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PubMed2004

TNF/LTA polymorphisms and risk for gastric cancer/duodenal ulcer in the Korean population.

The tumor necrosis factor-alpha (TNF) and lymphotoxin-alpha (LTA) are proinflammatory cytokines with immunoregulatory effects. TNF is also known to inhibit gastric acid secretion. Previously we have shown that the known proinflammatory genotypes, IL-1B -31C/+ and IL-1RN *2/*2, were not associated with increased risks for gastric cancer/duodenal ulcer in the Korean population. In this study, we tested the association between the polymorphisms of another candidate cytokine TNF/LTA and 341 gastric cancers, 133 duodenal ulcers, and 261 healthy controls. Five TNF promoter polymorphisms (-1031, -863, -857, -308, and -238) and two LTA polymorphisms (intron 1 and Thr26Asn) were analyzed. Individual polymorphisms were not associated with the gastric cancer and/or duodenal ulcer risk. When a haplotype analysis was performed with seven polymorphisms, differences in haplotype profile between the controls and gastric cancer and/or duodenal ulcer were not statistically significant. However, the frequencies of individual haplotypes C and D, which had opposite alleles at -1031, -863, and -857, showed statistically significant differences between the gastric cancer and duodenal ulcer (P=0.005 and P=0.02, respectively), suggesting that the TNF/LTA genotypes might play an opposite role in the pathogenesis of gastric cancer and duodenal ulcer.

Adult↗
PubMed2003

Cationic trypsinogen and pancreatic secretory trypsin inhibitor gene mutations in neonatal hypertrypsinaemia.

Neonatal hypertrypsinaemia with normal sweat chloride detected during CF screening may be related to trypsin activation. We have looked for mutations of the cationic trypsinogen (PRSS1) and pancreatic secretory trypsin inhibitor (PSTI) genes in 50 hypertrypsinaemic neonates with known CFTR genotypes and negative sweat test. No mutations were found in either gene. Two silent polymorphisms were detected in the PRSS1 gene. A polymorphism in the promoter region and an intronic polymorphism of the PSTI gene were found. No difference was observed in the frequency of PRSS1 or PSTI polymorphisms in neonates carrying or not carrying CF mutations. These results do not provide an indication for an increased frequency of mutations in the PRSS1 and PSTI genes in this group of neonates with transient hypertrypsinaemia.

Carrier Proteins↗
PubMed1993

Vb6 T-cell receptor elements in artiodactyls: conservation and germline polymorphisms.

By use of primers specific for human T-cell receptor (Tcr) Vb6 gene elements, a typing system for Tcr Vb variability in several artiodactyl species has been established. The amplified polymorphic locus is homologous to the human Vb6 gene element. Like the human counterpart, the artiodactyl Vb6 element contains a polymorphic intronic simple (gt)n repeat stretch. Extensive length polymorphism of this simple repeat sequence in some artiodactyls should allow efficient association studies in a multiplex approach, especially including MHC class II genes. On the protein level the Vb regions display little variability in the inter-species comparison among artiodactyls. The amino acid substitutions are not concentrated in the putative complementarity determining regions, suggesting evolutionary conservation. In addition, the simple repetitive element has been preserved in the same genomic location for more than 7 x 10(7) years. Similar evolutionary persistence has already been demonstrated for a (gt)n(ga)m repeat stretch in the second intron of the MHC-DRB locus. The reasons for these parallel developments in evolution are so far not clear, but they may point to a biological meaning if not function of the intronic simple repeat element.

Amino Acid Sequence↗
PubMed1998

Genetic analysis of the insulin receptor gene in Chinese patients with extreme insulin resistance.

BACKGROUND: Many patients with extreme insulin resistance in combination with acanthosis nigricans are reported to have defective insulin receptor genes. Because acanthosis nigricans is commonly accompanied by severe hyperinsulinemia and obesity, and obesity is a major factor in insulin resistance, this study was initiated to assess the prevalence of mutations in the insulin receptor gene in Chinese patients with extreme insulin resistance defined by hyperinsulinemia, obesity and acanthosis nigricans. METHODS: Exons 1-22 of the insulin receptor gene were amplified by polymerase chain reaction (PCR) by from genomic DNA from 13 young subjects with clinical and metabolic features of extreme insulin resistance. They were also screened for nucleotide variation using single-strand conformation polymorphism (SSCP) combined with nucleotide sequence analysis. RESULTS: Variant SSCP patterns were detected in exons 1, 3, 6, 11, 12 and 17 of the insulin receptor gene. However, sequencing of amplified DNA fragments revealed that none of the variations were mutations. The SSCP variant in exon 1 was caused by a novel intron polymorphism (G-->T at position 13, 5' intron), while the SSCP variant in exon 12 was caused by a novel silent polymorphism Thr789 (ACG-->ACA). Variants in exons 3 and 17 corresponded to known silent polymorphisms: Gln276 (CAA-->CAG) and His1068 (CAC-->CAT), respectively. Another three variants in exons 3, 6 and 11 were also identified as known polymorphisms in the flanking introns. In addition, two alterations, a silent polymorphism Gly8 (GGA-->GGG) and a polymorphism in the 3' flanking intron (T-->G at position 74), were observed in exon 1 of the insulin receptor gene. CONCLUSIONS: Although the prevalence of insulin receptor gene mutations in this Chinese study population might be underestimated because of the sensitivity of SSCP, these results suggest that mutations at the insulin receptor locus are uncommon in subjects with features of hyperinsulinemia, obesity and acanthosis nigricans.

Adolescent↗
PubMed2006

Porcine APP cDNAs: molecular cloning and characterization, expression analysis, chromosomal localization and SNP analysis.

The human amyloid precursor protein (APP) is the precursor of Abeta, a peptide with the potential to create amyloid plaques in neurons. Mutations in the human APP gene are associated with the familial form of Alzheimer's disease. In addition, differential expression of three alternative pre-mRNA APP splicing variants of 695, 751, and 770 amino acids is linked to the pathogenesis. In this study, two novel transcript variants of porcine APP have been identified, producing isoforms of 695 and 751 amino acids, respectively. These are highly homologous to APP orthologues from other vertebrate species. Expression analyses revealed that the gene is expressed in all 30 examined porcine tissues and in a selected subset of these, differential representation of the three major APP transcript variants was observed. The APP isoform of 770 amino acids clearly predominates in non-neuronal tissues while in porcine cerebellum, the APP isoforms of 695 and 770 amino acids are expressed at equivalent levels. Employing a somatic cell hybrid panel, the APP gene was mapped to porcine chromosome 13 in either the 13q41 or 13q46-q49 region. A large pig population was screened for single nucleotide polymorphisms (SNPs) in APP exon 17 and flanking intron sequences. No missense mutations were detected; however, the allele frequencies of two silent mutations and two intron polymorphisms varied significantly among breeds.

Amino Acid Sequence↗
PubMed1995

Complete subtyping of the HLA-A locus by sequence-specific amplification followed by direct sequencing or single-strand conformation polymorphism analysis.

A variety of reasons related to the HLA class I system has complicated the application of molecular approaches to HLA class I typing. Here we present a PCR-based HLA-A typing strategy considering the sequence variations of the two most polymorphic exons which allows complete subtyping of the HLA-A locus. The method is based on a sequence-specific amplification identifying the serologically defined HLA-A specificities. The PCR products generated by these group-specific primers bear the sequence information necessary for a postamplification specificity step. The primer pairs are located within one exon, either exon 2 or exon 3, which avoids amplification of polymorphic intron sequences allowing subsequent single-strand conformation polymorphism analysis and facilitating direct sequencing. Using this method we investigated 48 cell lines and 153 clinical samples. 23 PCR reactions are performed per individual for the assignment of the serological specificities A1-A80. The reproducibility was 100% in all cell lines and 85 clinical samples typed on two separate occasions. With the exception of 13 out of 231 possible serological combinations all homozygous and heterozygous combinations of A1-A80 can be distinguished by specific amplification patterns. Comparing the PCR based typing results with those of serology in 12% a discrepancy was found. Solid-phase sequencing or SSCP analysis of the group-specific PCR fragments allowed complete subtyping of the HLA-A locus. This strategy can identify all 48 HLA-A alleles based on the sequence variations of the 2nd and 3rd exon. 1128 homozygous and heterozygous allele combinations are possible for the HLA-A locus. Only 4 out of these 1128 allele combinations remained unresolved.

Alleles↗
PubMed2003

Haplotype structure of TP53 locus in Indian population and possible association with head and neck cancer.

It has been proposed that a constellation of three TP53 polymorphisms (intron 3 16 bp duplication, codon 72 BstUI, and intron 6 Nci I RFLP at nt 13494) constitute a haplotype predictive of increased cancer risk. We have estimated the allele frequency of these polymorphisms in three endogamous Indian ethnic populations from three different geographic locations (viz. Iyer from south India, Brahmin from central India and Mahishya from eastern India), as well as in head and neck squamous cell carcinoma (HNSCC) patients, and in ethnically matched normal individuals from the eastern region of India. The genotype distributions and allele frequencies of the three polymorphisms in all but one population, as well as in patients, showed a good fit to Hardy-Weinberg equilibrium. Strong linkage disequilibria were observed between all loci in every population examined, except for the 16bp-Nci I haplotype in the Mahishya population. The Mahishya population differed significantly from the other two populations with respect to differences in allele frequency and haplotype frequency. Although there were no significant differences in genotypic frequency at any of the loci between HNSCC patients and the matched control population, the minor allele frequency of codon 72 and intron 3 16 bp polymorphisms showed significant variation. Variation in overall haplotype frequency between patients and normal individuals was significant (p = 0.036) when two rare haplotypes 2-1-2 and 1-2-1 were combined. The rare haplotype 2-1-2 was found to be modestly over represented in HNSCC patients as compared to normal individuals.

DNA↗
PubMed2005

Association of functional polymorphisms of SLC11A1 with risk of esophageal cancer in the South African Colored population.

Several environmental factors have been implicated in the etiology of esophageal cancer (EC). The purpose of this study was to assess the likelihood that variation in the SLC11A1 gene contributes to EC susceptibility, possibly due to its role in inflammation and iron metabolism. The regions of the gene containing potential functional polymorphisms, including the promoter region and exon 2, were investigated. The study cohort included 105 EC South African Colored patients with squamous cell carcinoma (SCC) and 110 population-matched controls, with South African Colored referring to individuals of mixed ancestry. A significantly decreased frequency of the -237C-->T promoter polymorphism was observed in the patient group with EC compared with the population-matched control group (P < 0.002, chi(2) with Yates's correction=7.87). A statistically significant disease association was also observed with allele 3 of the 5'-(GT)n promoter polymorphism (P < 0.0006, chi(2) with Yates's correction=10.16), but only in the absence of the T-allele at nucleotide position -237 following allelic stratification. Four novel variants were identified in intron 1 (IVS1-28C-->T) and exon 2 (112G-->A, 148delGACCAGCCC, 157insGACCAGCCCAG). The novel intronic polymorphism, IVS1-28C-->T, was also significantly associated with EC (P < 0.05, chi(2) with Yates's correction=2.52). We demonstrate association of genetic variation in both the promoter region and intron 1 of the SLC11A1 gene with EC susceptibility.

Black People↗
PubMed2005

Identification of hippocampus-related candidate genes for Alzheimer's disease.

Alzheimer's disease (AD) is a complex multifactorial disease in which many genetic and environmental factors are involved. We performed an association study using 376 AD patients and 376 control subjects. We studied 35 single nucleotide polymorphisms in 35 genes that were significantly downregulated or upregulated only in the AD hippocampus compared with control and found that 9 single nucleotide polymorphisms were associated with AD. Our data indicated that single nucleotide polymorphisms could highly reflect differences in gene expression. Furthermore, an intronic polymorphism (+9943T/C) in POU2F1 was most significantly associated with AD (p = 0.0007). Our results suggest that POU2F1 is a candidate gene for AD.

Aged↗
PubMed2005

Molecular characterization of histidinemia: identification of four missense mutations in the histidase gene.

Histidinemia (MIM235800) is characterized by elevated histidine in body fluids and decreased urocanic acid in blood and skin and results from histidase (histidine ammonia lyase, EC 4.3.1.3) deficiency. It is the most frequent inborn metabolic error in Japan. Although the original description included mental retardation and speech impairment, neonatal screening programs have identified the majority of histidinemic patients with normal intelligence. Molecular characteristics of histidase in histidinemia have not been determined, and cytogenetically visible deletions of 12q22-24.1 in which histidase gene resides have not been identified in histidinemic patients. In order to investigate whether individuals with this disorder have small deletions, additions, or point mutations in the histidase gene, we screened genomic DNA isolated from 50 histidinemic individuals who were discovered by the neonatal screening program. The methods employed included polymerase chain reaction (PCR) amplification of exons 1-21 of the histidase gene, followed by mutation detection enhancement gel electrophoresis and sequencing of the PCR products displaying heteroduplex bands. Four missense mutations (R322P, P259L, R206T, and R208L), two exonic polymorphisms (T141T c.423A-->T and P259P c.777A-->G), and two intronic polymorphisms (IVS6-5T-->C and IVS9+25A-->G) were identified. The frequencies of each polymorphism estimated either by dot blot allele-specific oligonucleotide hybridization, restriction enzyme digestion, or direct sequencing of the PCR products amplified from 50 unrelated normal individuals were 0.28, 0.30, 0.40, and less than 0.01, respectively. Mutation analysis of one family demonstrated that the patient inherited R322P from the mother and P259L from the father. This report describes the first mutations occurring in the coding region of the histidase structural gene in patients with histidinemia.

Amino Acid Metabolism, Inborn Errors↗
PubMed2005

HLA-DQA1 introns 2 and 3 sequencing: DQA1 sequencing-based typing and characterization of a highly polymorphic microsatellite at intron 3 of DQA1*0505.

DQA1 class II gene encodes the alpha-chain of the human leukocyte antigen (HLA)-DQ heterodimer. Sequencing-based typing (SBT) for HLA genes is the most powerful methodology described. However, most of the SBT procedures reported for HLA class II genes are not able to define complete exon 2 region. For that purpose, we have characterized introns 2 and 3 from most DQA1 alleles to design amplification procedures that were able to obtain complete exon 2 and 3 sequences from DQA1 genes. This coding information allowed us to reduce the number of ambiguities for DQA1 typing. DQA1 intron 2 and 3 characterization demonstrated the presence of two polymorphisms for alleles with the same exons 2 and 3 sequence from DQA1*05 group. Different samples including the DQA1*050101 alleles showed a single nucleotide polymorphism at position 53 of intron 2 (G53T). Additional haplotypic analysis showed the possible association of T53 allele with the Ax-Cw5-B18-DR17-DQ2 extended haplotype. On the other hand, DQA1*0505 sequencing from different control samples noticed the existence of a microsatellite (TTTC/AAAG)n located at position 126 of intron 3. Fragment length analysis demonstrated a high polymorphism for this short tandem repeat system (0505STR), defining alleles that ranged from 8 to 20 repetitions in our population.

Base Sequence↗
PubMed1997

Presenilin-1 polymorphism in Alzheimer's disease and vascular dementia.

Recent reports suggest an association between an intronic polymorphism at the 3' position of exon 8 of the presenilin-1 (PS-1) gene and late-onset Alzheimer's disease (AD), but little is known about its role in the pathogenesis of AD. By genotyping 193 Japanese patients with vascular dementia or AD, and 186 elderly control subjects, we have shown no association between vascular dementia and this PS-1 polymorphism, though PS-1 genotype 1/1 and allele 1 frequencies were both significantly higher among patients with AD than among controls. These results argue for a specific role of PS-1 allele 1 in the pathogenesis of AD, rather than suggesting a broader role for this allele as, for example, in vascular dementia.

Age of Onset↗
PubMed2001

A single nucleotide polymorphism in the 3'untranslated region of the CDKN2A gene is common in sporadic primary melanomas but mutations in the CDKN2B, CDKN2C, CDK4 and p53 genes are rare.

In this report we present the results of mutational analysis of the CDKN2B, CDKN2C, CDK4, p53 genes and 5'UTR of the CDKN2A gene in a set of 44 sporadic primary melanomas, which had been earlier analysed for mutations in the CDKN2A (p16/p14(ARF)) gene. No tumour-associated mutations were detected except in 1 melanoma where we found a CC>T* deletion-mutation in the codon 151-152 (exon 5) of the p53 gene. On the basis of our preliminary results, we did extended genotyping of the 500 C>G and 540 C>T polymorphisms in the 3'UTR of the CDKN2A gene in 229 melanoma cases and 235 controls. The T-allele frequency (for 540 C>T polymorphism) in melanomas was significantly higher than in controls (0.14 vs. 0.08; chi(2) = 5.95, p = 0.01; OR = 1.71, 95%CI = 1.11-2.66). The heterozygote frequency for this polymorphism was 0.26 (59/229) in melanomas compared to 0.13 (30/235) in healthy controls (chi(2) = 11.4; p = 0.0007; OR = 2.34, 95% CI = 1.40-3.92). The frequency of the 500 C>G polymorphism in the 3'UTR in the CDKN2A gene was not significantly higher in melanomas compared to healthy controls. The 500 C>G polymorphism, however, was in linkage disequilibrium with approximately 50 kb apart the C>A intronic polymorphism in the CDKN2B gene (determined in 44 melanomas and 90 controls; Fisher exact test, p<0.0001). Finally, the sequence analysis of genomic DNA isolated from T cell lymphocytes of healthy individuals exhibited that the codon reported as last of exon 2 of the CDKN2C gene is rather the first codon of exon 3.

3' Untranslated Regions↗
PubMed2002

Evaluation of single-nucleotide polymorphisms in CAPN1 for association with meat tenderness in cattle.

Micromolar calcium activated neutral protease (CAPN1) was evaluated as a candidate gene for a quantitative trait locus (QTL) on BTA29 affecting meat tenderness by characterization of nucleotide sequence variation in the gene. Single-nucleotide polymorphisms (SNP) were identified by sequencing all 22 exons and 19 of the 21 introns in two sires (Piedmontese x Angus located at the U.S. Meat Animal Research Center in Clay Center, NE; Jersey x Limousin located at AgResearch in New Zealand) of independent resource populations previously shown to be segregating meat tenderness QTL on BTA29. The majority of the 38 SNP were found in introns or were synonymous substitutions in the coding regions, with two exceptions. Exons 14 and 9 contained SNP that were predicted to alter the protein sequence by the substitution of isoleucine for valine in Domain III of the protein, and alanine for glycine in Domain II of the protein. The resource populations were genotyped for these two SNP in addition to six intronic polymorphisms and two silent substitutions. Analysis of genotypes and shear force values in both populations revealed a difference between paternal CAPN1 alleles in which the allele encoding isoleucine at position 530 and glycine at position 316 associated with decreased meat tenderness (increased shear force values) relative to the allele encoding valine at position 530 and alanine at position 316 (P < 0.05). The association of maternal alleles with meat tenderness phenotypes is consistent with the hypothesis of CAPN1 as the gene underlying the QTL effect in two independent resource populations and presents the possibility of using these markers for selective breeding to reduce the numbers of animals with unfavorable meat tenderness traits.

Alleles↗
PubMed2005

Genetic study of the myelin oligodendrocyte glycoprotein (MOG) gene in schizophrenia.

Schizophrenia (SCZ) is a neuropsychiatric disorder that affects approximately 1% of the general population. The human leukocyte antigen (HLA) system has been implicated in several genetic studies of SCZ. The myelin oligodendrocyte glycoprotein (MOG) gene, which is located close to the HLA region, is considered a candidate for SCZ due to its association with white matter abnormalities and its importance in mediating the complement cascade. Four polymorphisms in the MOG gene (CA)n (TAAA)n, and two intronic polymorphisms, C1334T and C10991T, were investigated for the possibility of association with SCZ using 111 SCZ proband and their families. We examined the transmission of the alleles of each of these polymorphisms with the transmission disequilibrium test. We did not observe significant evidence for biased transmission of alleles at the (CA)n (chi2=2.430, 6 df, P=0.876) (TAAA)n (chi2=3.550, 5 df, P=0.616), C1334T (chi2=0.040, 1 df, P=0.841) and C10991T (chi2=0.154, 1 df, P=0.695) polymorphisms. Overall haplotype analysis using the TRANSMIT program was also not significant (chi2=7.954, 9 df, P=0.539). Furthermore, our results comparing mean age at onset in the genotype groups using the Kruskal-Wallis Test were not significant. Our case-control analyses (182 cases age-, sex- and ethnicity-matched with healthy controls) and combined z-score [(CA)n: z-score=-1.126, P=0.130; (TAAA)n: z-score=-0.233, P=0.408; C1334T: z-score=0.703, P=0.241; C10991T: z-score=0.551, P=0.291] were also not significant. Although our data are negative, the intriguing hypothesis for MOG in SCZ may warrant further investigation of this gene.

Adult↗
PubMed1997

Loss of heterozygosity of the retinoblastoma and p53 genes in primary cervical carcinomas with human papillomavirus infection.

OBJECTIVE: Paired DNA samples from 55 primary uterine cervical carcinomas and normal bloods were studied for chromosomal allelic loss (loss of heterozygosity; LOH) of the retinoblastoma (Rb) and p53 gene loci by polymerase chain reaction (PCR) or PCR-restriction fragment length polymorphism analysis. All the study samples contained at least one of the oncogenic human papillomavirus (HPV) type 16 and/or 18 sequences. And the relationships between allelic losses of these genes and conventional clinicopathological parameters were evaluated. METHODS: In order to detect LOH of the Rb gene in cervical cancers, we analyzed four polymorphic intronic sites (intron 1, 17, 20, and 25) of the Rb gene and one additional microsatellite near the Rb locus (D13S118). For detection of the LOH in p53, three intragenic polymorphisms (exon 1, exon 4, intron 6) and one microsatellite distal to the p53 gene (D17S5) were examined. RESULTS: By analyzing this system, we could increase the heterozygosity of the Rb and p53 loci up to 0.91 and 1, respectively. The observed allelic loss rates of the Rb and p53 loci in informative cases were 14% (7/50) and 5.5% (3/55), respectively. The patients with LOH at the D13S118 locus also had the allelic loss of the Rb gene, whereas only one of the four patients with LOH at the D17S5 locus showed a concomittant allelic loss of the p53 gene. The frequency of cervical cancer with one LOH at the Rb or p53 loci was 20% (11/55). No shifted bands were observed in the PCR-single-strand conformation polymorphism analysis of the p53 gene. The LOH of the Rb or p53 gene was not significantly associated with other parameters including clinical stage, histological type, degree of differentiation, status of HPV infection, and p53 gene mutation. CONCLUSION: Concerning the results above, we conclude that the allelic imbalance of the Rb or p53 gene itself is not implicated as a major contributing factor in the malignant transformation or the tumor progression in HPV-positive uterine cervical cancers.

Adult↗
PubMed2003

Genetic variation in lectin-like oxidized low-density lipoprotein receptor 1 (LOX1) gene and the risk of coronary artery disease.

BACKGROUND: We examined the association of 3 polymorphisms in the lectin-like oxidized LDL receptor-1 (LOX1 or OLR1) gene with coronary artery disease in the Women's Ischemia Syndrome Evaluation (WISE) study population. METHODS AND RESULTS: The WISE sample comprised 589 white and 122 black women who underwent angiography for suspected ischemia. The sample was divided into 3 groups: <20% stenosis (38.7%), 20% to 49% stenosis (24.9%), and >or=50% stenosis (35.3%). The three LOX1 polymorphisms (intron 4/G-->A, intron 5/T-->G, and 3' UTR/T-->C) were in linkage disequilibrium and thus behaved as a single polymorphism. The frequency of the 3'UTR/T allele was significantly higher in whites than blacks (49% versus 19%; P<0.0001). Among white women, the frequency of the 3'UTR/T allele carriers (TC+TT genotypes) increased gradually from 67.9% to 75.0% and 79.2% in the <20%, 20% to 49%, and >or=50% stenosis groups, respectively (chi2 trend=6.23; P=0.013). Logistic regression analyses indicated that APOE (odds ratio, 1.90; P=0.007) and LOX1 (odds ratio, 1.67; P=0.025) genotypes were independently associated with the risk of disease and that there was no interaction between the two genes. The 3'UTR/T allele carriers also had significantly higher IgG anti-oxLDL levels than individuals carrying the CC genotype (0.94+/-0.20 versus 0.86+/-0.16; P=0.032). Furthermore, our electrophoretic mobility shift assay data show that the 3'UTR polymorphic sequence affects the binding of a putative transcription factor in an allele-specific manner. CONCLUSIONS: Our data suggest that common genetic variation in the LOX1 gene may be associated with the risk of coronary artery disease in white women.

3' Untranslated Regions↗