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Книги з теми "Associated gene"

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Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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1

Jones, Richard Julian. Novel gene therapy for EBV-associated malignancies. Birmingham: University of Birmingham, 2003.

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2

Berns, Kenneth I., and Catherine Giraud, eds. Adeno-Associated Virus (AAV) Vectors in Gene Therapy. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80207-2.

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3

Millar, Anna L. Frequency estimation of endometrial cancer associated with microsatellite instability and mismatch repair gene defects. Ottawa: National Library of Canada, 1999.

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4

Musk, P. Molecular events associated with the activation of a temperature sensitive p160 v-abl gene product. Manchester: UMIST, 1993.

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5

Small, Cherrie-Lee. The analysis of gene transcripts associated with conidiation in the insect pathogenic fungus, Metarhizium anisopliae. St. Catharines, Ont: Brock University, Dept. of Biological Sciences, 2004.

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6

Murray, Paul G. Epstein-Barr virus gene expression in the pathogenesis of Hodgkin's Disease and other EBV-associated diseases. Wolverhampton: University of Wolverhampton, 1996.

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7

Lai, Joe Heng. A polymorphic locus in the promoter region of the IGFBP3 gene is associated with mammographic breast density. Ottawa: National Library of Canada, 2003.

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8

Kellough, Gene Ross. The ancestry of Gene Ross: Including the Ross line and associated lines of Bennett, Grimes, Llewellyn, Knighton, Turnbull and Kyle. Seneca, S.C. (600 Old Salem Rd., Seneca 29678): G.R. Kellough, 1986.

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9

United, States Dept of Energy Assistant Secretary for Environment Safety and Health. Human radiation experiments associated with the U.S. Department of Energy and its predecessors. Washington, DC: U.S. Dept. of Energy, 1995.

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10

Flavin, Nora. Cloning and characterisation of the bovine activin receptor type II gene (ActRII): Its localisation to chromosome 2 (BTA2) by somatic cell genetic analysis and the genotyping of an associated microsatelltie UCD2. Dublin: University College Dublin, 1996.

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11

Harper, Katherine. Studies of cytotoxic t-lymphocyte associated genes. Uxbridge: Brunel University, 1990.

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12

Farid, Waliyar, Collette L, Kenmore Peter E, International Crops Research Institute for the Semi-arid Tropics., and Food and Agriculture Organization of the United Nations., eds. Beyond the gene horizon: Sustaining agricultural productivity and enhancing livelihoods through optimization of crop and crop-associated biodiversity with emphasis on semi-arid tropical agroecosystems : proceedings of a workshop 23-25 September 2002, Patancheru, India. Andhra Pradesh, India: ICRISAT, 2003.

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13

Gene, Stipe, ed. State Senator Gene Stipe's A gathering of heroes. Heavener, Okla: Spring Mountain, 2000.

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14

Brezinski-Caliguri, Donna Jean. A genetic approach to the identification of genes associated with tumorigenicity in gliomas. [s.l: s.n.], 1991.

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15

Sprowl, Jason A. Identification of PKCa-dependent genes associated with growth arrest in Saccharomyces cerevisiae. Sudbury, Ont: Laurentian University, 2004.

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16

Hagens, Olivier. An investigation of two novel genes associated with Wnt signalling in Drosophila melanogaster. Brighton, UK: University of Sussex, 2000.

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17

S, Lakshmi M., ed. The genetics of cancer: Genes associated with cancer invasion, metastasis, and cell proliferation. San Diego: Academic Press, 1997.

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18

Guennoun, Souad. L' ultime parcours de Jean Genet: Tanger, Rabat, Casablanca, Larache. Paris Casablanca: Paris-Méditerranée Tarik Editions, 2001.

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19

L' ultime parcours de Jean Genet: Tanger, Rabat, Casablanca, Larache. Casablanca: Tarik éditions, 2001.

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20

The prizefighter and the playwright: Gene Tunney and Bernard Shaw. Richmond Hill, Ont: Firefly Books, 2010.

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21

Kusz-Zamelczyk, Kamila. Gene Mutations Associated with Male Infertility. INTECH Open Access Publisher, 2012.

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22

Barbetti, F., F. Guaraldi, and L. Ghizzoni, eds. Diabetes Associated with Single Gene Defects. S. Karger AG, 2017. http://dx.doi.org/10.1159/isbn.978-3-318-06025-6.

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23

1938-, Berns Kenneth I., and Flotte T. R, eds. Adeno-associated virus vectors for gene therapy. Amsterdam: Elsevier, 2005.

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24

Giraud, Catherine, and Kenneth I. Berns. Adeno-Associated Virus Vectors in Gene Therapy. Brand: Springer, 2012.

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25

Adeno-Associated Viral Vectors for Gene Therapy. Elsevier, 2005. http://dx.doi.org/10.1016/s0075-7535(05)x1016-6.

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26

Flotte, Terence R., and Kenneth I. Berns. Adeno-Associated Virus Vectors for Gene Therapy. Elsevier Science & Technology Books, 2005.

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27

Adeno-Associated Virus (Aav) Vectors in Gene Therapy. Springer-Verlag Telos, 1996.

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28

Giraud, Catherine, and Kenneth I. Berns. Adeno-Associated Virus (AAV) Vectors in Gene Therapy. Springer London, Limited, 2012.

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29

(Editor), Terence R. Flotte, and Kenneth I. Berns (Editor), eds. Adeno-associated Virus Vectors for Gene Therapy: Volume 31. Elsevier Science, 2005.

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30

Philippe, Moullier, ed. Adeno-associated Virus: Methods and Protocols. Humana Pr Inc, 2011.

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31

Moullier, Philippe, and Richard O. Snyder. Adeno-Associated Virus: Methods and Protocols. Humana Press, 2016.

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32

Adeno-Associated Virus (Aav): Vectors in Gene Therapy (Current Topics in Microbiology and Immunology). Springer-Verlag, 1996.

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33

Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Cystic fibrosis-associated liver disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0022.

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Pathophysiology 162Clinical features 162Diagnosis 163Management 164Cystic fibrosis (CF) is an autosomal recessive disease resulting from mutations in the gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) (see Chapter 21). CFTR functions as a transmembrane chloride channel in the apical membrane of most secretory epithelia and the disease thus affects lungs, pancreas, exocrine glands, gut, and liver. In CF-associated liver disease the biliary tract is most commonly involved in a spectrum from asymptomatic to biliary cirrhosis. The liver disease runs from mild and subclinical to severe cirrhosis and portal hypertension. Clinical disease is seen in 4–6% of cases, but there are biochemical abnormalities in 20–50%. At autopsy, fibrosis is present in 20% and steatosis in 50%....

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34

Keszei, Andras Peter. Role of the thiazide-sensitive sodium chloride cotransporter gene in primary hypertension associated with hypercalciuria. 2006.

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35

Said, Harun M., Adrian Staab, and Carsten Hagemann. Brain-Cancer Associated Tumor Marker Genes Expression Pattern in Humans. Nova Science Publishers, Incorporated, 2011.

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36

Saab, Yolande. Renin-angiotensin-associated gene polymorphism frequencies in the Lebanese population and their association with depressive disorders. 2004.

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37

Food and Agriculture Organization of the. Beyond the Gene Horizon: Sustaining Agricultural Productivity and Enhancing Livelihoods Through Optimization of Crop and Crop-Associated Biodiv. ICRISAT, 2003.

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38

Setnik, Beatrice. Alterations in brain gene expression and other factors associated with resistance and vulnerability to learned helplessness in rats. 2005.

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39

Food and Agriculture Organization of the. Beyond the Gene Horizon: Sustaining Agricultural Productivity and Enhancing Livelihoods Through Optimization of Crop and Crop-Associated Biodiv. ICRISAT, 2003.

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40

Biloshytsky, Vadym, and Roman Cregg. Pioneering use of gene therapy for pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0083.

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The landmark paper discussed in this chapter is ‘Gene therapy for pain: Results of a Phase I clinical trial’, published by Fink et al. in 2011. In this study, the first of its kind, researchers studied the efficacy and safety of a modified herpes simplex virus (HSV) vector used to deliver PENK, which encodes proenkephalin, which is cleaved into the enkephalin peptides Met-enkephalin and Leu-enkephalin, which induce analgesia by acting on opioid receptors. The development of the HSV vector was based in part on results studies in which adenovirus, adeno-associated virus, or non-viral vectors were used to overexpress genes. Overexpression of a variety of large molecules leads to a reduction in pain-related behaviour in animals. Gene therapy in the treatment of chronic pain seems to offer a promising alternative to systemic or highly invasive therapies. However, additional research is needed to determine the safety, effectiveness, and cost-efficiency of this approach.

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41

Kakefuda, Mary Sue. Molecular characterization of a gene of unknown function associated with a NAD(P)H nitrate reductase genomic clone from rice. 1988.

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42

Kolomietz, Elena. Identification of the deleted gene(s) associated with the Philadelphia rearrangement responsible for poor outcome in ~20% of patients with CML. 2003.

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43

Retroviral mediated gene transfer and expression of the multidrug resistance-associated protein 1 for hematopoietic chemoprotection: Preclinical trials in a canine model. Ottawa: National Library of Canada, 2000.

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44

Organization of centromeric domains in interphase nuclei of hepatocytes from Xenopus laevis: Changes associated with novo activation of the vitellogenin gene family. Ottawa: National Library of Canada, 1994.

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45

Powell, Craig M. PTEN and Autism With Macrocepaly. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0010.

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Phosphatase and Tensin homolog deleted on chromosome 10 (PTEN) is a gene encoding an intracellular signaling molecule. PTEN was originally discovered as the gene responsible for a subset of familial hamartoma (tumor) syndromes associated with increased risk for certain cancers (Nelen et al., 1997) and as a gene often mutated in human cancers and tumor cell lines (Li et al., 1997; Steck et al., 1997). More recently, mutations in PTEN have been linked genetically to the clinical phenotype of autism or developmental delay with macrocephaly (Boccone et al., 2006; Butler et al., 2005; Buxbaum et al., 2007; Goffin, Hoefsloot, Bosgoed, Swillen, & Fryns, 2001; Herman, Butter, et al., 2007; McBride et al., 2010; Orrico et al., 2009; Stein, Elias, Saenz, Pickler, & Reynolds, 2010; Varga, Pastore, Prior, Herman, & McBride, 2009; Zori, Marsh, Graham, Marliss, & Eng, 1998). This chapter examines the role of PTEN in intracellular signaling, the link between PTEN signaling pathways and other autism-related genes and signaling pathways, the genetic relationship between PTEN and autism, model systems in which effects of Pten deletion on the brain have been studied, and promising preclinical data identifying therapeutic targets for patients with autism/macrocephaly associated with PTEN mutations.

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46

Hastie, Nick, and Eve Miller-Hodges. WT1 and its disorders. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0329_update_001.

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Mutations in the Wilms tumour suppressor gene, WT1, are associated with Wilms tumour in childhood. However, in addition WT1 has a key role in renal development, emerging roles in podocyte function, and a potential role in tissue regeneration. An understanding of WT1 is of increasing importance to clinical practice. WT1 is a complex gene with multiple isoforms. It is crucial for normal embryonic development, especially kidney development, where it is necessary for mesenchymal-to-epithelial transition to form the nephron. WT1 mutations lead to abnormalities in renal and genitourinary development, causing diseases such as Denys–Drash syndrome and Frasier syndrome as well as Wilms tumour. Recently, WT1 mutations have been recognized as a significant cause of isolated steroid-resistant nephrotic syndrome in children and young adults, without other associated syndromic features. WT1 continues to be expressed in adult podocytes, where it acts as a transcriptional activator of many podocyte genes. However, the specific role of WT1 in adult podocyte function remains poorly understood.

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47

Fabbri, Chiara, and Alessandro Serretti. The treatment of bipolar disorder in the era of personalized medicine: myth or promise? Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0031.

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Bipolar disorder (BD) is a chronic disease associated with high personal and socio-economic burden. Genetics accounts for 20–95% of variability in central nervous system drug disposition and pharmacodynamics, thus genetic markers are considered a promising way to develop tailored treatments and improve the prognosis of the disease. Among mood stabilizers, lithium response was the most investigated phenotype and the most replicated genes are involved in synaptic plasticity (BDNF), serotonergic (SLC6A4) and dopaminergic (DRD1) neurotransmission, and second messenger cascades (GSK3B). Relevant pharmacogenetic findings regarding other mood stabilizers are hyperammonaemia (CPS1 gene) and hepatic dysfunction (POLG gene) induced by valproate and immune-mediated cutaneous hypersensitivity reactions (HLA-B*1502) induced by lamotrigine or carbamazepine. Polymorphisms in cytochrome (CYP) P450 genes are expected to provide useful information particularly in case of polypharmacy. Despite few pharmacogenetic tests are currently recommended, the development of pharmacogenetics in other fields of medicine provides an encouraging perspective.

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48

Paylor, Richard, Alexia M. Thomas, Surabi Veeraragavan, and Corinne M. Spencer. Putting Into Perspective the Use of the Fmr1 Knockout Mouse as a Model for Autism Spectrum Disorder. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0007.

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Chapter 7 is concerned with the presence of autism spectrum disorder (ASD) in individuals with Fragile X Syndrome (FXS). It is estimated that 21–50% of individuals with FXS meet the criteria for autism or autism with pervasive developmental delay not otherwise specified. Importantly, recent findings indicate that approximately 2–6% of individuals with ASDs have a mutation in the FMR1 gene, making it one of the most significant single genes associated with the presence of ASD.

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49

Harms, Matthew B., and Timothy M. Miller. Amyotrophic Lateral Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0027.

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Recent advances in sequencing technologies have dramatically expanded the number of genes associated with amyotrophic lateral sclerosis, including rare but highly penetrant causative mutations as well as common risk alleles. This chapter discusses these gene discoveries and how they have implicated a diverse array of biological pathways essential for motor neuron health and have begun to inform our understanding of ALS pathogenesis as a heterogeneous and multistep process. Insights from these discoveries are leading to a new generation of targeted therapies directed at specific genes and are poised to inform how patients with amyotrophic lateral sclerosis are evaluated and treated in the clinic.

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50

Ganger, Jennifer. The Genetics of Spoken Language. Edited by Jeffrey L. Lidz, William Snyder, and Joe Pater. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780199601264.013.32.

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This chapter reviews recent research on the genetics of spoken language, both behavioral and molecular, and explains the methodologies for non-geneticists. Twin studies, which have benefited from statistical advances and larger sample sizes in recent decades, have progressed from merely establishing the presence of heritability in language to making claims about whether sub-domains of language (such as vocabulary and syntax) share common genes. Molecular studies have identified at least ten promising genes associated with reading impairment, Specific Language Impairment, and speech-language impairment, but in most cases have only begun to explore the pathways from gene to behavior.

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