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Genetic Indicators (genetic + indicator)

Distribution by Scientific Domains

Life Sciences	50%

Selected Abstracts

Genetic indicators of herbicide stress in the pacific oyster Crassostrea gigas under experimental conditions

ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 3 2000
Dario Moraga
Abstract This study examined use of the oyster Crassostrea gigas as a bioindicator of experimental pollution caused by two concentrations of five pesticides (atrazine, isoproturon, alachlore, metolachlore, and diuron) used in agricultural and urban activities. The effect of these pesticides on the genetic structure of the marine bivalve was studied as part of an environmental biomonitoring project. This research was performed on two natural estuarine populations sampled along the French Atlantic coast as part of an ongoing monitoring program to survey the ecosystem of Brittany using two approaches: identifying the genetic markers based on the alleles and genotypes associated with pollution effects, and searching for a correlation between these markers and the sensitivity or tolerance of individuals under stress conditions. Results indicate a differential survival of individuals subjected to the various pollutants examined. The sensitivity of alleles and genotypes to environmental stress can be assessed based on the significant differences in allele and genotype frequencies observed between resistant and sensitive individuals when subjected to the pesticides. This genetic study included examination of five enzyme systems (Ak, Pgi, Cap, Pgm, and Mdh) involved in physiologic processes. A total of six alleles and five genotypes at three loci (Ak, Pgi, and Pgm) were identified as being markers of resistance or sensitivity. It is hypothesized that these markers could be used as potential genetic markers in estuarine ecosystem monitoring. [source]

CLINICAL STUDY: Predicting the effect of naltrexone and acamprosate in alcohol-dependent patients using genetic indicators

ADDICTION BIOLOGY, Issue 3 2009
Wendy Ooteman
ABSTRACT Acamprosate and naltrexone are effective medications in the treatment of alcoholism. However, effect sizes are modest. Pharmacogenomics may improve patient-treatment-matching and effect sizes. It is hypothesized that naltrexone exerts its effect through genetic characteristics associated with the dopaminergic/opioidergic positive reinforcement system, whereas acamprosate works through the glutamatergic/GABAergic negative reinforcement system. Alcohol-dependent subjects were randomly assigned to either acamprosate or naltrexone. Subjects participated in a cue-exposure experiment at the day before and at the last day of medication. Reductions in cue-induced craving and physiological cue reactivity were measured. Differential effects of naltrexone and acamprosate on these outcomes were tested for different polymorphisms of the opioid, dopamine, glutamate and GABA-receptors. Significant matching effects were found for polymorphisms at the DRD2, GABRA6 and GABRB2 gene. In addition, a trend was found for the OPRM1 polymorphism. This provides evidence for the matching potential of genotypes. It is expected that more effective treatments can be offered when genetic information is used in patient-treatment-matching. [source]

Genome-wide array-based comparative genomic hybridization analysis of pancreatic adenocarcinoma: Identification of genetic indicators that predict patient outcome

CANCER SCIENCE, Issue 3 2007
Panayiotis Loukopoulos
We analyzed the subchromosomal numerical aberrations of 44 surgically resected pancreatic adenocarcinomas by array-based comparative genomic hybridization. The aberration profile ranged widely between cases, suggesting the presence of multiple or complementary mechanisms of evolution in pancreatic cancer, and was associated with lymph node metastasis and venous or serosal invasion. A large number of small loci, previously uncharacterized in pancreatic cancer, showed non-random loss or gain. Frequent losses at 1p36, 4p16, 7q36, 9q34, 11p15, 11q13, 14q32-33, 16p13, 17p11-13, 17q11-25, 18q21-tel, 19p13, 21q22 and 22q11-12, and gains at 1q25, 2p16, 2q21-37, 3q25, 5p14, 5q11-13, 7q21, 7p22, 8p22, 8q21-23, 10q21, 12p13, 13q22, 15q13-22 and 18q11 were identified. Sixteen loci were amplified recurrently. We identified novel chromosomal alterations that were significantly associated with a range of malignant phenotypes. Gain of LUNX, HCK, E2F1 and DNMT3b at 20q11, loss of p73 at 1p36 and gain of PPM1D at 17q23 independently predicted patient outcome. Expression profiling of amplified genes identified Smurf1 and TRRAP at 7q22.1, BCAS1 at 20q13.2-3, and VCL at 10q22.1 as potential novel oncogenes. Our results contribute to a complete description of genomic structural aberrations and the identification of potential therapeutic targets and genetic indicators that predict patient outcome in pancreatic adenocarcinoma. (Cancer Sci 2007; 98: 392,400) [source]