Terri M. King

University of Texas Medical School, Houston, Texas, United States

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Publications (32)138.82 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Matrix metalloproteinases (MMPs) are a family of endopeptidases that mediate vascular remodeling by degrading extracellular matrix components, such as collagen and elastin. On the basis of accumulating evidence that implicates increased MMP-2 (gelatinase A) and MMP-9 (gelatinase B) amounts and activity in the pathogenesis of aneurysms, the authors investigated the genetic association between polymorphisms in MMP-2 and MMP-9 and sporadic intracranial aneurysms. Eight polymorphisms located in MMP-2 and MMP-9 were genotyped, and the association of these variations with disease was assessed in a Caucasian population consisting of 125 patients with intracranial aneurysms and 234 ethnically matched healthy volunteers. Polymorphisms in the MMP-2 gene and the haplotypes generated from these polymorphisms were not associated with the occurrence of intracranial aneurysms. However, a polymorphism located in the 3' untranslated region of MMP-9 showed a significant association with disease in the study population, with individuals carrying the TT genotype at increased risk for developing intracranial aneurysms (odds ratio 1.91, p = 0.005). Haplotypes containing the T allele of this polymorphism also showed a comparable association with disease. Similar results were obtained in an analysis of these polymorphisms in a subgroup of patients who presented with ruptured aneurysms. The study findings support a role for MMP-9, but not MMP-2, in the pathogenesis of intracranial aneurysms.
    Journal of Neurosurgery 10/2006; 105(3):418-23. DOI:10.3171/jns.2006.105.3.418 · 3.23 Impact Factor
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    ABSTRACT: Matrix metalloproteinases (MMPs) are a family of endopeptidases that mediate vascular remodeling by degrading extracellular matrix components, such as collagen and elastin. On the basis of accumulating evidence that implicates increased MMP-2 (gelatinase A) and MMP-9 (gelatinase B) amounts and activity in the pathogenesis of aneurysms, the authors investigated the genetic association between polymorphisms in MMP-2 and MMP-9 and sporadic intracranial aneurysms. Eight polymorphisms located in MMP-2 and MMP-9 were genotyped, and the association of these variations with disease was assessed in a Caucasian population consisting of 125 patients with intracranial aneurysms and 234 ethnically matched healthy volunteers. Polymorphisms in the MMP-2 gene and the haplotypes generated from these polymorphisms were not associated with the occurrence of intracranial aneurysms. However, a polymorphism located in the 3' untranslated region of MMP-9 showed a significant association with disease in the study population, with individuals carrying the TT genotype at increased risk for developing intracranial aneurysms (odds ratio 1.91, p = 0.005). Haplotypes containing the T allele of this polymorphism also showed a comparable association with disease. Similar results were obtained in an analysis of these polymorphisms in a subgroup of patients who presented with ruptured aneurysms. The study findings support a role for MMP-9, but not MMP-2, in the pathogenesis of intracranial aneurysms.
    Journal of Neurosurgery 10/2006; 105(3):418-23. DOI:10.3171/jns.2006.105.3.418 · 3.23 Impact Factor
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    ABSTRACT: Polymorphisms in genes encoding proteins involved in the inflammatory response may lead to a differential response to a noxious stimulus. We hypothesized that proinflammatory alleles at candidate loci would predispose patients undergoing lung resection to cardiopulmonary complications with a presumed inflammatory cause. We determined the genotypes at six candidate loci in 155 patients who underwent 160 lung resection operations at our center. We correlated these results with data from our clinical database, constructed a model predicting the risk of postoperative complications, and assessed its adequacy using receiver operating characteristic curve methodology. Preexisting cardiovascular disease (p < 0.001), primary lung cancer (p = 0.009), extent of lung resection (p = 0.042), interleukin 6 genotype (p = 0.017), and tumor necrosis factor genotype (p = 0.005) were significantly associated with complications. The odds ratio for complications for rare allele homozygosity was 3.9 (95% confidence interval, 1.4 to 10.4) for interleukin 6 and 15.3 (95% confidence interval, 1.7 to 131.4) for tumor necrosis factor. In multivariate analysis we found that cardiovascular disease (p < 0.001; odds ratio, 4.0 [95% confidence interval, 1.9 to 8.6]), interleukin 6 genotype (p = 0.027; odds ratio, 1.8 [95% confidence interval, 1.1 to 3.1]), and tumor necrosis factor genotype (p = 0.011; odds ratio, 2.5 [95% confidence interval, 1.2 to 5.1]) were independently predictive of complications, with an area under the receiver operating characteristic curve for the entire model of 0.765. Carriage of specific alleles, and homozygosity in particular, at loci within the interleukin 6 and tumor necrosis factor genes appears to contribute to the risk of experiencing an adverse event after lung resection.
    The Annals of thoracic surgery 06/2005; 79(5):1704-10. DOI:10.1016/j.athoracsur.2004.10.010 · 3.65 Impact Factor
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    ABSTRACT: A Mexican family with partial congenital nephrogenic diabetes insipidus (NDI) that resulted from a mutation in the aquaporin-2 water channel (AQP2) was characterized, and the source of this rare mutation was traced to the family's town of origin in Mexico. Affected individuals with profound polyuria and polydipsia were homozygous for an autosomal recessive missense V168M mutation in the AQP2 gene. Expression in oocytes revealed that, although retained in the endoplasmic reticulum (ER) to a great extent, a considerable amount of the partially functional AQP2-V168M was expressed at the plasma membrane, and that its ER retention was less than AQP2-T126M, a functional mutant in severe recessive NDI. None of the affected AQP2-V168M individuals had neurologic deficits, which also suggested a milder form of the disease. The homozygous individuals reported subjective improvement in polyuria and polydipsia with the use of dDAVP (1-desamino-8-D-arginine-vasopressin). When clinically tested, infusion of dDAVP at variable doses produced a partial increase in the urinary osmolality in homozygous individuals and decreased their water intake. Heterozygotes were unaffected when compared with controls. Samples were obtained from the population of the Mexican town of origin of the family; 30% of the population was heterozygous for the V168M AQP2 mutation and 1% was homozygous for the mutation. The high frequency of this rare mutation in the town provides evidence for an important health care problem in the village with consequences for future generations.
    Journal of the American Society of Nephrology 06/2004; 15(5):1223-31. · 9.47 Impact Factor
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    ABSTRACT: The concentration of a novel 65 kDa oncofetal protein, p65, was measured in the sera of patients with prostatic malignancies using an enzyme-linked immunosorbent assay. The prostate cancer sera were positive for p65 in 40 out of 59 cases (68%), while only 7 of 79 normal sera (9%) and 12 of 61 sera from patients with benign diseases (20%) were positive. The detection system had an overall sensitivity of 68% and a specificity of 86%. Elevated p65 levels correlated positively with the pathologic stages of the prostate cancer. Using this marker in concert with PSA may increase our ability to evaluate treatment response and aid in early detection of prostate cancer.
    Oncology Reports 09/2003; 10(5):1387-92. DOI:10.3892/or.10.5.1387 · 2.19 Impact Factor
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    ABSTRACT: Enteroaggregative Escherichia coli (EAEC) infection can be identified in 26% of travelers with diarrhea and is associated with fecal interleukin (IL)-8 production. We hypothesized that single-nucleotide polymorphisms (SNPs) in the IL-8 gene are associated with EAEC-related symptoms. Fecal IL-8 production and IL-8 SNPs at 5 loci were identified in 69 US students who remained in Mexico for 5 weeks; 23 subjects had EAEC-associated diarrhea, 7 were asymptomatic EAEC carriers, 22 had nonspecific diarrhea, and 17 were asymptomatic without an enteropathogen. The chances of having EAEC-associated diarrhea were significantly increased among those with the AA genotype at the -251 position (odds ratio [OR], 208.51; 95% confidence interval [CI], 28.5-1525.36) and among those with AT genotype (OR, 14.3; 95% CI, 1.98-105.74), compared with those with the TT genotype at the -251 position. Among subjects with EAEC-associated diarrhea, the AA genotype at the -251 position produced greater concentrations of fecal IL-8 than those with the AT or TT genotype (P=.0053). In the present study, the AA genotype at the -251 position was associated with the occurrence of EAEC-associated diarrhea and increased levels of fecal IL-8.
    The Journal of Infectious Diseases 09/2003; 188(4):506-11. DOI:10.1086/377102 · 5.78 Impact Factor
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    ABSTRACT: In molecular epidemiologic studies, optimizing the use of available biological specimens while minimizing the cost is always a challenge. This is particularly true in pilot studies, which often have limited funding and involve small numbers of biological samples too small for assessment of recently developed biomarkers. In this study we examined several statistical approaches for determining how many experimental subjects to use in a biomarker study and how many repeated measurements to make on each sample, given specific funding considerations and the correlated nature of the repeated measurements. A molecular epidemiology study of DNA repair and aging in basal cell carcinoma was used to illustrate the application of the statistical methods proposed. Our methods extend traditional designs on biomarker studies with repeated measurements to including funding constraints.
    Annals of Epidemiology 04/2003; 13(3):204-8. · 2.15 Impact Factor
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    ABSTRACT: PURPOSE: In molecular epidemiologic studies, optimizing the use of available biological specimens while minimizing the cost is always a challenge. This is particularly true in pilot studies, which often have limited funding and involve small numbers of biological samples too small for assessment of recently developed biomarkers.METHODS: In this study we examined several statistical approaches for determining how many experimental subjects to use in a biomarker study and how many repeated measurements to make on each sample, given specific funding considerations and the correlated nature of the repeated measurements.RESULTS: A molecular epidemiology study of DNA repair and aging in basal cell carcinoma was used to illustrate the application of the statistical methods proposed.CONCLUSIONS: Our methods extend traditional designs on biomarker studies with repeated measurements to including funding constraints.
    Annals of Epidemiology 03/2003; 13(3):204-208. DOI:10.1016/S1047-2797(02)00261-2 · 2.15 Impact Factor
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    Terri M King
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    ABSTRACT: Interactions between multiple biological phenotypes are difficult to model. Simultaneous equation modelling (SEM), as used in econometric modelling, may prove an effective tool for this problem. Generalized linear models were used to derive the structural equations defining the interactions between cholesterol, glucose, triglycerides and high-density lipoprotein cholesterol (HDL-C). These structural equations were then applied, using SEM, to Cohort 2 data (replicates 1-100) to estimate the phenotypic structure underlying the simulation. The goal was to determine if this empiric method of deriving structural equations for use in SEM was able to recover the simulation model better than generalized linear models. First, the underlying structural equations were estimated using generalized linear model techniques, which found strong a relationship between glucose, triglycerides and HDL-C. Using these structural equations, I used SEM to evaluate these relationships jointly. I found that a combination of the empiric structural equations and the SEM method was better at recovering the underlying simulated relationship between biologic measures than generalized linear modelling. The empiric SEM procedure presented here estimated different relationships between dependent variables than generalized linear modelling. The SEM procedure using empirically developed structural equations was able to recover the underlying simulation relationship partially and thus holds promise as a technique for complex phenotype analysis. Robust methods for determining the structural equations must be developed for application of SEM to population data.
    BMC Genetics 02/2003; 4 Suppl 1(Suppl 1):S10. DOI:10.1186/1471-2156-4-S1-S10 · 2.36 Impact Factor
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    ABSTRACT: Susceptibility to pulmonary fibrosis following environmental insults or cytotoxic cancer therapies has a genetic component. In mouse strains differing in susceptibility to bleomycin-induced lung fibrosis, we show highly significant linkage to only two loci. The first locus on chromosome 17 in the major histocompatibility complex (MHC), LOD = 17.4, named Blmpf1, is highly significant in both males and females, and accounts for approximately 20% of the phenotypic variance. We confirmed the presence of Blmpf1 in MHC congenic mice and narrowed the region to 2.7 cM in a reduced MHC congenic strain. The second locus on chromosome 11, LOD = 5.6, named Blmpf2, is significant in males only. A model including an interaction between Blmpf1 and Blmpf2 best fit the data in males. We confirmed Blmpf2 in a chromosome substitution strain, C57BL/6J-11(C3H), and found that its presence reduces the severity of fibrosis. Functional studies of bleomycin hydrolase activity indicate that this enzyme modulates bleomycin-induced pulmonary fibrosis, suggesting that it may be a candidate gene for Blmpf2. The data suggest sex-specific models of susceptibility to bleomycin-induced lung fibrosis, with an interaction between Blmpf2 and Blmpf1 for the more susceptible males and Blmpf1 as the major locus in females. A putative mechanism for the interaction between the two loci in males is that bleomycin hydrolase functions as an MHC class I epitope-processing protease.
    Human Molecular Genetics 09/2002; 11(16):1855-63. DOI:10.1093/hmg/11.16.1855 · 6.68 Impact Factor
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    ABSTRACT: To report on the accuracy of probands providing information on specific cancer types in their families and the ability of investigators to document these reports. Accurate information on the health status of family members is critical when studying familial patterns of diseases. However, collecting these data require significant resources. We identified 143 patients with prostate cancer from the University of Texas M. D. Anderson Cancer Center who had reported at least 1 first-degree relative with cancer. There were 263 first-degree relatives identified, for whom we confirmed diagnoses using medical records, death certificates, and verbal confirmation. The data are reported in summary statistics and compared with chi-square analysis. We documented 78% of the reports, with an accuracy rate of 81.6%. We found that accuracy was highly related to the site reported. Accuracy and documentation levels were not related to the age or income of the proband. The education level was significantly associated with the ability to document cancer, but not with the accuracy of the report. The accuracy and documentation differed by the relationship of the first-degree relative to the proband. Proband reporting of cancer in first-degree relatives varies widely by site, with common metastatic sites the most inaccurate. No reliable demographic factors were found that would reasonably predict the ability to document the accuracy of the report. We found a significant proportion of proband-reported prostate cancer was, in reality, benign prostatic hyperplasia. We propose a strategy of targeting male relatives and reports of cancer in common metastatic sites for aggressive follow-up.
    Urology 05/2002; 59(4):546-50. DOI:10.1016/S0090-4295(01)01598-9 · 2.13 Impact Factor
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    ABSTRACT: The International Genetic Epidemiology Society (IGES) has examined the charges against James V. Neel and his colleagues contained in the recently published book by Patrick Tierney entitled Darkness in El Dorado: How Scientists and Journalists Devastated the Amazon (W.W. Norton, 2000). The book implicates Neel in causing or promoting an epidemic of measles among the Yanomamö Indians of Venezuela in 1968 leading to "hundreds if not thousands" of deaths by using a "dinosaur" vaccine (Edmonston B) as a deliberate "experiment" to test his "eugenic" theories. Tierney also attempts to link this research, funded by the Atomic Energy Commission (AEC), with a broader tapestry of human radiation experiments. To investigate these serious charges, the IGES undertook a thorough examination of most source documents referenced in Tierney's book, Neel's field logs, notes, first-hand reports, contemporary writings, film sound tracks, etc., and conducted interviews with many relevant persons. The IGES finds that these allegations are false. Neel was not a eugenicist and was in fact highly critical of both the scientific basis of eugenics and its coercive social policies. In this regard, Tierney has grossly misrepresented Neel's views on a wide range of social implications of modern civilization for the long-term health of the gene pool. Far from causing an epidemic of measles, Neel did his utmost to protect the Yanomamö from the ravages of the impending epidemic by a vaccination program using a vaccine that was widely used at the time and administered in an appropriate manner. There was nothing experimental about the vaccination program, which in fact severely hindered the primary scientific objectives of the expedition. Although the research was funded in large part by the AEC, there was no element of radiation research and the work had no connection with the ethical abuses that have been reported from AEC-sponsored radiation research, such as studies of heavy isotopes. Neel's seminal contributions to a broad range of topics in human genetics have been extensively chronicled elsewhere. His research on the Yanomamö in particular has provided unique insights into the evolutionary biology of our species, the role of sociocultural practices, such as kinship relationships and selective pressures in shaping the genetic diversity of primitive population isolates, as well as the general picture of health in such populations. The IGES decries the damage done to the reputation of one of its founders and its first President and the misperception this book may have caused about the conduct of research in genetic epidemiology. Ethical issues about scientific research in primitive populations deserve serious and wide discussion, but the IGES condemns the gross misrepresentation of the facts and demonization of the principal characters in this book.
    Genetic Epidemiology 10/2001; 21(2):81-104. · 2.95 Impact Factor
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    [Show abstract] [Hide abstract]
    ABSTRACT: The International Genetic Epidemiology Society (IGES) has examined the charges against James V. Neel and his colleagues contained in the recently published book by Patrick Tierney entitled Darkness in El Dorado: How Scientists and Journalists Devastated the Amazon (W.W. Norton, 2000). The book implicates Neel in causing or promoting an epidemic of measles among the Yanomamö Indians of Venezuela in 1968 leading to “hundreds if not thousands” of deaths by using a “dinosaur” vaccine (Edmonston B) as a deliberate “experiment” to test his “eugenic” theories. Tierney also attempts to link this research, funded by the Atomic Energy Commission (AEC), with a broader tapestry of human radiation experiments. To investigate these serious charges, the IGES undertook a thorough examination of most source documents referenced in Tierney’s book, Neel’s field logs, notes, first-hand reports, contemporary writings, film sound tracks, etc., and conducted interviews with many relevant persons. The IGES finds that these allegations are false. Neel was not a eugenicist and was in fact highly critical of both the scientific basis of eugenics and its coercive social policies. In this regard, Tierney has grossly misrepresented Neel’s views on a wide range of social implications of modern civilization for the long-term health of the gene pool. Far from causing an epidemic of measles, Neel did his utmost to protect the Yanomamö from the ravages of the impending epidemic by a vaccination program using a vaccine that was widely used at the time and administered in an appropriate manner. There was nothing experimental about the vaccination program, which in fact severely hindered the primary scientific objectives of the expedition. Although the research was funded in large part by the AEC, there was no element of radiation research and the work had no connection with the ethical abuses that have been reported from AEC-sponsored radiation research, such as studies of heavy isotopes.Neel’s seminal contributions to a broad range of topics in human genetics have been extensively chronicled elsewhere. His research on the Yanomamö in particular has provided unique insights into the evolutionary biology of our species, the role of sociocultural practices, such as kinship relationships and selective pressures in shaping the genetic diversity of primitive population isolates, as well as the general picture of health in such populations. The IGES decries the damage done to the reputation of one of its founders and its first President and the misperception this book may have caused about the conduct of research in genetic epidemiology. Ethical issues about scientific research in primitive populations deserve serious and wide discussion, but the IGES condemns the gross misrepresentation of the facts and demonization of the principal characters in this book. Genet. Epidemiol. 21:81–104, 2001. © 2001 Wiley-Liss, Inc.
    Genetic Epidemiology 09/2001; 21(2):81-104. DOI:10.1002/gepi.1020 · 2.95 Impact Factor
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    ABSTRACT: An unresolved issue in research on child survival is the extent to which familial mortality risk in infancy is due to biological influences net of sociodemographic and economic factors. We examine the effect of consanguinity on early childhood mortality in an Old Order Amish settlement by using the inbreeding coefficient, an explicit measure of the degree of relatedness in one's ancestry. Inbreeding has a net positive effect on neonatal and postneonatal deaths. We find social, demographic, and population-based sociocultural explanations for this effect among the Amish population which is known to experience certain genetically transmitted defects associated with mortality.
    Demography 06/1999; 36(2):263-71. DOI:10.2307/2648113 · 1.93 Impact Factor
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    ABSTRACT: Analysis of the role of candidate genes as risk factors for age-dependent hereditary conditions often ignores the importance of dependence among sibships or other family clusters for age of onset. We examined the performance of several methods of survival analysis with dependent data using Collaborative Study on the Genetics of Alcoholism families as submitted for GAW11. Additionally, an arbitrary truncation of cluster size was performed to explore the potential impact of heterogeneity of family size on the resulting inferences concerning the role of candidate genes. Our results showed substantial differences in attribution of risk to candidate genes according to whether the method utilized allowed for dependence in onset age and according to whether the sample was truncated or arbitrarily stratified. Further work needs to be done to clarify the importance of properly accounting for dependent data in age-dependent phenotypes and in integrating these methods into widely used genetic analysis computer programs.
    Genetic Epidemiology 01/1999; 17 Suppl 1(S1):S97-102. DOI:10.1002/gepi.1370170717 · 2.95 Impact Factor
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    ABSTRACT: We report results when one alcoholism related quantitative trait, monoamine oxidase B (MAOB), is analyzed by the variance components approach for linkage [Amos, 1994; Amos et al., 1996] using the Collaborative Study on the Genetics of Alcoholism data set provided for the Genetic Analysis Workshop 11. We used two different covariate models, one with age at interview, sex, ethnicity, and smoking status and the other with age at interview, sex, and ethnicity. The univariate analysis showed 24 markers on four different chromosomes (1, 4, 9, and 12) to have evidence for linkage with the quantitative trait (single-point and multipoint linkage). However, when outliers for MAOB were removed, the significant evidence for linkage disappeared.
    Genetic Epidemiology 01/1999; 17 Suppl 1(S1):S49-54. DOI:10.1002/gepi.1370170709 · 2.95 Impact Factor
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    ABSTRACT: We report the results of the analysis of three measures of alcoholism and six associated symptoms using transmission disequilibrium (TDT) analysis on data from the Collaborative Study on the Genetics of Alcoholism data set. Implementation of identity-by-state (IBS) routines for error checking revealed 10 reported full siblings that were rejected as a full sibling to all of their purported full siblings with p < 0.05. TDT analysis revealed two loci with significant transmission disequilibrium (p < 0.001) on chromosomes 1 and 7. Analysis by parental origin found alleles at three loci displaying significant disequilibrium in the transmission of the paternal alleles for at least three of the nine tested traits. These loci are on chromosomes 6, 9, and 13. Analyses of Caucasian families alone and the use of a single affected individual from each family also yielded significant results for the loci on chromosomes 6, 9, and 13.
    Genetic Epidemiology 01/1999; 17 Suppl 1(S1):S277-81. DOI:10.1002/gepi.1370170747 · 2.95 Impact Factor
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    Terri M. King, Jill Barnholtz, Grier P. Page
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    ABSTRACT: This report summarizes our analysis of the auditory and visual event related evoked potentials. These data were collected as a component of the Collaborative Study on the Genetics of Alcoholism and distributed as a part of the data available for the Genetic Analysis Workshop 11. For this analysis, we collapsed the data collected from eight leads using principal components methods. Using four collapsed variables derived from the principal components, we used regression analysis to adjust for environmental and demographic variables. We then fit the best fitting regression model and calculated the residuals. Using the residuals, we performed segregation analysis using S.A.G.E. Finally, we applied Markov chain Monte Carlo reverse jump methods to identify areas with potential quantitative trait loci. Our findings indicate that there may be an underlying genetic component to the potentials.
    Genetic Epidemiology 01/1999; 17 Suppl 1(S1):S199-204. DOI:10.1002/gepi.1370170734 · 2.95 Impact Factor
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    ABSTRACT: We performed two-point linkage analysis during a genome-wide search for susceptibility genes that predispose to alcohol dependence with the Collaborative Study on the Genetics on Alcoholism (COGA) data made available for the Genetic Analysis Workshop 11 (GAW11). For chromosomes 1 and 4 our findings supported results reported by Reich et al. [1998] based on the same data. We found similarity between our findings in regions on chromosomes 8 and 10 and reported results for schizophrenia linkage studies. Differences between our results with COGA data and those obtained by Reich et al. [1998] are due to our use of a lod score method versus their use of the affected relative pair (sib pair) method.
    Genetic Epidemiology 01/1999; 17 Suppl 1(S1):S295-300. DOI:10.1002/gepi.1370170750 · 2.95 Impact Factor
  • Cancer Epidemiology Biomarkers & Prevention 09/1998; 7(8):729. · 4.32 Impact Factor

Publication Stats

649 Citations
138.82 Total Impact Points

Institutions

  • 2003–2004
    • University of Texas Medical School
      • Department of Internal Medicine
      Houston, Texas, United States
    • Fred Hutchinson Cancer Research Center
      Seattle, Washington, United States
  • 1995–2003
    • University of Texas MD Anderson Cancer Center
      • Department of Epidemiology
      Houston, Texas, United States
  • 2002
    • University of Houston
      Houston, Texas, United States
  • 2001
    • University of Texas Health Science Center at Houston
      • Medical School
      Houston, Texas, United States
  • 1996
    • Johns Hopkins Bloomberg School of Public Health
      • Department of Epidemiology
      Baltimore, Maryland, United States
  • 1994
    • Memorial Sloan-Kettering Cancer Center
      New York, New York, United States