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The @DISEASE$ of @GENE$ C26304T is related with the susceptibility to radiation injury.
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The promoter polymorphisms of @GENE$, investigated in this study, do not influence the severity of @DISEASE$ outcome by 5 years.
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If confirmed by others, our results indicate that more intensive @DISEASE$ prophylaxis is needed for patients with at least one IL-2 G allele, possibly directed toward blunting early host cell production of @GENE$.
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The de novo origin of an @GENE$ (Arg677ter) mutation in a patient with simplex @DISEASE$ suggests that this common autosomal dominant RP mutation can arise independently in the population and supports the hypothesis of a mutational hotspot in the RP1 gene.
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We identified a polymorphism in the @GENE$ gene associated with @DISEASE$.
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In this large, prospective study, we found little evidence that the two previously described polymorphisms in the CD14 and @GENE$ genes are associated with risks of future @DISEASE$.
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These findings suggest that the @GENE$ polymorphisms may form a genetic susceptibility factor for @DISEASE$ in men.
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This suggests that the VNTR of the 5'-flanking region of the @GENE$ gene influences blood pressure levels in obesity-associated @DISEASE$.
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The Arg3500Gln @DISEASE$ in the apolipoprotein B gene, which is responsible for familial defective @GENE$ and is present in approximately 1 in 1000 persons in Denmark, causes severe hypercholesterolemia and increases the risk of ischemic heart disease.
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The finding of @GENE$ germ-line mutation in all patients with familial @DISEASE$ suggests that genetic screening should be useful in our population to identify affected individuals within a kindred and allow early detection of MEN1-related tumours.
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A broad protective effect of @GENE$ S180L against @DISEASE$ per se is not discernible.
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These findings are consistent with our initial observation for @DISEASE$ and further support the hypothesis that @GENE$ genotype may influence individual susceptibility to the development of certain cancer.
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The @GENE$ 3'UTR microsatellite is associated with @DISEASE$, and the most represented alleles in patients were accompanied by a more prolonged protein expression in activated lymphocytes from controls.
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Although requiring replication in larger samples, these findings provide preliminary evidence that sequence variation in @GENE$ is associated with susceptibility to @DISEASE$, particularly in males.
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These results suggest that @GENE$ may have a role in the repair of 8-OH-dG adducts in prostate tissue and hOGG1 Ser326Cys polymorphism is associated with @DISEASE$ risk.
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our data indicate significant associations between @GENE$ haplotypes and @DISEASE$ risk but do not support a relation between ADIPOR2 variability and the disease.
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The results of our study of Turkish prostate cancer patients suggest that mutation of the @GENE$ gene may be an important risk factor for @DISEASE$.
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although we were unable to support an association between @GENE$ A61G and @DISEASE$, the AA genotype might play a disease-modifying role differentially according to gender.
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VDR overexpression in @DISEASE$ is independently associated with @GENE$ and KRAS mutations.
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@GENE$ polymorphisms apparently play no role in promoting hypertensive renal damage, and do not influence endothelial-mediated @DISEASE$ in never-treated men with essential hypertension.
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These data represent an important negative finding and suggest that, while @GENE$ is implicated in rare Mendelian susceptibility to mycobacterial disease, the common variants studied here do not have a major influence on susceptibility to @DISEASE$ in The Gambian population.
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The polymorphisms of @GENE$, ALDH2, and CYP2E1 were significantly different in Korean patients with @DISEASE$ and Korean control subjects without alcoholism, but ADH3 and OPRM1 did not differ between the two groups.
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We provide evidence that variants of @GENE$, XRCC3, and ERCC4/XPF genes, particularly in combination, contribute to @DISEASE$ susceptibility.
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The polymorphisms of these two loci on the @GENE$) gene are unlikely to contribute to the etiology of @DISEASE$ in the Korean population.
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Our results suggest a potential protective role for @GENE$ in both VaD and @DISEASE$, whereas TNF-alpha may act as a risk factor only for VaD, and not for AD.
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Our results indicate that genetic polymorphisms affecting knee @DISEASE$ vary between populations (Japanese versus Caucasian) and sexes and indicate a role for ASPN, COMP, @GENE$, and COL2A1 in Caucasians.
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There are no statistically significant differences in the frequencies of the Rad52 mutations between the control group and sporadic ovarian cancer patients and between the control groups and familial breast/ovarian cancer patients, indicating that these two mutations of the @GENE$ do not play a major role in the initiation of sporadic @DISEASE$ and familial breast/ovarian cancer.
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An element of the innate immune system (@GENE$) has profound effects upon modulating the acquired allergen-specific immunoglobulin responses among those with an inherited @DISEASE$ predisposition.
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The authors emphasize the usefulness of tau protein level measurement and determination of @GENE$ allele in diagnosis of @DISEASE$.
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The two @GENE$ polymorphisms were found to be associated with all five bone measures (L2L4 and femoral neck DXA as well as heel SOS, BUA and @DISEASE$ index) in the whole sample.
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Our analysis of the entire coding region and three parts of the promoter of the @GENE$ gene failed to show an association between genetic polymorphisms and AAA, suggesting that variations in the MMP2 gene do not contribute to the development of @DISEASE$.
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This @DISEASE$ provides further evidence supporting a role of @GENE$ amplitude reduction as an endophenotype for disinhibited psychopathology.
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Our findings support the hypothesis of the pivotal role of the G glycoprotein @GENE$ pathway in the @DISEASE$ of RSV bronchiolitis and propose CX3CR1 as a potential therapeutic target.
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Chinese individuals >or=50 years of age carrying the AG genotype of NFKBIA may be at an increased risk of developing @DISEASE$, and the GG genotype of @GENE$ may be considered as a prognostic factor for Swedish CRC patients.
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The @GENE$ gene and Hemicentin-1 genes do not appear to be involved in a statistically significant fraction of @DISEASE$ AMD cases in the Japanese population.
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Our findings suggest that the @GENE$ A2 allele is associated with hormone levels, and interacts with insulin levels and diet to affect breast density levels and potentially @DISEASE$ risk.
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In conclusion, we suggest that the @GENE$ genotype of the Gly482Ser polymorphism of the PGC-1 gene should be considered as a risk factor for the development of @DISEASE$ in Caucasians.
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Our findings suggest that interactions between moderate-high meat consumption and the @GENE$ gene A52C polymorphism may increase the risk of @DISEASE$.
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This study suggested that G894T @DISEASE$ in @GENE$ gene might serve as a major risk factor to the pathogenesis of P-CHD in this study population.
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These findings may reflect the interaction of @GENE$ with the underlying genetic and phenotypic complexity that characterizes both @DISEASE$ and normal cognition and brain development.
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The results suggest that the polymorphic alleles of @GENE$ and IL-1Ra studied play little or no part in the susceptibility to @DISEASE$ among these patients with systemic vasculitis.
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The @GENE$-159 SNP might not play a major role in the development of @DISEASE$ in German children.
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The -2849 IL-10 promoter polymorphism is associated with autoantibody production and subsequent joint @GENE$ in @DISEASE$.
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This study suggest that @GENE$-@DISEASE$ polymorphisms may contribute to the risk of pancreatic cancer in our study population.
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These results suggest an association between the @GENE$) C242T polymorphism and vascular aging, which might be mediated by the increase of @DISEASE$.
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Our data suggest that @GENE$ gene polymorphisms may play an important role in the @DISEASE$ of vessel stenosis in Korean population.
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Therefore, @GENE$ is unlikely to play a major role in the @DISEASE$ of PD.
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@GENE$ overexpression in @DISEASE$ is independently associated with PIK3CA and KRAS mutations.
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The results of our study show that @GENE$ is positively associated with the CTLA-4 A/G genotype, similarly to T1DM, thus providing further supporting evidence of the @DISEASE$ origin of this form of diabetes mellitus of the adult.
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Polymorphism of @GENE$ -819C/T SNP site is associated with susceptibility to @DISEASE$ in Chinese Han people; at least five haplotypes of IL-10 gene promoter (ATA, ACC, GCC, ATC and ACA) exist in Chinese Han people.
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These findings indicate that @GENE$ exonic variants may contribute to the risk of @DISEASE$ in the Chinese population, and these variant genotypes may modulate the risk of lung cancer associated with smoking.
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These findings indicate that the promoter polymorphism of @GENE$ is a genetic factor conferring predisposition to @DISEASE$, and that it contributes considerably to disease pathogenesis in patients that were SE negative.
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There is no evidence that mutations in exon 17 of the @GENE$ gene are involved in the @DISEASE$ of human IBD.
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This study suggests that the Asn allele in the @GENE$ gene may be related to a reduced risk of @DISEASE$ among postmenopausal women by increasing their blood SHBG levels.
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allograft TNFbeta and @GENE$ gene polymorphisms may be useful markers to predict the severity of @DISEASE$ recurrence among HCV+ patients after liver transplantation.
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Thus, our study suggested that apo C III is an independent risk factor for atherosclerotic @DISEASE$ in Chinese @GENE$ 2 diabetes.
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C1014T SNP of @GENE$ does not appear to be associated with susceptibility to @DISEASE$ in Japanese patients.
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The @GENE$ -55 C/T polymorphism was associated with a higher atherogenic profile and modified the risk for the development of @DISEASE$.
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We conclude that the two polymorphisms in the @GENE$ gene studied are not a major factor contributing to @DISEASE$ in our population.
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This is the first report that @GENE$, IL8, and PPARG genes are important in relation to @DISEASE$-related risk of sporadic CRC.
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In the present case-control study, we found no evidence of an association between the Glu298Asp variant of the @GENE$ gene and @DISEASE$/MI among Taiwanese.
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@GENE$ genotypes predicted both the severity of baseline @DISEASE$ and relative responsiveness to antipsychotic treatment.
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The present study provides additional evidence that SNPs in the proximal promoter region of the @GENE$ gene contribute to the development of @DISEASE$.
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The results reported in this study suggest that @GENE$ polymorphism is a genetic susceptibility factor involved in the carcinogenesis of @DISEASE$, and also that the analysis of the allelic profile of populations in different geographic locations may help to understand the incidence of cervical cancer worldwide.
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@GENE$ polymorphism T1277C (tyrosine-402 --> histidine-402) is strongly associated with both dry and wet @DISEASE$ and points to a possible role for inflammation in the pathogenesis of AMD.
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In @DISEASE$, the protective effect of @GENE$ wt/Delta 32 is more pronounced in early years of infection and appears to be abrogated by the SDF1-3'A genotype.
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Our data support LBP-1c/CP2/@GENE$ as a candidate gene/risk factor for @DISEASE$ and provide justification for future studies to investigate the role of this gene in Alzheimer's disease.
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These findings indicate that the @GENE$ gene may be a candidate for the genetic regulation of common age-related @DISEASE$ like osteoporosis and spondylosis, and we provide the first evidence suggesting that this gene may be involved in the etiology of human diseases.
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The R121W mutation in @GENE$ is a predisposing factor for the development of @DISEASE$ in Okinawans.
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the APE1 Asp148Glu polymorphism is highly predictive for @DISEASE$, and cumulative cigarette smoking modifies the associations between the @GENE$ Arg399Gln and the XPD Lys751Gln polymorphisms and lung cancer risk.
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These results suggest that @GENE$ Asp148Glu and XRCC1 Arg399Gln polymorphisms might modify the risk of @DISEASE$ attributable to cigarette smoking exposure.
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A frameshifting 2-@GENE$ pair insertion at codon 99 of the RPGR gene produced typical @DISEASE$ and carrier findings (but no tapetallike reflex) in this family.
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Our findings suggest that the @GENE$ gene may be implicated in the susceptibility to spontaneous @DISEASE$ of methamphetamine psychosis and that, as an intracellular adapter protein, PICK1 may play a role in the pathophysiology of methamphetamine psychosis.
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Mutations in the @GENE$ gene do not appear to account for the variability in expression of the common Jewish @DISEASE$ mutation.
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In conclusion, these results suggest that the @GENE$ gene may contribute to the genetic susceptibility to @DISEASE$.
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@GENE$ polymorphism is not a useful marker for predicting the susceptibility or severity to @DISEASE$ for Taiwanese.
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Our results suggest that polymorphisms of the @GENE$ gene may play a role in the pathogenesis of @DISEASE$.
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We conclude that @GENE$ is associated with both the development of @DISEASE$ and ABO incompatibility.
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The current study suggests a possible role of SNPs rather than mutations in @GENE$ in POAG @DISEASE$ in the Indian population.
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the evidence for an association between @GENE$ I1307K and @DISEASE$ is not compelling.
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This study suggests that certain null @GENE$ and GSTT1 genotypes may be associated with an elevated risk of @DISEASE$ which may be modified by interaction of the two genetic polymorphisms and cigarette smoking.
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Our findings are consistent with the notion that genetic variation in the @GENE$ neurotransmitter system contributes to the pathogenesis of @DISEASE$.
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The AA genotype of HMOX1 reduced the incidence of @DISEASE$, possibly due to the high expression level of @GENE$.
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We demonstrated that the @GENE$ Pro185Ala polymorphism contributed to a predisposition to male factor @DISEASE$ in the Estonian population.
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We can speculate that susceptibility to the development of @DISEASE$ could be influenced by the 1704G/T polymorphism of the @GENE$ gene, independently of diabetes.
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Mutations in exon 6 of @GENE$ existed in the patients with FAD and @DISEASE$, and the two missense mutations were probably pathological by nature.
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These findings support the hypothesis that these two @GENE$ variants may contribute to the risk of developing @DISEASE$.
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Together these data implicate that @GENE$ is the first really strong genetic factor identified in a common complex @DISEASE$.
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The @GENE$ gene is likely to be involved in the genetic vulnerability for @DISEASE$.
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Our results confirm the positive association between CHL1 gene and @DISEASE$ and indicate that @GENE$ may be involved in the etiology of schizophrenia.
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Unlike previously reported positive association, in this population, there is no evidence that susceptibility to @DISEASE$ is associated with HLA-@GENE$.
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The results of our study indicate that @DISEASE$ diseases are caused, in part, by impairment of the IL-12 signal cascade, which downregulates IgE production, and that the mutation of the @GENE$) chain gene is one of the causative genes for atopy.
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Our findings suggest that in the H. pylori-infected southern European population, the cagA genotype and the @GENE$(*)0602 gene confer an increased risk for distal @DISEASE$.
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The results indicated that @GENE$ G1649C and SP-A2 A1660G, polymorphisms in the collagen region of SP-A2, might be one of the contributing factors to genetic predisposition and severity of clinical markers of @DISEASE$.
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This large case-control study argues for an only minor-if any-role of the @GENE$ and ECE-1 genotype for the risk of @DISEASE$ development.
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All together, our results show that genome wide patterns of alteration differ between @GENE$ and KRAS @DISEASE$ lung ADC, describe two models of oncogenic cooperation involving either EGFR mutation and CDKN2A deletion or cyclin amplification and TP53 inactiva
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These results suggest that the @GENE$ -463G>A polymorphism does not significantly affect the susceptibility to @DISEASE$ in Koreans.
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Our results highlight the potential protective effect of @GENE$*06 alleles on the course of @DISEASE$.
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These results suggest that the polymorphisms in the @GENE$ gene and the IL-4 receptor alpha chain gene play no role in the development of @DISEASE$ in patients who have normal IgE productivity.
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The @GENE$ polymorphisms associated with rheumatoid arthritis in a Japanese population are not associated per se with @DISEASE$ in a Spanish population.
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