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PubMed2005

Genetic variations in the human gelatinase A (matrix metalloproteinase-2) promoter are not associated with susceptibility to, and severity of, chronic periodontitis.

BACKGROUND: Gelatinase A (matrix metalloproteinase-2 [MMP-2]) has been shown to play an important role in the pathogenesis of several disorders, including periodontal diseases. In this study, we test the hypothesis that variations in this gene influence the development and severity of chronic periodontitis. METHODS: Four promoter polymorphisms (-1575G/A, -1306C/T, -790T/G, and -735C/T) were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods in 149 patients with mild to severe chronic periodontitis and 127 age-matched controls in the Czech population. RESULTS: No significant differences in distribution of the -1575G/A, -1306C/T, and -735C/T variants between periodontitis and control groups were detected in our study. However, a trend to decreased frequency of the -790 GG homozygotes was observed in patients with chronic periodontitis compared to healthy controls (P = 0.036, P (corr) >0.05). Haplotype analysis of four single nucleotide polymorphisms (SNP) in the MMP-2 gene showed no significant association of any haplotype with chronic periodontitis. CONCLUSION: Our findings suggest that polymorphisms in the MMP-2 gene promoter do not contribute significantly to the interindividual periodontitis susceptibility and/or severity in European Caucasians, and they are not regulatory variants in this disease.

Adult↗
PubMed2005

The Autism Genome Project: goals and strategies.

Autism is a complex neurodevelopmental disorder with a broad spectrum of symptoms and varying severity. Currently, no biological diagnosis exists. Although there has been a significant increase in autism genetics research recently, validated susceptibility genes for the most common, sporadic forms of autistic disorder, as well as familial autism, have yet to be identified. The identification of autism-susceptibility genes will not only assist in the identification and/or development of better medications that can help improve the health and neurodevelopment of children with autism, but will also allow for better perinatal diagnosis. The Autism Genome Project (AGP) is a large-scale, collaborative genetics research project initiated by the National Alliance for Autism Research and the National Institutes of Health, and is aimed at sifting through the human genome in search of autism-susceptibility genes. Phase I of the AGP will consist of genome-wide scans utilizing both SNP array and microsatellite technologies. Linkage analysis will subsequently be performed on approximately 1500 pedigrees as will downstream fine-mapping and sequencing of the critical linkage intervals. Ultimately, the vision will be to identify the exact nucleotide variants within genes which give rise to predisposition. The AGP intends to move the field of autism clinical management forward by answering questions about the causal mechanisms underlying the pathophysiology of autism. From this knowledge, therapeutic targets for drug treatments, and ultimately, a newborn screening diagnostic that would allow for early intervention, can begin to be developed.

Autistic Disorder↗
PubMed2006

The ATGL gene is associated with free fatty acids, triglycerides, and type 2 diabetes.

Adipose triglyceride lipase (ATGL) was recently described to predominantly perform the initial step in triglyceride hydrolysis and therefore seems to play a pivotal role in the lipolytic catabolism of stored fat in adipose tissue. In the first study investigating genetic variations within the ATGL gene in humans, 12 polymorphisms identified via sequencing and database search were studied in 2,434 individuals of European ancestry from Utah. These polymorphisms and their haplotypes were analyzed in subjects not taking diabetes medication for association with plasma free fatty acids (FFAs) as primary analysis, as well as triglycerides and glucose as a secondary analysis (n = 1,701, 2,193, or 2,190, respectively). Furthermore, type 2 diabetes (n = 342 of 2,434) was analyzed as an outcome. FFA concentrations were significantly associated with several single nucleotide polymorphisms (SNPs) of ATGL (P values from 0.015 to 0.00003), consistent with additive inheritance. The pattern was similar when considering triglyceride concentrations. Furthermore, two SNPs showed associations with glucose levels (P < 0.00001) and risk of type 2 diabetes (P < 0.05). Haplotype analysis supported and extended the shown SNP association analyses. These results complement previous findings of functional studies in mammals and elucidate a potential role of ATGL in pathways involved in components of the metabolic syndrome.

Adult↗
PubMed2006

Allelic drop-out may occur with a primer binding site polymorphism for the commonly used RFLP assay for the -1131T>C polymorphism of the Apolipoprotein AV gene.

Apolipoprotein AV (ApoAV) gene variant, -1131T>C, is associated with increased triglyceride concentrations in all ethnic groups studied. An MseI based RFLP analysis is the most commonly used method for genotyping this SNP. We genotyped a large cohort comprising 1185 Asian Indians and 173 UK Caucasians for -1131T>C using an ARMS-PCR based tetra-primer method. For quality control, we re-genotyped approximately 10% random samples from this cohort utilizing the MseI RFLP, which showed a 2.9% (3/102) genotyping error rate between the two methods. To investigate further, we sequenced the 900 bp region around the -1131T>C polymorphism in 25 Asian Indians and 15 UK Caucasians and found a number of polymorphisms including the -987C>T polymorphism. Further analysis of the -987C>T SNP showed a higher rare allele frequency of 0.23 in Asian Indians (n = 158) compared to 0.09 in the UK Caucasians (n = 157). This SNP is located 4 bp from the 3' end of the RFLP forward primer and is in weak linkage disequilibrium with -1131T>C variant (r2 = 0.084 and D' = 1). Repeated RFLP analysis of seven subjects heterozygous for -987C>T (seven times), showed discordant results with the sequence at -1131T>C SNP nearly one third (15/49) of the time. We conclude that presence of -987C>T polymorphism in the forward primer of the MseI RFLP assay may lead to allelic drop-out and generate unforeseen errors in genotyping the -1131T>C polymorphism. Our results also emphasise the need for careful quality control in all molecular genetic studies, particularly while transferring genotyping methods between various ethnic groups.

Alleles↗
PubMed2006

Genetic association between COPD and polymorphisms in TNF, ADRB2 and EPHX1.

There is evidence of a hereditary component in chronic obstructive pulmonary disease (COPD). A number of genetic association studies have been performed to find susceptibility genes of COPD. The current authors performed a case-control, genetic-association study and a meta-analysis of 16 studies, involving seven polymorphisms in three well-studied genes: microsomal epoxide hydroxylase (EPHX1); tumour necrosis factor; and beta2-adrenoreceptor. A total of 492 Caucasian smokers and former smokers were recruited from hospital databases and population cohort studies. In the present study, a protective effect of the EPHX1 Tyr113His polymorphism was found (homozygous odds ratio (OR) 0.5). In the meta-analysis, homozygotes for this single nucleotide polymorphism (SNP) also had a pooled OR of 0.5. The same effect has been found in several lung cancer studies. Effects for other candidate SNPs were weak or statistically insignificant, and probable genotyping error was common. In conclusion, the present data and meta-analysis support a role for microsomal epoxide hydroxylase in the aetiology of chronic obstructive pulmonary disease.

Adult↗
PubMed2005

Linkage disequilibrium mapping via cladistic analysis of phase-unknown genotypes and inferred haplotypes in the Genetic Analysis Workshop 14 simulated data.

We recently described a method for linkage disequilibrium (LD) mapping, using cladistic analysis of phased single-nucleotide polymorphism (SNP) haplotypes in a logistic regression framework. However, haplotypes are often not available and cannot be deduced with certainty from the unphased genotypes. One possible two-stage approach is to infer the phase of multilocus genotype data and analyze the resulting haplotypes as if known. Here, haplotypes are inferred using the expectation-maximization (EM) algorithm and the best-guess phase assignment for each individual analyzed. However, inferring haplotypes from phase-unknown data is prone to error and this should be taken into account in the subsequent analysis. An alternative approach is to analyze the phase-unknown multilocus genotypes themselves. Here we present a generalization of the method for phase-known haplotype data to the case of unphased SNP genotypes. Our approach is designed for high-density SNP data, so we opted to analyze the simulated dataset. The marker spacing in the initial screen was too large for our method to be effective, so we used the answers provided to request further data in regions around the disease loci and in null regions. Power to detect the disease loci, accuracy in localizing the true site of the locus, and false-positive error rates are reported for the inferred-haplotype and unphased genotype methods. For this data, analyzing inferred haplotypes outperforms analysis of genotypes. As expected, our results suggest that when there is little or no LD between a disease locus and the flanking region, there will be no chance of detecting it unless the disease variant itself is genotyped.

Chromosome Mapping↗
PubMed2003

Microchip capillary gel electrophoresis with electrochemical detection for the analysis of known SNPs.

A novel microchip-based single nucleotide polymorphism (SNP) screening system has been developed. The system utilizes capillary gel electrophoresis (CGE) with electrochemical detection in a chip-based format to accomplish rapid scoring of a mock SNP site. The accuracy of the thermostable polymerase and the advantages of coupling this technique to microfluidics are demonstrated. An electrochemically labeled chain terminator is used in the single base extension (SBE) reaction, in which the terminator is incorporated only when its Watson-Crick complementary base is present at the mock SNP site. The resulting electrochemically active extension product is subsequently separated from any excess terminator by CGE and detected by sinusoidal voltammetry. Although no attempts at optimization have been made, the analysis is performed in less than 4 min. The technique presented could lead to a fast, simple, and cost effective SNP scoring system.

DNA Primers↗
PubMed2006

Quantitative analysis of chimerism after allogeneic stem cell transplantation by real-time polymerase chain reaction with single nucleotide polymorphisms, standard tandem repeats, and Y-chromosome-specific sequences.

We compared the results of chimerism analyses with real-time SNP-PCR to those obtained by the classical STR-PCR method in 135 hematopoietic stem cell transplantation recipients. Using 10 different SNP gene loci, the SNP-PCR method was able to discriminate patient from donor cells in 125 of 135 cases (93%), whereas the use of 11 different STR gene loci with the STR-PCR analysis using agarose or polyacrylamide gel resolution resulted in accurate donor-host discrimination in all patients. Of the 470 analyzed samples we found in 74% concordant results for both chimerism methods. In all 26% discordant cases the SNP-chimerism method showed mixed chimerism (MC), whereas the STR-method found complete chimerism (CC). As a consequence, the SNP-PCR chimerism analysis method detected a MC prior to the occurrence of relapse significantly earlier than the STR-PCR chimerism method (120 vs. 30 days, P < 0.007). The probability of relapses was significantly higher in patients with increasing MC (70%) compared to 30% in patients with CC (P < 0.00001) associated with a significantly shorter overall survival in patients with increasing MC. The multivariate Cox model showed that chimerism analsis with SNP-PCR was the only significant risk factor predicting relapse (RR 6.08, P < 0.0001).Furthermore, we analyzed the chimerism status in male recipients with a female donor in 580 samples of 134 patients using quantitative real-time PCR of Y-chromosome-specific sequences and compared the results with interphase XY-fluorescent in situ hybridization (FISH). MC without signs of relapse was detected in 35% of samples using quantitative real-time PCR of Y-chromosome-specific sequences. The detected Y-DNA amounts were low compared to the amounts detected in 104 samples of 42 patients with leukemic relapse at the time of analysis (P < 0.0001). Quantitative real-time PCR of Y-chromosome-specific sequences detected therefore an increasing MC with high residual host DNA amounts approximately 143 days (mean) prior to the occurrence of relapse. By comparing the results of Y-chromosome PCR with the XY-FISH analysis we found concordant results in 73% in patients with myeloablative regimens. The XY-FISH could detect 12 relapses, whereas the Y-chromosome PCR detect 36 relapses by MC (P < 0.005). Residual host cells gradually decreased during the posttransplant period from a mean of 5.4 ng (first months) to 0.5 ng (above 5 years) without evidence of relapses. The probability of relapses was significantly higher in patients with increasing MC (100%) compared to 8% in patients with CC (P < 0.00001) associated with a significantly shorter overall survival in patients with increasing MC. The multivariate Cox model showed that chimerism analysis of Y-chromosome-specific sequences is an important risk factor for relapse (RR 17.0, P < 0.0001). We conclude that the use of real-time SNP or Y-PCR may be superior to the STR-PCR or interphase XY-FISH methods in detecting patients who are at high risk for relapse after transplant.

Adolescent↗
PubMedDate not supplied

Cytotoxic effect of sodium nitroprusside on cancer cells: involvement of apoptosis and suppression of c-myc and c-myb proto-oncogene expression.

Nitric oxide (NO) is an unstable free radical gas known as an effector molecule of macrophage cytotoxicity against cancer cells. Although several mechanisms of NO-mediated cytotoxicity have been proposed, this phenomenon remains to be characterized in detail. To explore the mechanisms by which NO kills cancer cells, we made use of sodium nitroprusside (SNP), which releases NO in the culture medium. SNP showed a dose-dependent cytotoxic effect on NA cells, an epithelial cancer cell line. When NA cells were killed by SNP, high levels of NO2- (stable end product of NO) were detected in the culture medium. The cell death induced by SNP was mediated by apoptosis, as demonstrated by the presence of nuclear condensation and blebbing of the nuclear membrane, and internucleosomal DNA fragmentation quantified by a specific ELISA. Northern blot analysis revealed that c-myc mRNA expression of NA cells was rapidly reduced by treatment with SNP. RT-PCR analysis showed that c-myb mRNA was expressed in untreated NA cells, and c-myb mRNA level of NA cells was dose-dependently reduced by treatment with SNP. These results indicate that SNP exerts its cytotoxic effect on NA cells through spontaneous release of NO. Cytotoxicity induced by SNP is at least partially mediated via the process known as apoptosis. Our results also suggest that down-regulation of c-myc and c-myb proto-oncogenes might be involved in SNP-induced cytotoxicity.

Antineoplastic Agents↗
PubMed2006

A scan statistic for identifying chromosomal patterns of SNP association.

We have developed a single nucleotide polymorphism (SNP) association scan statistic that takes into account the complex distribution of the human genome variation in the identification of chromosomal regions with significant SNP associations. This scan statistic has wide applicability for genetic analysis, whether to identify important chromosomal regions associated with common diseases based on whole-genome SNP association studies or to identify disease susceptibility genes based on dense SNP positional candidate studies. To illustrate this method, we analyzed patterns of SNP associations on chromosome 19 in a large cohort study. Among 2,944 SNPs, we found seven regions that contained clusters of significantly associated SNPs. The average width of these regions was 35 kb with a range of 10-72 kb. We compared the scan statistic results to Fisher's product method using a sliding window approach, and detected 22 regions with significant clusters of SNP associations. The average width of these regions was 131 kb with a range of 10.1-615 kb. Given that the distances between SNPs are not taken into consideration in the sliding window approach, it is likely that a large fraction of these regions represents false positives. However, all seven regions detected by the scan statistic were also detected by the sliding window approach. The linkage disequilibrium (LD) patterns within the seven regions were highly variable indicating that the clusters of SNP associations were not due to LD alone. The scan statistic developed here can be used to make gene-based or region-based SNP inferences about disease association.

Chromosome Mapping↗
PubMed2005

Genetic variants in the calpain-10 gene and the development of type 2 diabetes in the Japanese population.

Variation in the gene encoding the cysteine protease calpain-10 has been linked and associated with risk of type 2 diabetes. We have examined the effect of three polymorphisms in the calpain-10 gene (SNP-43, Indel-19, and SNP-63) on the development of type 2 diabetes in the Japanese population in a pooled analysis of 927 patients and 929 controls. We observed that SNP-43, Indel-19, and SNP-63 either individually or as a haplotype were not associated with altered risk of type 2 diabetes with the exception of the rare 111/221 haplogenotype (odds ratio (OR) =3.53, P=0.02). However, stratification based on the median age-at-diagnosis in the pooled study population (<50 and > or =50 years) revealed that allele 2 of Indel-19 and the 121 haplotype were associated with reduced risk in patients with later age-at-diagnosis (age-at-diagnosis > or =50 years OR=0.82 and 0.80, respectively; P=0.04 and 0.02). Thus, variation in the calpain-10 gene may affect risk of type 2 diabetes in Japanese, especially in older individuals.

Adult↗
PubMed2006

High amino acid variation in the intracellular domain of the pig prolactin receptor (PRLR) and its relation to ovulation rate and piglet survival traits.

Two polymorphisms of the porcine prolactin receptor (PRLR) gene were previously related to litter size by several authors; however, the magnitude and direction of such effects varied depending on the population analyzed. We have sequenced the complete coding region of the porcine PRLR gene and found 6 nonconservative SNP: C1217T (Leu/Pro406), C1283A (Asp/Ala428), G1439A (Lys/Arg480), T1528A (Met/Leu510), G1600A (Gly/Ser534), and G1789A (Gly/Ser597), within exon 10 of the gene, which encodes the entire intracytoplasmic domain of the protein. Eight haplotypes were found and were segregating at different frequencies in 6 porcine breeds. The effects of each individual SNP and haplotype were evaluated in an Iberian x Meishan F2 population using a univariate mixed-inheritance animal model. Significant effects on the number of corpora lutea were found for PRLR haplotypes (P < 0.012), confirming the previously reported associations of PRLR in this process and highlighting the importance of performing analysis of haplotypes rather than of individual SNP. Suggestive effects or tendencies were found for heart rate at birth (P < 0.10), rectal temperature (P < 0.05), and oxygen saturation (P < 0.10) 1 h after birth, and time to first suckle (P < 0.10). We found greater than expected levels of amino acid variability within the intracellular domain of the porcine PRLR, which have been associated with differences in the number of corpus lutea of sows and the preweaning survivability of piglets.

Amino Acid Sequence↗
PubMed2005

Genes, age, and alcoholism: analysis of GAW14 data.

A genetic analysis of age of onset of alcoholism was performed on the Collaborative Study on the Genetics of Alcoholism data released for Genetic Analysis Workshop 14. Our study illustrates an application of the log-normal age of onset model in our software Genetic Epidemiology Models (GEMs). The phenotype ALDX1 of alcoholism was studied. The analysis strategy was to first find the markers of the Affymetrix SNP dataset with significant association with age of onset, and then to perform linkage analysis on them. ALDX1 revealed strong evidence of linkage for marker tsc0041591 on chromosome 2 and suggestive linkage for marker tsc0894042 on chromosome 3. The largest separation in mean ages of onset of ALDX1 was 19.76 and 24.41 between male smokers who are carriers of the risk allele of tsc0041591 and the non-carriers, respectively. Hence, male smokers who are carriers of marker tsc0041591 on chromosome 2 have an average onset of ALDX1 almost 5 years earlier than non-carriers.

Age of Onset↗
PubMed2006

Thermodynamic analyses of the specific interaction between two C:C mismatch base pairs and silver (I) cations.

We have already found that a single silver (I) cation specifically binds to a single C:C mismatch base pair in heteroduplex, which increases the melting temperature (T(m)) of heteroduplex involving a single C:C mismatch base pair by about 4 degrees C. Here, to examine the properties of the interaction between two C:C mismatch base pairs and silver (I) cations, we analyzed the effect of silver (I) cations on the thermal stability of heteroduplexes involving two C:C mismatch base pairs. The positions of the two C:C mismatch base pairs in heteroduplex did not significantly affect the magnitude of the increase in T(m) upon addition of silver (I) cation, suggesting that the binding affinity of the first silver (I) cation with one of the two C:C mismatch base pairs and that of the second silver (I) cation with the other of the two mismatch base pairs may be independent of the positions of the two mismatch base pairs. The larger magnitude of the increase in T(m) for the second silver (I) cation binding than that observed for the first silver (I) cation binding suggests that the binding affinity for the second silver (I) cation may be significantly higher than that for the first silver (I) cation. Our results certainly support the idea that addition of the metal cation is a promising strategy for the mismatch base pair detection in the heteroduplex analysis and may eventually lead to progress in SNP genotyping.

Base Pair Mismatch↗
PubMed2005

A novel polymorphism in secretory phospholipase A2-IID is associated with body weight loss in chronic obstructive pulmonary disease.

RATIONALE: Chronic and systemic inflammation, a potential cause of body weight loss in patients with chronic obstructive pulmonary disease (COPD), may be associated with the proinflammatory properties of secretory phospholipases A2 (sPLA2s), especially the group II subfamily sPLA2s. OBJECTIVES: We tested our hypothesis that the individual susceptibility to body weight loss in patients with COPD is attributed to the genetic variances of this sPLA2 gene region. METHODS: A total of 12 single nucleotide polymorphisms (SNPs) encompassing the sPLA2 gene region were determined in 276 male patients with COPD. MEASUREMENTS AND MAIN RESULTS: We first analyzed our patients whose body mass index (BMI) was at the bottom 100 (BMI, 17.13 +/- 1.29 kg/m2) and at the top 100 (23.83 +/- 1.98) in relation to SNPs. Both the Fisher's exact test (odds ratio, 2.36; 95% confidence interval, 1.34-4.18; p = 0.004) and logistic regression analysis (odds ratio, 2.10; 95% confidence interval, 1.13-3.90; p = 0.019) showed statistical significance between one SNP (National Center for Biotechnology Information SNP reference: rs584367) and the reduction of BMI in the recessive model in patients with COPD. Using all the patients, a significant difference between the values of BMI (log transformed) of the mutant group (CT + TT) and that of the nonmutant group (CC) of this SNP (mean [SE], 1.293 [0.005] vs. 1.317 [0.006]; p = 0.003) was found after adjustment for age, smoking habit, and pulmonary function (analysis of covariance). Importantly, this SNP caused a change in amino acids in sPLA2-IID protein (Gly80Ser). CONCLUSIONS: These results suggest that sPLA2-IID may be one of the susceptibility genes that contribute to body weight loss in patients with COPD.

Aged↗
PubMed2006

Association of the NRG1 gene and schizophrenia: a meta-analysis.

We investigated the association of the NRG1 gene and schizophrenia using meta-analytic techniques, combining all published data while restricting our analysis to studies investigating the most commonly reported single marker (SNP8NRG221533). We also investigated whether ancestry (European vs East Asian) and study design (family-based vs case-control) moderated any association. We found no evidence for an association of SNP8NRG221533 with schizophrenia, and significant between-study heterogeneity, which persisted when family-based studies were combined separately. However, when haplotype-based P-values were combined, there was evidence in support of an association of NRG1 with schizophrenia, and no evidence of between-study heterogeneity. Our meta-analysis provides support for the association of NRG1 with schizophrenia, but indicates that firmly establishing the role of NRG1 gene in schizophrenia by genetic association requires much larger sample sizes than have hitherto been reported. Association analyses and replications should take place at the level of the gene, rather than at the level of SNP, haplotype, or functional variant. Meta-analysis would then be carried out on the basis of the combination of P-values.

Asian People↗
PubMed2004

Concurrent analysis of loss of heterozygosity (LOH) and copy number abnormality (CNA) for oral premalignancy progression using the Affymetrix 10K SNP mapping array.

Like most human cancers, oral squamous cell carcinoma (SCC) is characterized by genetic instabilities. In this study, a single platform (Affymetrix 10K SNP mapping array) was used to generate both loss of heterozygosity (LOH) and DNA copy number abnormality (CNA) read-outs for precise and high-resolution genetic alteration profiles. As a proof of principle, we performed this concordant analysis on a panel of deletion and trisomy cell lines with known chromosomal alterations and the precise LOH and CNA regions were detected as expected. Using a previously described oral SCC progression model system, we identified a set of genomic regions that may be associated with the malignancy progression, including chromosome regions 3pter-3p35.3, 3p14.1-3p13, 11p, 11q14.3-11q22.2, and 11q13.5-11q14.1. These data show that it is feasible to utilize high-density SNP arrays to generate concordant LOH and CNA profiles at high resolution.

Carcinoma, Squamous Cell↗
PubMed2006

Candidate lung tumor susceptibility genes identified through whole-genome association analyses in inbred mice.

We performed a whole-genome association analysis of lung tumor susceptibility using dense SNP maps ( approximately 1 SNP per 20 kb) in inbred mice. We reproduced the pulmonary adenoma susceptibility 1 (Pas1) locus identified in previous linkage studies and further narrowed this quantitative trait locus (QTL) to a region of less than 0.5 Mb in which at least two genes, Kras2 (Kirsten rat sarcoma oncogene 2) and Casc1 (cancer susceptibility candidate 1; also known as Las1), are strong candidates. Casc1 knockout mouse tumor bioassays showed that Casc1-deficient mice were susceptible to chemical induction of lung tumors. We also found three more genetic loci for lung adenoma development. Analysis of one of these candidate loci identified a previously uncharacterized gene Lasc1, bearing a nonsynonymous substitution (D102E). We found that the Lasc1 Glu102 allele preferentially promotes lung tumor cell growth. Our findings demonstrate the prospects for using dense SNP maps in laboratory mice to refine previous QTL regions and identify genetic determinants of complex traits.

Adenoma↗