE$ but not endometriosis.
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Our results indicate that common variants in the @GENE$, CHEK2 or ERBB2 genes are not involved in modifying breast cancer survival or the risk of tumour-characteristic-defined @DISEASE$.
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Although a possible interaction between @GENE$ gene C/T polymorphism and SP-1 transcription factor has been reported in the literature, we did not find any evidence for this the difference among clinical staging, pathological grading, or responsiveness to hormonal therapy in @DISEASE$.
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The @GENE$ gene 5 bp D/I within 3'-UTR polymorphism taking on genetic variation among the different races of mankind may not play a critical role in the development of @DISEASE$ in Chinese Hans of Hefei region in Anhui province.
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Our results suggest that @GENE$ *1/*1 and NAT2 @DISEASE$ genotypes might modulate the effect of carcinogenic arylamines contained in tobacco smoke, and that the modulation of NAT2 intermediate and slow acetylator genotype has a tendency to present a higher risk for highly differentiated tumors among heavy-smokers.
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Systematic screening of 431 @DISEASE$ children and adults for mutations in the coding sequence and the minimal core promoter of @GENE$ reveals that genetic variation in the transcriptionally essential region of the MC4R promoter is not a significant cause of severe obesity in humans.
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This study, together with an in vitro functional study, suggests that the @GENE$ gene is an important susceptibility locus for @DISEASE$ on chromosome11q13.
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These results provide strong evidence for pathogenic variant(s) in the 276-kb region harboring @GENE$ that influence intermediate @DISEASE$ phenotypes and risk for AD.
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we identified @GENE$ to be associated with an increased risk for @DISEASE$, which was modified by smoking.
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Patients with @DISEASE$ and @GENE$ exon 19 deletions have a longer survival following treatment with gefitinib or erlotinib compared with those with the L858R mutation.
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These results warrant prolonged medical surveillance and may indicate a clinically important interaction between @GENE$ heterozygosity and radiation in the development of @DISEASE$.
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Presence of the @GENE$ gene promoter polymorphisms was found to be a negative prognostic parameter in patients with @DISEASE$.
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To summarize, alterations of the @GENE$ gene do not lead to clinically relevant @DISEASE$ predisposition and are therefore most unlikely to contribute to familial ovarian cancer.
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The @GENE$ gene may, therefore, be a susceptibility gene in some vitiligo patients, further supporting the epidermal @DISEASE$ model for vitiligo pathogenesis.
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We conclude that the @GENE$ gene Bst U I polymorphism is a suitable genetic marker of @DISEASE$.
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@GENE$ @DISEASE$ genotype is related to endothelium-dependent arterial dilation in the early stage of type 2 diabetes mellitus and in healthy individuals.
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Our findings suggest that @GENE$ may be involved in the pathogenesis of micro- and macrovascular complications in @DISEASE$, and that determination of MBL status might be used to identify patients at increased risk of developing these complications.
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it is likely that @GENE$ gene does not have a major role in diabetes and CHD in our populations, although we can not exclude a minor contribution of the PPARalpha gene to the risk of @DISEASE$ associated with Type 2 diabetes through a modulation of atherogenic plasma lipids.
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We observed no statistically significant interaction between @GENE$ genotype and asbestos exposure for @DISEASE$ risk.
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@GENE$ could be directly involved in protecting critical enzymes or organelles against oxidative damage; PON2 may thus predispose to the development of microvascular @DISEASE$.
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These data suggest that the Ala allele of @GENE$ may modify @DISEASE$ risk among current smokers, but is not an independent risk factor for breast cancer.
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Our results suggest that @GENE$ is one of the genes that contributes to susceptibility to @DISEASE$, and that the association of the TNF/LTA haplotypes to asthma may be defined by the polymorphism in the LTA promoter region in the Japanese population.
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The present investigation provides no evidence that the variable repeat located in the regulatory sequences of the @DISEASE$ gene @GENE$ is associated with the risk of developing POAG or exfoliation glaucoma.
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These results indicate that mutations in NLGN3 and @GENE$ genes are responsible for at most a small fraction of @DISEASE$ cases and additional screenings in other autistic populations are needed to better determine the frequency with which mutations in NLGN3 and NLGN4 occur in autism.
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Our results suggest that inherited variability in DNA repair capacity, as reflected by polymorphisms in @GENE$ and APE1, is a risk factor for @DISEASE$.
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Our findings of an increased risk of systemic sclerosis in @GENE$ D and eNOS 894T allele carriers suggest that these polymorphisms may contribute to the @DISEASE$ of the disease.
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in a large study sample, we were unable to find robust evidence of an association of the Pro129Thr @GENE$ variant with overweight, @DISEASE$, and any related quantitative traits among the examined whites.
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These data suggest that the @GENE$ 469KK genotype could be a genetic risk factor for @DISEASE$ in Type 2 diabetes mellitus.
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Polymorphism of IL-12 @GENE$ gene was not found to be associated with the presence or severity of @DISEASE$, suggesting that it does not play an important role in the development of this disease.
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We conclude that @DISEASE$ polymorphism of @GENE$ gene, as an independent variable, is not associated with reflux nephropathy in children with vesicoureteral reflux.
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A strong interaction between SNP309 status and tumor p53 status appears to modify the association between @GENE$ status and @DISEASE$ survival.
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Our results suggest that H. pylori interacts with @GENE$ and that there are functional allelic differences that affect susceptibility to @DISEASE$.
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the truncating @GENE$ SNP is not important in this group of Th1 dominated granulomatous @DISEASE$.
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Result showed that the @DISEASE$ of the Turkish population seemed to develop without any alterations in @GENE$ Glu298Asp genotype frequency and the serum nitric oxide level.
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These results indicate that gain-of-function variants of T helper @GENE$ 2 cytokine genes may play a role in increasing the severity of RSV @DISEASE$, which appears more pronounced after the first half-year of life.
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The results of our study indicate that atopic diseases are caused, in part, by impairment of the IL-12 signal cascade, which downregulates IgE production, and that the mutation of the @GENE$) chain gene is one of the causative genes for @DISEASE$.
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We conclude that @GENE$ coding sequence mutations are not an important factor in the aetiology of @DISEASE$.
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Our data suggest that polymorphisms of the @GENE$, CCKAR and CCKBR genes do not play a major role in @DISEASE$ symptoms (even though significant associations were found among polymorphisms at the -388 and -333 loci of the CCKAR gene and hallucinations, the rate was nonsignificant after Bonferroni correction).
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Our findings suggest that @GENE$ Cys557Ser is an ancient variant that confers risk of single and multiple primary @DISEASE$, and this risk extends to carriers of the BRCA2 999del5 mutation.
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We did not find significant evidence to support an association of @GENE$ allele 5A or MMP-1 allele 2G with @DISEASE$ in Norwegian and Swedish populations.
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Our findings suggest that the @GENE$ SNP309 may be a risk factor for the occurrence and advanced neck @DISEASE$ of NPC in Chinese population.
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We conclude that polymorphism in the @GENE$ gene may influence @DISEASE$ and tamoxifen treatment response in early-onset breast carcinomas.
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Our data showed that @GENE$ genetic polymorphisms might be useful as prognostic genetic markers for @DISEASE$ in the clinical setting.
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We conclude that this mutation appears to be a frequent @GENE$ gene polymorphism causing no impaired function of the enzyme and no measurable @DISEASE$ in the general population.
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Our results suggest that the +1730 G/A polymorphism of the @GENE$ gene may not be associated with the risk of @DISEASE$ in the Korean population, which was not the case in the Japanese population.
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This @DISEASE$ suggests a role, in at least a group of patients, for the @GENE$ mutation in genetic susceptibility to MS.
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There was no association between @GENE$ alleles and the CagA status of infected individuals, although certain alleles show significant association to the @DISEASE$ status in different populations.
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The 67G allele of @GENE$ may be a contributing factor in the pathogenesis of @DISEASE$.
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Although the mechanism underlying the association is unclear, the findings are of interest because @GENE$ may provide a link between coagulation and @DISEASE$ pressure regulation.
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We conclude that the structure of this @GENE$ promoter region does not have a large impact on the expression of @DISEASE$ characteristics in the present Swedish population.
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The genotype-phenotype analysis showed a significant association (@GENE$.001) between @DISEASE$ and the presence of mutations at codon 694 in exon 10 (both M694V and M694I).
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The @GENE$ polymorphism Tyr402His appears indicative of @DISEASE$ pathogenesis.
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