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PubMed1988

Differing amounts of genetic polymorphism in testes and male accessory glands of Drosophila melanogaster and Drosophila simulans.

We surveyed genetic polymorphism by two-dimensional gel electrophoresis of male reproductive tract proteins in 20 isofemale lines each of Drosophila melanogaster and Drosophila simulans. After classifying 244 such proteins of Drosophila melanogaster and 271 of Drosophila simulans by their distribution between testes and accessory glands within the reproductive tract, significant correlations were found between genetic polymorphism and tissue distribution. In both species, gland-specific proteins were significantly more polymorphic than testis-specific proteins, as well as those found in both testes and glands. Simultaneously, in Drosophila simulans, proteins found in roughly equivalent relative abundance in both testes and glands were significantly less variable than gland-specific and testis-specific proteins, as well as those with a quantitative difference in relative abundance between testes and glands. These correlations may reflect general differences in variability between extracellular and intracellular proteins and between proteins with broad as opposed to tissue-specific distributions.

Animals↗
PubMed2003

Genetic polymorphisms in the estrogen receptor alpha gene and risk of breast cancer: results from the Shanghai Breast Cancer Study.

Estrogen receptor (ER) is a ligand-activated transcription factor that mediates estrogen actions in target tissues. Several common polymorphisms of the ER-alpha gene have been reported to be associated with alterations in receptor expression and function. We evaluated the hypothesis that genetic polymorphisms in the ER-alpha gene may be associated with breast cancer risk in a population-based case-control study conducted in urban Shanghai during 1996-1998. Two RFLPs at the ER-alpha gene locus, denoted as PvuII and XbaI, were examined in 1069 breast cancer cases and 1166 age frequency-matched controls. PvuII polymorphism was associated with an increased risk of breast cancer with the age-adjusted odds ratios for genotypes Pp and pp being 1.3 [95% confidence interval (CI), 1.0-1.7) and 1.4 (95% CI, 1.1-1.8), respectively, comparing to genotype PP. The XbaI polymorphism was associated with a nonsignificantly elevated risk. The odds ratios for genotypes Xx and xx were 1.2 (95% CI, 0.7-1.9) and 1.3 (95% CI, 0.8-2.0), respectively, and the elevated risks were mainly confined to older or postmenopausal women. No apparent synergetic effect of these two polymorphisms was identified. Results of this study indicate that genetic polymorphisms in the ER-alpha gene may play a role in the etiology of breast cancer.

Adult↗
PubMed1985

Genetic polymorphism of human factor I (C3b inactivator).

Genetic polymorphism of human factor I (C3b inactivator) has been described using polyacrylamide gel isoelectric focusing electrophoresis of neuraminidase-treated EDTA plasma samples followed by electrophoretic blotting technique. In 435 individuals three different common patterns were observed, and these were controlled by two common alleles at a single locus. The results of typing family material confirmed autosomal codominant Mendelian inheritance. Two common alleles were designated FI*B and FI*A, and gene frequencies were estimated to be 0.8931 and 0.1069 for FI*B and FI*A, respectively. The distribution of phenotypes fitted the Hardy-Weinberg equilibrium. Linkage studies failed to show close linkage between factor I and the major histocompatibility complex.

Complement C3b Inactivator Proteins↗
PubMed2001

Genetic polymorphisms and lipid response to dietary changes in humans.

BACKGROUND: Previous studies on the effects of genetic polymorphisms on the serum cholesterol response to dietary treatments were often inconsistent and frequently involved small numbers of subjects. MATERIALS AND METHODS: We studied the effect of 10 genetic polymorphisms on the responses of serum cholesterol to saturated and trans fat, cholesterol and the coffee diterpene, cafestol, as measured in 26 dietary trials performed over 20 years in 405 mostly normolipidaemic subjects. RESULTS: Apoprotein A4 360-2 allele attenuated the response of low-density lipoprotein cholesterol to dietary cholesterol, but not in women. Subjects with the cholesteryl ester transfer protein TaqIb-1 allele had -0.02 to -0.05 mmol L-1 smaller responses of high-density lipoprotein cholesterol to diet than those with the 2/2 genotype. The effects of the other eight polymorphisms on cholesterol response were either inconsistent with results in previous studies or need to be replicated in other studies. CONCLUSIONS: Apoprotein A4360 and cholesteryl ester transfer protein TaqIb polymorphisms may affect dietary responses. However, no one single genotype was a major determinant of a subject's lipid response to diet. Therefore, knowledge of these genotypes by themselves is of little use in the identification of subjects who may or may not benefit from dietary treatment.

Adolescent↗
PubMed2004

Thiopurine S-methyltransferase genetic polymorphism in the Thai population.

AIMS: To determine the incidence of the thiopurine S-methyltransferase (TPMT) genetic polymorphism in the Thai population. METHODS: Genomic DNAs were isolated from peripheral blood leucocytes of 200 healthy Thais. The frequencies of five allelic variants of the TPMT gene, TPMT*2, *3A, *3B, *3C and *6 were determined using allele specific polymerase chain reaction (PCR) or PCR-Restriction fragment length polymorphism technique. RESULTS: Of the 200 Thai subjects participating in this study, 181 subjects (90.5%) were homozygous for TPMT*1, 18 subjects (9.0%) were heterozygous for TPMT*1/*3C. Only one subject (0.5%) was homozygous for TPMT*3C. The frequency of TPMT*3C mutant allele was 0.050. CONCLUSIONS: Although the TPMT*3C is the most prevalent mutant allele in Asian populations, the frequency of this defective allele is significantly higher in Thais than has been reported in other Asian populations.

Adult↗
PubMed2001

Apolipoprotein E genetic polymorphism and stroke subtypes in a Bangladeshi hospital-based study.

The association between apolipoprotein E (apoE) genetic polymorphism and stroke has not been concordant in different racial populations. We investigated the association between apoE genotypes and stroke subtypes by a case-control study in Bangladesh for the first time among south Asian countries. First-ever-stroke patients (n=227; cerebral infarction, n=147, cerebral hemorrhage, n=80) and 190 controls were recruited from a hospital in Dhaka, Bangladesh. The diagnosis of stroke was based on CT and clinical findings. Cerebral infarction was classified anatomically into cortical and penetrating region. Infarction in the cortical region was further categorized etiologically into thrombosis and embolism. Cerebral hemorrhage was considered as a whole in all analyses. ApoE genotypes were determined by restriction fragment length polymorphism. In the multivariate conditional logistic regression analysis adjusted for potential confounders both the epsilon3/epsilon4 genotype and epsilon4 carrier conferred an approximately 3-fold increased risk for cerebral thrombosis in the cortical artery region (OR 3.5, 95% CI 1.2 to 10.4 and OR 3.1, 95% Cl 1.1 to 9.0, respectively) compared with epsilon3/epsilon3 genotype. However, when the analysis was restricted to the elderly (>60 years), epsilon 2 carrier was associated with a risk of hemorrhagic stroke (OR 19.2, 95% CI 1.3 to 295.2). Our study suggested that both apoE epsilon3/epsilon4 genotype and epsilon4 carriers were risk factors for cerebral thrombosis in cortical artery region, whereas epsilon 2 carrier was a risk factor for hemorrhagic stroke in the elderly.

Aged↗
PubMed1979

Genetic polymorphism in normal human fibroblasts as analyzed by two-dimensional polyacrylamide gel electrophoresis.

Two dimensional gel electrophoresis has been used to measure the degree of genetic polymorphism among the proteins of normal human fibroblasts. Autoradiographic analysis of the gel protein profiles from radioactively labeled cells allowed comparison of as many as 300 discrete polypeptides at a time. In addition, a newly developed technique for double label autoradiography was used to increase the sensitivity of the system for detection of small differences in the protein profiles of different cell lines. Only about 1.2% of the proteins of different cell lines were found to differ in their electrophoretic mobility. This corresponds to an average heterozygosity of approximately 0.6%. Previous studies of genetic polymorphism using different methods of one-dimensional electrophoretic analysis have estimated the average heterozygosity of the human population at about 6.7%. Detailed mathematical analysis shows the variation of the observed from the expected number of differences to be statistically highly significant. While the reasons for this difference are not clear, the observation of low levels of genetic polymorphism on two-dimensional gels should enhance the usefulness of this technique for detection of altered proteins in inherited disease.

Adult↗
PubMed2006

Lack of association between COPD and transforming growth factor-beta1 (TGFB1) genetic polymorphisms in Koreans.

OBJECTIVE: Many genetic variations have been suggested as genetic risk factors for the development of chronic obstructive pulmonary disease (COPD), including single nucleotide polymorphisms in the transforming growth factor-beta1 (TGFB1) gene. We attempted to elucidate the association between TGFB1 genetic polymorphisms and COPD among Koreans. DESIGN: The genotypes of 102 male patients with COPD and 159 volunteers with similar distributions of age, sex and smoking intensity, as well as normal pulmonary function, were determined for three previously associated TGFB1 single nucleotide polymorphisms (SNPs), -10807G/A (rs2241712) and -509T/C (rs1800469), located in or near the promoter, and 29T/C (rs1982073), located in exon 1 of the TGFB1 gene. RESULTS: No significant associations between COPD and the three TGFB1 SNPs could be identified. In addition, the haplotypes composed of three TGFB1 SNPs were not associated with the presence of COPD. CONCLUSION: These results differ from previous reports involving Caucasians, and might reflect racial differences in the pathogenesis of COPD.

Chi-Square Distribution↗
PubMed2005

Assessment of the role of genetic polymorphism in venous thrombosis through artificial neural networks.

PURPOSE: To assess the role of genetic polymorphisms in venous thrombosis events (VTE) using Artificial Neural Networks (ANNs), a model for solving non-linear problems frequently associated with complex biological systems, due to interactions between biological, genetic and environmental factors. METHODS: A database was generated from a case-control study of venous thrombosis, using 238 patients and 211 controls. The database of 64 variables included age, gender and a panel of 62 genetic variants. Three different ANNs were compared, with logistic regression for the accuracy of predicting cases and controls. RESULTS: ANNs yielded a better performance than the logistic regression algorithm. Indeed, through ANNs models, the 62 variables related to genetic variants were first reduced to a set of 9, and then of 3 (MTHFR 677 C/T, FV arg506gln, ICAM1 gly214arg). CONCLUSIONS: The findings of this study illustrate the power of ANN in evaluating multifactorial data, and show that the different sensitivities of the models of elaboration are related to the characteristics of the data. This may contribute to a better understanding of the role played by genetic polymorphisms in VTE, and help to define, if possible, a test panel of genetic variants to estimate an individual's probability of developing the disease.

Adolescent↗
PubMed2004

Genetic polymorphisms of cytochrome P450 enzymes and the effect on interindividual, pharmacokinetic variability in extensive metabolizers.

Genetic polymorphisms of cytochrome P450 (CYP) enzymes are one of the factors that contribute to the pharmacokinetic (PK) variability of drugs. PK variability is observed in the bimodal distribution between extensive metabolizers (EMs) and poor metabolizers (PMs). PK variability may also exist between individuals genotyped as homozygous EMs and heterozygous EMs. This may carry implications for drug dosing and drug response (e.g., risk of therapeutic failure or drug toxicity). Studies have reported significant PK differences between homozygous and heterozygous EMs. Some literature suggests that this distinction may be of clinical relevance. Due to study design limitations and data that are either sparse or conflicting, generalizations regarding the potential impact of the CYP genotype, within EMs, are difficult. Optimally designed clinical trials are needed. This review evaluates the potential impact of CYP genetic polymorphisms on interindividual PK variability of drugs within an EM population.

Biotransformation↗
PubMed2006

Maternal smoking during pregnancy and genetic polymorphisms in the Ah receptor, CYP1A1 and GSTM1 affect infant birth size in Japanese subjects.

Genetic susceptibility to tobacco smoke might have relation to adverse pregnancy outcomes. To estimate the effects of maternal smoking and genetic polymorphisms on infant birth weight and length, we conducted a prospective cohort study of 293 women who delivered singleton live births in Sapporo, Japan. Birth weight and length were significantly lower among infants born to continuously smoking women having the aryl hydrocarbon receptor (AhR) wild type genotype (Arg/Arg; 211 g +/- 76 g; 1.2 cm +/- 0.4 cm, p < 0.01 and p < 0.01, respectively), the CYP1A1 variant genotype (m1/m2 + m2/m2; 170 g +/- 64 g, 0.8 cm +/- 0.3 cm, p < 0.01 and p < 0.05, respectively), or the GSTM1 null genotype (171 g +/- 58 g, 0.6 cm +/- 0.3 cm, p < 0.01 and p < 0.05, respectively). When combinations of these genotypes were considered, birth weight and length were significantly lower for infants of continuously smoking women in the AhR wild type + CYP1A1 variant group (315 g +/- 116 g; 1.7 cm +/- 0.6 cm, p < 0.01 and p < 0.01, respectively) and in the CYP1A1 variant + GSTM1 null group (237 g +/- 92 g; 1.3 cm +/- 0.5 cm, p < 0.05 and p < 0.01, respectively). These genotypes did not confer adverse effects among women who had never smoked; therefore, maternal smoking in combination with maternal AhR, CYP1A1 and GSTM1 genetic polymorphisms may adversely affect infant birth size.

Adult↗
PubMed2003

[Analysis on GST-Pi genetic polymorphism in children with acute leukemia].

OBJECTIVES: To study the frequency distribution patterns of the genetic polymorphisms for glutathione S-transferase Pi (GST-Pi) in children with acute leukemia, and explore the possible relationship of GST-Pi gene mutation to the vulnerability of children with leukemia and the chemotherapeutic response. METHOD: Direct DNA sequencing was applied to detect the genotype polymorphism in 85 healthy children as the control group and 120 children with acute leukemia. The distribution difference of the genotypes between them was analyzed. RESULTS: Gene mutation rate of GST-Pi exon5 was 47.5% in children with acute leukemia, significantly higher than that of 31.8% in the control group (OR = 1.944, 95% CI 1.088-3.473), and this polymorphism distribution pattern was similar to that reported abroad. The mutation rate was much higher in ALL group than in others groups and was not significantly between the AML children and the control group. The overall mutation rate of B-lineage ALL (60.3%) was markedly higher than that of T-ALL (47.1%), but the homozygous mutation rate of the latter group (17.6%) was much higher than that of the former group (3.4%) (P < 0.05). The average survival time of the children with wild type exon5 was 24 months, longer than that of the mutation group (17.6 months), however with no statistical difference (P > 0.05). The genotype of exon5 had no effect on the survival time of AML children. No Ala(114)Val variant genotype of GST-Pi exon6 reported in literatures was found in this study, but two new mutant genotypes were discovered. A/G hybridity at 99 loci of exon6 was found in one healthy child and such hybrid genotype did not result in amino acid alteration. G-->T/G bases hybridity at 103 loci of exon6 occurred in two children with leukemia, leading to GAC of Asp (aspartic acid) replaced by TAC of Try (tyrosine) at 147 loci of the protein peptide chain, producing Asp(147) Try hybrid mutation with a genotypic frequency of 1.7%. CONCLUSION: The gene mutation of GST-Pi exon5 is one of the potential vulnerable factors in leukemogenesis of the Chinese children and the genetic polymorphism of exon6 in Chinese is greatly different from that in other races. The role of the newly discovered variant genotype Asp(147) Try in leukemogenesis remains to be further studied.

Adolescent↗
PubMed1997

Molecular mechanisms of genetic polymorphisms of drug metabolism.

One of the major causes of interindividual variation of drug effects is genetic variation of drug metabolism. Genetic polymorphisms of drug-metabolizing enzymes give rise to distinct subgroups in the population that differ in their ability to perform certain drug biotransformation reactions. Polymorphisms are generated by mutations in the genes for these enzymes, which cause decreased, increased, or absent enzyme expression or activity by multiple molecular mechanisms. Moreover, the variant alleles exist in the population at relatively high frequency. Genetic polymorphisms have been described for most drug metabolizing enzymes. The molecular mechanisms of three polymorphisms are reviewed here. The acetylation polymorphism concerns the metabolism of a variety of arylamine and hydrazine drugs, as well as carcinogens by the cytosolic N-acetyltransferase NAT2. Seven mutations of the NAT2 gene that occur singly or in combination define numerous alleles associated with decreased function. The debrisoquine-sparteine polymorphism of drug oxidation affects the metabolism of more than 40 drugs. The poor metabolizer phenotype is caused by several "loss of function" alleles of the cytochrome P450 CYP2D6 gene. On the other hand, "ultrarapid" metabolizers are caused by duplication or amplification of an active CYP2D6 gene. Intermediate metabolizers are often heterozygotes or carry alleles with mutations that decrease enzyme activity only moderately. The mephenytoin polymorphism affects the metabolism of mephenytoin and several other drugs. Two mutant alleles of CYP2C19 have so far been identified to cause this polymorphism. These polymorphisms show recessive transmission of the poor or slow metabolizer phenotype, i.e. two mutant alleles define the genotype in these individuals. Simple DNA tests based on the primary mutations have been developed to predict the phenotype. Analysis of allele frequencies in different populations revealed major differences, thereby tracing the molecular history and evolution of these polymorphisms.

Acetylation↗
PubMed2006

Association of VEGF genetic polymorphisms with prostate carcinoma risk and clinical outcome.

OBJECTIVES: Vascular endothelial growth factor (VEGF) is a potent stimulus of angiogenesis that has an important role in many human malignancies including prostate carcinoma (PCa). We evaluated the role of the functional VEGF polymorphisms as genetic markers for PCa susceptibility and prognosis. METHODS: The study included 101 patients with PCa and [corrected] 100 age-matched healthy men. The VEGF genotypes -1154G>A were identified by allele-specific polymerase chain reaction (AS-PCR) and the genotypes -634G>C and 936C>T were identified by restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR). RESULTS: A negative association was found between VEGF -1154AA genotype and PCa risk (OR=0.27; P=0.009). Furthermore, the presence of the VEGF -1154A allele appeared to be associated with a decreased [corrected] risk of higher tumor grade (OR=0.37; P=0.01). A significant increased risk of prostate cancer was associated with the VEGF -634 (GC+CC) combined genotype (OR=1.95; P=0.02). The VEGF -634C allele was associated with the aggressive phenotype of prostate cancer as defined by the high histological grade (OR=3.48; P=0.007). The VEGF -1154A/-634G haplotype was negatively associated with PCa risk (OR=0.48; P=0.005) and high tumor grade compared to low grade (OR=0.37; P=0.02). CONCLUSIONS: Genetic variations in the VEGF may predict not only PCa risk but also tumor aggressiveness.

Adult↗
PubMed2006

Association between beta2-adrenergic receptor genetic polymorphisms and total serum IgE in asthmatic patients of Chinese Han nationality.

BACKGROUND: beta(2)-Adrenergic receptor (beta(2)-AR) polymorphisms occurring at amino acid position 16 (Arg-Gly) and 27 (Gln-Glu) are known to be functionally relevant and also disease-modifying in subjects with asthma. It has been found in Caucasoid asthmatic patients that the Gln27 genotype beta(2)-AR was associated with an increase in total serum IgE levels. The association between beta(2)-AR genetic polymorphisms and total serum IgE in asthmatic patients of Chinese Han nationality remains to be established. OBJECTIVES: It was the aim of this study to investigate the association between beta(2)-AR genetic polymorphisms and total serum IgE in asthmatic patients of Chinese Han nationality. METHODS: All 59 asthmatic patients investigated (27 males and 32 females, aged between 16 and 60 years) were people of Chinese Han nationality. They were tested for their total serum IgE levels with the enzyme-linked immunosorbent assay test, and beta(2)-AR genetic polymorphisms were tested with the polymerase chain reaction allele-specific oligonucleotide hybridization assay. RESULTS: There was a significant difference of serum IgE levels among three beta(2)-AR 27 loci groups (p < 0.0001), with the highest IgE level [(1.24 +/- 0.25) x 10(6) IU/l] in the Gln/Gln group and the lowest IgE level [(0.48 +/- 0.06) x 10(6) IU/l] in the Glu/Glu group. No polymorphism of beta(2)-AR 16 loci was found to be associated with total serum IgE (p > 0.05). CONCLUSIONS: Our research suggested that in asthmatic patients of Chinese Han nationality, the beta(2)-AR genetic polymorphism at 27 loci could be associated with serum IgE levels and it might therefore play an important role in the determination of phenotypes of bronchial asthma.

Adolescent↗
PubMedDate not supplied

Genetic analysis of a cross-pollinated species, Secale cereale L., for the character with polymorphic genetic basis.

Theoretical basis and an algorithm of calculations for frequencies of genes and genotypes in the population of species with obligate cross-pollination under assessment for the character of polymorphic genetic basis are proposed. Use of four rye populations and the F1 and F2 from their crossings allows to determine genetic control of beta-amylase spectrum through identification of two genes, establishment of the allele number in each gene, and showing the linkage between beta-Amy-1 and the gene for self-incompatibility S2.

Alleles↗
PubMedDate not supplied

Genetic polymorphisms and heart failure.

Heart failure is a complex clinical syndrome. There is evidence for a genetic contribution to the pathophysiology of heart failure. Considering the fundamental role of neurohormonal factors in the pathophysiology and progression of cardiac dysfunction and hypertrophy, variants of genes involved in this system are logical candidate genes in heart failure. In this report, genetic polymorphisms of the major neurohormonal systems in heart failure will be discussed. Studies on polymorphisms of the renin-angiotensin-aldosterone system (RAAS), adrenergic receptor polymorphisms, endothelin (receptor) polymorphisms, and a group of miscellaneous polymorphisms that may be involved in the development or phenotypic expression of heart failure will be reviewed. Research on left ventricular hypertrophy is also included. The majority of genetic association studies focused on the ACE I/D polymorphism. Initial genetic associations have often been difficult to replicate, mainly due to problems in study design and lack of power. Promising results have been obtained with genetic polymorphisms of the RAAS and sympathetic system. Considering the evidence so far, a modifying role for these polymorphisms seems more likely than a role of these variants as susceptibility genes. Besides the need for larger studies to examine the effects of single nucleotide polymorphisms and haplotypes, future studies also need to focus on the complexity of these systems and study gene-gene interactions and gene-environment interactions.

Heart Failure↗
PubMed1999

Genetic polymorphism of human O6-alkylguanine-DNA alkyltransferase: identification of a missense variation in the active site region.

O6-Alkylguanine-DNA alkyltransferase (AGT, EC 2.1.1.63) is a principle DNA repair protein in repairing O6-alkylguanine in DNA, a major premutagenic lesion produced by environmental and therapeutic alkylating agents. AGT plays a critical role in protecting cells against mutation and cytotoxicity induced by these alkylating agents. The existence of a large interindividual variation in human AGT activity level has been observed and we hypothesize that genetic polymorphism of AGT could be an important determinant for this variation. The present study reports the identification of a novel missense polymorphism in the human AGT gene. The polymorphic alteration occurs at codon 143 in exon 5, converting isoleucine (ATC) to valine (GTC). Because Ile143 is adjacent to the alkyl acceptor Cys145 of the AGT active site and is conserved among mammalian AGTs, amino acid substitution at this position may affect the function of AGT. The codon 143 polymorphism appears to be linked to another new polymorphic alteration at codon 178, which converts lysine (AAG) to arginine (AGG). Because it has been reported that human AGT can be truncated at position 176 without loss of activity, the codon 178 polymorphism may not affect AGT activity. The codon 143/178 polymorphism was found in two of 90 (2%) esophageal cancer patients residing in a high incidence area of China, but was not detected in 60 normal individuals residing in the same area. Six of 28 (210%) non-cancer Caucasian individuals, however, were found to carry this polymorphic allele, suggesting a significant ethnic difference in distribution of this codon 143/178 polymorphism between Chinese and Caucasian individuals. In addition, we confirmed the existence of a codon 84 genetic polymorphism previously identified in a Japanese population, which converts leucine (CTT) to phenylalanine (TTT). The distribution of codon 84 polymorphism was 16%, 20% and 36%, respectively, in the Chinese esophageal cancer patients, Chinese and Caucasian non-cancer individuals. Coexistence of codons 84 and 143/178 polymorphic alterations was found in one Caucasian individual. In all the Chinese (n = 150) and Caucasian (n = 28) samples examined, we were unable to detect a previously reported codon 160 polymorphism (Gly to Arg) which occurred in 10-25% of the Japanese individuals and was shown to affect the reaction of AGT with the drug O6-benzylguanine. The functional significance of the codon 143/178 genetic polymorphism of human AGT and its role in determining an individual's susceptibility to environmental alkylating carcinogens and response to alkylating chemotherapeutic drugs both remain to be studied.

Adult↗