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Journal articles on the topic 'Diseases - genetic mapping'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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1

Smith, M. J., and P. N. Goodfellow. "Gene mapping and genetic diseases." Current Opinion in Cell Biology 1, no. 3 (1989): 460–65. http://dx.doi.org/10.1016/0955-0674(89)90006-9.

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2

Mynett-Johnson, Lesley A., and Patrick McKeon. "The molecular genetics of affective disorders: An overview." Irish Journal of Psychological Medicine 13, no. 4 (1996): 155–61. http://dx.doi.org/10.1017/s0790966700004444.

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AbstractObjective: Genetic mapping, the method of comparing an inheritance pattern of a disease to that of a chromosomal region, has brought about a revolution in the field of human inherited diseases. Diseases which exhibit a more complex pattern of inheritance now afford the next challange in the application of genetic mapping to the field of human disease. This article aims to review the application of genetic mapping to affective disorders.Method: Review of literature concerning the molecular genetics of affective disorders.Findings: This article describes the evidence for a genetic role i

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3

Afanasenko, Olga S., and Kapiton V. Novozhilov. "Problems of rational use of genetic resources of plants resistance to diseases." Ecological genetics 7, no. 2 (2009): 38–43. http://dx.doi.org/10.17816/ecogen7238-43.

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The decision of a complex problem of rational use of plants genetic resources of resistance to diseases is based on principles of maintenance of a genetic diversity of resistance. The development of methodology of grain crops breeding with durable resistance to diseases is based on knowledge of evolutionary potential of most harmful pathogens and genetics of host-pathogen interactions. For molecular mapping of genes determined barley resistance to net blotch, spot blotch and scald double haploid barley populations were developed. Molecular mapping of genomes both plants and pathogens will prom

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Suarez-Pajes, Eva, Ana Díaz-de Usera, Itahisa Marcelino-Rodríguez, Beatriz Guillen-Guio, and Carlos Flores. "Genetic Ancestry Inference and Its Application for the Genetic Mapping of Human Diseases." International Journal of Molecular Sciences 22, no. 13 (2021): 6962. http://dx.doi.org/10.3390/ijms22136962.

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Admixed populations arise when two or more ancestral populations interbreed. As a result of this admixture, the genome of admixed populations is defined by tracts of variable size inherited from these parental groups and has particular genetic features that provide valuable information about their demographic history. Diverse methods can be used to derive the ancestry apportionment of admixed individuals, and such inferences can be leveraged for the discovery of genetic loci associated with diseases and traits, therefore having important biomedical implications. In this review article, we summ

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Ommen, G. J. B. van, and P. L. Pearson. "Long-range mapping in the research and diagnosis of genetic disease." Genome 31, no. 2 (1989): 730–36. http://dx.doi.org/10.1139/g89-131.

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This paper reviews current genetic and molecular biological methods that may be used in the so-called "reverse genetics" approach. These methods are the mapping, isolation, and study of the chromosomal DNA containing a previously unidentified gene responsible for a genetic disease, beginning with its chromosomal localization. In principle, the reverse genetics methodology follows the same path for different diseases studied. An overall outline of the steps to be undertaken is given and discussed. Several stages are illustrated with reference to current research in the fields of Duchenne muscul

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Casals, Ferran, Youssef Idaghdour, Julie Hussin, and Philip Awadalla. "Next-generation sequencing approaches for genetic mapping of complex diseases." Journal of Neuroimmunology 248, no. 1-2 (2012): 10–22. http://dx.doi.org/10.1016/j.jneuroim.2011.12.017.

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7

Bulayeva, Kazima B., Suzanne M. Leal, Tatiana A. Pavlova, et al. "Mapping genes of complex psychiatric diseases in Daghestan genetic isolates." American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 132B, no. 1 (2004): 76–84. http://dx.doi.org/10.1002/ajmg.b.30073.

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8

Houwing-Duistermaat, Jeanine J., and Robert C. Elston. "Linkage Disequilibrium Mapping of Complex Genetic Diseases Using Multiallelic Markers." Genetic Epidemiology 21, S1 (2001): S576—S581. http://dx.doi.org/10.1002/gepi.2001.21.s1.s576.

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9

Shulman, Eldad David, and Ran Elkon. "Genetic mapping of developmental trajectories for complex traits and diseases." Computational and Structural Biotechnology Journal 19 (2021): 3458–69. http://dx.doi.org/10.1016/j.csbj.2021.05.055.

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10

Dominiczak, AF, and K. Lindpaintner. "Genetics of Hypertension: A Current Appraisal." Physiology 9, no. 6 (1994): 246–51. http://dx.doi.org/10.1152/physiologyonline.1994.9.6.246.

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Recent advances in molecular genetics have made it possible to approach the study of complex polygenic multifactorial diseases such as hypertension. Two major approaches, the candidate gene and genetic mapping, have been used to investigate models of genetic hypertension in the rat.

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11

Xu, Shizhong, and William R. Atchley. "Mapping Quantitative Trait Loci for Complex Binary Diseases Using Line Crosses." Genetics 143, no. 3 (1996): 1417–24. http://dx.doi.org/10.1093/genetics/143.3.1417.

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Abstract A composite interval gene mapping procedure for complex binary disease traits is proposed in this paper. The binary trait of interest is assumed to be controlled by an underlying liability that is normally distributed. The liability is treated as a typical quantitative character and thus described by the usual quantitative genetics model. Translation from the liability into a binary (disease) phenotype is through the physiological threshold model. Logistic regression analysis is employed to estimate the effects and locations of putative quantitative trait loci (our terminology for a s

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12

Einarsdottir, Elisabet, Inez Egerbladh, Lars Beckman, Dan Holmberg, and Stefan A. Escher. "The genetic population structure of northern Sweden and its implications for mapping genetic diseases." Hereditas 144, no. 5 (2007): 171–80. http://dx.doi.org/10.1111/j.2007.0018-0661.02007.x.

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13

Shearman, Jeremy R., and Alan N. Wilton. "Origins of the Domestic Dog and the Rich Potential for Gene Mapping." Genetics Research International 2011 (January 17, 2011): 1–6. http://dx.doi.org/10.4061/2011/579308.

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The unique breeding structure of the domestic dog makes canine genetics a useful tool to further the understanding of inherited diseases and gene function. Answers to the questions of when and where the dog was domesticated from the wolf are uncertain, but how the modern diversity of dog breeds was developed is documented. Breed development has resulted in many genetically isolated populations which are segregating for different alleles for disease and morphological and behavioral traits. Many genetic tools are available for dog research allowing investigation into the genetic basis of these p

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14

Anderson, Timothy J. C., Philip T. LoVerde, Winka Le Clec’h, and Frédéric D. Chevalier. "Genetic Crosses and Linkage Mapping in Schistosome Parasites." Trends in Parasitology 34, no. 11 (2018): 982–96. http://dx.doi.org/10.1016/j.pt.2018.08.001.

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15

Collins, Andrew, Winston Lau, and Francisco M. De La Vega. "Mapping Genes for Common Diseases: The Case for Genetic (LD) Maps." Human Heredity 58, no. 1 (2004): 2–9. http://dx.doi.org/10.1159/000081451.

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16

Mitchell-Olds, T. "Interval mapping of viability loci causing heterosis in Arabidopsis." Genetics 140, no. 3 (1995): 1105–9. http://dx.doi.org/10.1093/genetics/140.3.1105.

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Abstract The genetic basis of heterosis has implications for many problems in genetics and evolution. Heterosis and inbreeding depression affect human genetic diseases, maintenance of genetic variation, evolution of breeding systems, agricultural productivity, and conservation biology. Despite decades of theoretical and empirical studies, the genetic basis of heterosis has remained unclear. I mapped viability loci contributing to heterosis in Arabidopsis. An overdominant factor with large effects on viability mapped to a short interval on chromosome I. Homozygotes had 50% lower viability than

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17

KIMMEL, MAREK. "WHY MATHEMATICS IS NEEDED TO UNDERSTAND COMPLEX GENETICS DISEASES." Journal of Biological Systems 10, no. 04 (2002): 359–80. http://dx.doi.org/10.1142/s0218339002000688.

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We discuss mathematical approaches to population genetics and evolutionary theory in the context of complex genetic disease. Mechanisms, which we discuss, include gene-environment interaction in lung cancer as well as classical mechanisms of stabilization of genetic disease such as overdominance, antagonistic pleiotropy and recurring mutations. Specific modeling approaches discussed include: (1) Mathematical model of the evolution of disease chromosome applied to mapping of a disease gene. (2) Iterated Galton–Watson branching process applied to modeling of trinucleotide expansion in triplet-re

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18

Kane, Melissa, and Tatyana V. Golovkina. "Mapping Viral Susceptibility Loci in Mice." Annual Review of Virology 6, no. 1 (2019): 525–46. http://dx.doi.org/10.1146/annurev-virology-092818-015544.

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Genetic alleles that contribute to enhanced susceptibility or resistance to viral infections and virally induced diseases have often been first identified in mice before humans due to the significant advantages of the murine system for genetic studies. Herein we review multiple discoveries that have revealed significant insights into virus-host interactions, all made using genetic mapping tools in mice. Factors that have been identified include innate and adaptive immunity genes that contribute to host defense against pathogenic viruses such as herpes viruses, flaviviruses, retroviruses, and c

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19

Su, Xin-zhuan, Hongying Jiang, Ming Yi, Jianbing Mu, and Robert M. Stephens. "Large-scale Genotyping and Genetic Mapping in Plasmodium Parasites." Korean Journal of Parasitology 47, no. 2 (2009): 83. http://dx.doi.org/10.3347/kjp.2009.47.2.83.

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20

Liu, Chunyu. "Brain expression quantitative trait locus mapping informs genetic studies of psychiatric diseases." Neuroscience Bulletin 27, no. 2 (2011): 123–33. http://dx.doi.org/10.1007/s12264-011-1203-5.

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21

Puffenberger, Erik G., Robert N. Jinks, Carrie Sougnez, et al. "Genetic Mapping and Exome Sequencing Identify Variants Associated with Five Novel Diseases." PLoS ONE 7, no. 1 (2012): e28936. http://dx.doi.org/10.1371/journal.pone.0028936.

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22

Zhao, Huiying, Yuedong Yang, Yutong Lu, et al. "Quantitative mapping of genetic similarity in human heritable diseases by shared mutations." Human Mutation 39, no. 2 (2017): 292–301. http://dx.doi.org/10.1002/humu.23358.

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23

Gershon, Elliot S., Maria Martinez, Lynn R. Goldin, and Pablo V. Gejman. "Genetic mapping of common diseases: the challenges of manic-depressive illness and schizophrenia." Trends in Genetics 6 (1990): 282–86. http://dx.doi.org/10.1016/0168-9525(90)90233-v.

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24

Beckwith, Jon, and Joseph S. Alper. "Reconsidering Genetic Antidiscrimination Legislation." Journal of Law, Medicine & Ethics 26, no. 3 (1998): 205–10. http://dx.doi.org/10.1111/j.1748-720x.1998.tb01421.x.

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Until approximately twenty years ago, advances in the study of human genetics had little influence on the practice of medicine. In the 1980s, this changed dramatically with the mapping of the altered genes that cause cystic fibrosis (CF) and Huntington disease (HD). In just a few years, these discoveries led to DNA-based tests that enabled clinicians to determine whether prospective parents were carriers of CF or whether an individual carried the Huntington gene and, as a result, would almost certainly develop the disease.Observers interested in the social and economic implications of genetic

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25

Klimeš, I., K. Weston, D. Gašperíková, et al. "Mapping of genetic determinants of the sympathoneural response to stress." Physiological Genomics 20, no. 2 (2005): 183–87. http://dx.doi.org/10.1152/physiolgenomics.00054.2004.

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Activation of the sympathoadrenal system (SAS, comprising the sympathetic nervous system and the adrenal medulla) in response to stressful stimuli is an important defense mechanism as well as a contributor to several cardiovascular diseases. There is variability in the SAS response to stress, although the extent to which this is genetically regulated is unclear. Some rodent models, including the hereditary hypertriglyceridemic (hHTg) rat, are hyperresponsive to stress. We investigated whether quantitative trait loci (QTLs) that affect sympathoadrenal response to stress could be identified. Sec

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26

Jiang, Li, Peter Sørensen, Bo Thomsen, et al. "Gene prioritization for livestock diseases by data integration." Physiological Genomics 44, no. 5 (2012): 305–17. http://dx.doi.org/10.1152/physiolgenomics.00047.2011.

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Identifying causal genes that underlie complex traits such as susceptibility to disease is a primary aim of genetic and biomedical studies. Genetic mapping of quantitative trait loci (QTL) and gene expression profiling based on high-throughput technologies are common first approaches toward identifying associations between genes and traits; however, it is often difficult to assess whether the biological function of a putative candidate gene is consistent with a particular phenotype. Here, we have implemented a network-based disease gene prioritization approach for ranking genes associated with

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27

Thumamo Pokam, BenjaminD, D. Yeboah-Manu, L. Lawson, et al. "Mapping Mycobacterium tuberculosis genetic diversity in the Gulf of Guinea – Africa." International Journal of Mycobacteriology 9, no. 5 (2021): 57. http://dx.doi.org/10.4103/2212-5531.307108.

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28

Han, Jing, and Yongzhao Shao. "The Transmission Disequilibrium/Heterogeneity Test with Parental-Genotype Reconstruction for Refined Genetic Mapping of Complex Diseases." Journal of Probability and Statistics 2012 (2012): 1–14. http://dx.doi.org/10.1155/2012/256574.

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In linkage analysis for mapping genetic diseases, the transmission/disequilibrium test (TDT) uses the linkage disequilibrium (LD) between some marker and trait loci for precise genetic mapping while avoiding confounding due to population stratification. The sib-TDT (S-TDT) and combined-TDT (C-TDT) proposed by Spielman and Ewens can combine data from families with and without parental marker genotypes (PMGs). For some families with missing PMG, the reconstruction-combined TDT (RC-TDT) proposed by Knapp may be used to reconstruct missing parental genotypes from the genotypes of their offspring t

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29

Bolovan-Fritts, Cynthia A., and Jean A. Wiedeman. "Mapping the viral genetic determinants of endothelial cell tropism in human cytomegalovirus." Journal of Clinical Virology 25 (August 2002): 97–109. http://dx.doi.org/10.1016/s1386-6532(02)00089-6.

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30

Fedak, George, Dawn Chi, Colin Hiebert, et al. "Capturing Multiple Disease Resistance in Wheat through Intergeneric Hybridization." Biology 10, no. 7 (2021): 631. http://dx.doi.org/10.3390/biology10070631.

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Derivatives from 4 species from the secondary gene pool of wheat—1 diploid (T. monococcum), 2 tetraploid (T. carthlicum; T. timopheevi), and 1 hexaploid (T. miguschovae)—were screened for resistance to Fusarium head blight, leaf rust, stem rust, and stripe rust. Where screening, genetic studies, and mapping were completed it was shown that all species carried resistance to multiple plant diseases. Some derived lines carried resistance to up to four different diseases. Where mapping was completed, it was shown that different diseases mapped to different chromosomes within any one accession.

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31

Gorbunova, Viktoriya Nikolayevna. "Molecular genetics — a way to the individual personalized medicine." Pediatrician (St. Petersburg) 4, no. 1 (2013): 115–21. http://dx.doi.org/10.17816/ped41115-121.

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Review of modern technologies that are used for identification and mapping of genetic risk factors associated with different multifactorial diseases. The principles of the wide genomic association scan (GWAS) are accounted. A significance of this method is considered on the example of hereditary predisposition to autoimmune diseases. The role of MCH complex gene polymorphism and specific genetic risk factors in the autoimmunity forming and a possibility of multifactorial diseases personalized therapy with taking into account of the patient hereditary constitution are discussed.

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32

Uitto, Jouni. "Genetic Linkage Mapping of Heritable Skin Diseases: Positional Cloning Versus the Candidate Gene Approach." Journal of Investigative Dermatology 102, no. 6 (1994): 825–26. http://dx.doi.org/10.1111/1523-1747.ep12381904.

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33

Broeckel, Ulrich, and Nicholas J. Schork. "Identifying genes and genetic variation underlying human diseases and complex phenotypes via recombination mapping." Journal of Physiology 554, no. 1 (2003): 40–45. http://dx.doi.org/10.1113/jphysiol.2003.051128.

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34

Patterson, David. "Genetic mapping in chromosome 21 and its implications for Down's syndrome and other diseases." Somatic Cell and Molecular Genetics 13, no. 4 (1987): 365–72. http://dx.doi.org/10.1007/bf01534933.

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35

WITZIG, CLAUDIA, CHARLES S. WONDJI, CLARE STRODE, ROUSSEAU DJOUAKA, and HILARY RANSON. "Identifying permethrin resistance loci in malaria vectors by genetic mapping." Parasitology 140, no. 12 (2013): 1468–77. http://dx.doi.org/10.1017/s0031182013000024.

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SUMMARYIdentification of the major loci responsible for insecticide resistance in malaria vectors would aid the development and implementation of effective resistance management strategies, which are urgently needed to tackle the growing threat posed by resistance to the limited insecticides available for malaria control. Genome-wide association studies in the major malaria vector, Anopheles gambiae, have been hindered by the high degree of within-population structuring and very low levels of linkage disequilibrium hence we revisited the use of quantitative trait loci (QTL) mapping to study re

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Beck, Emily A., Mark C. Currey, Clayton M. Small, and William A. Cresko. "QTL Mapping of Intestinal Neutrophil Variation in Threespine Stickleback Reveals Possible Gene Targets Connecting Intestinal Inflammation and Systemic Health." G3: Genes|Genomes|Genetics 10, no. 2 (2019): 613–22. http://dx.doi.org/10.1534/g3.119.400685.

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Selection, via host immunity, is often required to foster beneficial microbial symbionts and suppress deleterious pathogens. In animals, the host immune system is at the center of this relationship. Failed host immune system-microbial interactions can result in a persistent inflammatory response in which the immune system indiscriminately attacks resident microbes, and at times the host cells themselves, leading to diseases such as Ulcerative Colitis, Crohn’s Disease, and Psoriasis. Host genetic variation has been linked to both microbiome diversity and to severity of such inflammatory disease

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Tomer, Yaron, and Terry F. Davies. "Searching for the Autoimmune Thyroid Disease Susceptibility Genes: From Gene Mapping to Gene Function." Endocrine Reviews 24, no. 5 (2003): 694–717. http://dx.doi.org/10.1210/er.2002-0030.

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Abstract The autoimmune thyroid diseases (AITD) are complex diseases that are caused by an interaction between susceptibility genes and environmental triggers. Genetic susceptibility, in combination with external factors (e.g., dietary iodine), is believed to initiate the autoimmune response to thyroid antigens. Abundant epidemiological data, including family and twin studies, point to a strong genetic influence on the development of AITD. Various techniques have been used to identify the genes contributing to the etiology of AITD, including candidate gene analysis and whole genome screening.

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38

Broekema, R. V., O. B. Bakker, and I. H. Jonkers. "A practical view of fine-mapping and gene prioritization in the post-genome-wide association era." Open Biology 10, no. 1 (2020): 190221. http://dx.doi.org/10.1098/rsob.190221.

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Over the past 15 years, genome-wide association studies (GWASs) have enabled the systematic identification of genetic loci associated with traits and diseases. However, due to resolution issues and methodological limitations, the true causal variants and genes associated with traits remain difficult to identify. In this post-GWAS era, many biological and computational fine-mapping approaches now aim to solve these issues. Here, we review fine-mapping and gene prioritization approaches that, when combined, will improve the understanding of the underlying mechanisms of complex traits and disease

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Wilfert, Lena, and Francis M. Jiggins. "Disease association mapping in Drosophila can be replicated in the wild." Biology Letters 6, no. 5 (2010): 666–68. http://dx.doi.org/10.1098/rsbl.2010.0329.

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Association and linkage mapping have become important tools in understanding the genetics of complex traits, including diseases in humans. As the success of association mapping is reduced by small effect sizes and limited power, linkage studies in laboratory-based model systems are still heavily used. But whether the results of these studies can be replicated in natural populations has been questioned. Here, we show that a polymorphism in the gene ref ( 2 ) P , which had previously been linked to sigma virus resistance in Drosophila melanogaster under laboratory conditions, also provides resis

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Müllerová, Jana, and Pavel Hozák. "Use of Recombinant Congenic Strains in Mapping Disease-Modifying Genes." Physiology 19, no. 3 (2004): 105–9. http://dx.doi.org/10.1152/nips.01512.2003.

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Previous research studies have established much information about single-gene diseases. However, other genes also influencing the outcome of a disease and genes involved in complex disease remain largely unknown. Here we report on recombinant congenic strains of mice, a powerful tool for genetic dissection of a complex trait.

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KADARMIDEEN, HAJA N., YONGJUN LI, and LUC L. G. JANSS. "Gene–environment interactions in complex diseases: genetic models and methods for QTL mapping in multiple half-sib populations." Genetical Research 88, no. 2 (2006): 119–31. http://dx.doi.org/10.1017/s0016672306008391.

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An interval quantitative trait locus (QTL) mapping method for complex polygenic diseases (as binary traits) showing QTL by environment interactions (QEI) was developed for outbred populations on a within-family basis. The main objectives, within the above context, were to investigate selection of genetic models and to compare liability or generalized interval mapping (GIM) and linear regression interval mapping (RIM) methods. Two different genetic models were used: one with main QTL and QEI effects (QEI model) and the other with only a main QTL effect (QTL model). Over 30 types of binary disea

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Yeh, Ming Te, Sara Capponi, Adam Catching, Simone Bianco, and Raul Andino. "Mapping Attenuation Determinants in Enterovirus-D68." Viruses 12, no. 8 (2020): 867. http://dx.doi.org/10.3390/v12080867.

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Enterovirus (EV)-D68 has been associated with epidemics in the United Sates in 2014, 2016 and 2018. This study aims to identify potential viral virulence determinants. We found that neonatal type I interferon receptor knockout mice are susceptible to EV-D68 infection via intraperitoneal inoculation and were able to recapitulate the paralysis process observed in human disease. Among the EV-D68 strains tested, strain US/MO-14-18949 caused no observable disease in this mouse model, whereas the other strains caused paralysis and death. Sequence analysis revealed several conserved genetic changes a

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Chubanov, Vladimir, and Thomas Gudermann. "Mapping TRPM7 Function by NS8593." International Journal of Molecular Sciences 21, no. 19 (2020): 7017. http://dx.doi.org/10.3390/ijms21197017.

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The transient receptor potential cation channel, subfamily M, member 7 (TRPM7) is a ubiquitously expressed membrane protein, which forms a channel linked to a cytosolic protein kinase. Genetic inactivation of TRPM7 in animal models uncovered the critical role of TRPM7 in early embryonic development, immune responses, and the organismal balance of Zn2+, Mg2+, and Ca2+. TRPM7 emerged as a new therapeutic target because malfunctions of TRPM7 have been associated with anoxic neuronal death, tissue fibrosis, tumour progression, and giant platelet disorder. Recently, several laboratories have identi

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44

Pinheiro, Andréa Poyastro, Patrick F. Sullivan, Josue Bacaltchuck, Pedro Antonio Schmidt do Prado-Lima, and Cynthia M. Bulik. "Genetics in eating disorders: extending the boundaries of research." Revista Brasileira de Psiquiatria 28, no. 3 (2006): 218–25. http://dx.doi.org/10.1590/s1516-44462006005000004.

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OBJECTIVE: To review the recent literature relevant to genetic research in eating disorders and to discuss unique issues which are crucial for the development of a genetic research project in eating disorders in Brazil. METHOD: A computer literature review was conducted in the Medline database between 1984 and may 2005 with the search terms "eating disorders", "anorexia nervosa", "bulimia nervosa", "binge eating disorder", "family", "twin" and "molecular genetic" studies. RESULTS: Current research findings suggest a substantial influence of genetic factors on the liability to anorexia nervosa

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Galjaard, Hans. "Genetic Technology in Health Care: A Global View." International Journal of Technology Assessment in Health Care 10, no. 4 (1994): 527–45. http://dx.doi.org/10.1017/s026646230000814x.

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AbstractClinical genetics services have become an integrated part of health care in nearly all European countries. The emphasis has been on postnatal cytogenetic, biochemical, and DNA diagnosis of congenital disorders, carrier detection, genetic counseling, and prenatal diagnosis. Use has been satisfactory, and very few ethical problems have arisen, apart from moral objections against abortion by minority groups. The progress of human gene mapping is associated with new perspectives in clinical genetics and will enable the identification of people at risk of major adult diseases. This prospect

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Kawashima, K. D., and H. Akashi. "The global population genetics of Dengue viruses revealed through temporal and spatial mapping of viral genetic variation." International Journal of Infectious Diseases 53 (December 2016): 154. http://dx.doi.org/10.1016/j.ijid.2016.11.377.

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47

Coetzee, Gerhard A. "Understanding Non-Mendelian Genetic Risk." Current Genomics 20, no. 5 (2019): 322–24. http://dx.doi.org/10.2174/1389202920666191018085511.

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This opinion paper highlights strategies for a better understanding of non-Mendelian genetic risk that was revealed by genome-wide association studies (GWAS) of complex diseases. The genetic risk resides predominantly in non-coding regulatory DNA, such as in enhancers. The identification of mechanisms, the causal variants (mainly SNPs), and their target genes are, however, not always apparent but are likely involved in a network of risk determinants; the identification presents a bottle-neck in the full understanding of the genetics of complex phenotypes. Here, we propose strategies to identif

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48

Saukko, Paula. "State of play in direct-to-consumer genetic testing for lifestyle-related diseases: market, marketing content, user experiences and regulation." Proceedings of the Nutrition Society 72, no. 1 (2013): 53–60. http://dx.doi.org/10.1017/s0029665112002960.

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Direct-to-consumer (DTC) genetic tests have aroused controversy. Critics have argued many of the tests are not backed by scientific evidence, misguide their customers and should be regulated more stringently. Proponents suggest that finding out genetic susceptibilities for diseases could encourage healthier behaviours and makes the results of genetics research available to the public. This paper reviews the state of play in DTC genetic testing, focusing on tests identifying susceptibilities for lifestyle-related diseases. It will start with mapping the market for the tests. The paper will revi

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Heward, Joanne, and Stephen C. L. Gough. "Genetic Susceptibility to the Development of Autoimmune Disease." Clinical Science 93, no. 6 (1997): 479–91. http://dx.doi.org/10.1042/cs0930479.

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1. Autoimmune diseases are common conditions which appear to develop in genetically susceptible individuals, with expression of disease being modified by permissive and protective environments. Familial clustering and data from twin studies provided the impetus for the search for putative loci. Both the candidate gene approach in population-based case-control studies and entire genome screening in families have helped identify susceptibility genes in a number of autoimmune diseases. 2. After the first genome screen in type 1 (insulin-dependent) diabetes mellitus it seems likely that most autoi

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Prokunina, Ludmila, and Marta E. Alarcón-Riquelme. "Regulatory SNPs in complex diseases: their identification and functional validation." Expert Reviews in Molecular Medicine 6, no. 10 (2004): 1–15. http://dx.doi.org/10.1017/s1462399404007690.

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Abstract:

Finding the genetic causes for complex diseases is a challenge. Expression studies have shown that the level of expression of many genes is altered in disease compared with normal conditions, but what lies behind these changes? Linkage studies provide hints as to where in the genome the genetic triggers – the mutations – might be located. Fine-mapping and association studies can give yet more information about which genes, and which changes in the genes, are involved in the disease. Recent examples show that single-nucleotide polymorphisms (SNPs), which are variations at the single-nucleotide

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