Relevant bibliographies by topics / Mutational mechanisms

Academic literature on the topic 'Mutational mechanisms'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Mutational mechanisms"

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Antić, Željko, Stefan H. Lelieveld, Cédric G. van der Ham, Edwin Sonneveld, Peter M. Hoogerbrugge, and Roland P. Kuiper. "Unravelling the Sequential Interplay of Mutational Mechanisms during Clonal Evolution in Relapsed Pediatric Acute Lymphoblastic Leukemia." Genes 12, no. 2 (February 2, 2021): 214. http://dx.doi.org/10.3390/genes12020214.

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Pediatric acute lymphoblastic leukemia (ALL) is the most common pediatric malignancy and is characterized by clonal heterogeneity. Genomic mutations can increase proliferative potential of leukemic cells and cause treatment resistance. However, mechanisms driving mutagenesis and clonal diversification in ALL are not fully understood. In this proof of principle study, we performed whole genome sequencing of two cases with multiple relapses in order to investigate whether groups of mutations separated in time show distinct mutational signatures. Based on mutation allele frequencies at diagnosis and subsequent relapses, we clustered mutations into groups and performed cluster-specific mutational profile analysis and de novo signature extraction. In patient 1, who experienced two relapses, the analysis unraveled a continuous interplay of aberrant activation induced cytidine deaminase (AID)/apolipoprotein B editing complex (APOBEC) activity. The associated signatures SBS2 and SBS13 were present already at diagnosis, and although emerging mutations were lost in later relapses, the process remained active throughout disease evolution. Patient 2 had three relapses. We identified episodic mutational processes at diagnosis and first relapse leading to mutations resembling ultraviolet light-driven DNA damage, and thiopurine-associated damage at first relapse. In conclusion, our data shows that investigation of mutational processes in clusters separated in time may aid in understanding the mutational mechanisms and discovery of underlying causes.
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Kim, Yoo-Ah, Mark D. M. Leiserson, Priya Moorjani, Roded Sharan, Damian Wojtowicz, and Teresa M. Przytycka. "Mutational Signatures: From Methods to Mechanisms." Annual Review of Biomedical Data Science 4, no. 1 (July 20, 2021): 189–206. http://dx.doi.org/10.1146/annurev-biodatasci-122320-120920.

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Mutations are the driving force of evolution, yet they underlie many diseases, in particular, cancer. They are thought to arise from a combination of stochastic errors in DNA processing, naturally occurring DNA damage (e.g., the spontaneous deamination of methylated CpG sites), replication errors, and dysregulation of DNA repair mechanisms. High-throughput sequencing has made it possible to generate large datasets to study mutational processes in health and disease. Since the emergence of the first mutational process studies in 2012, this field is gaining increasing attention and has already accumulated a host of computational approaches and biomedical applications.
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Dunson, David B., and Kenneth R. Tindall. "Bayesian Analysis of Mutational Spectra." Genetics 156, no. 3 (November 1, 2000): 1411–18. http://dx.doi.org/10.1093/genetics/156.3.1411.

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Abstract Studies that examine both the frequency of gene mutation and the pattern or spectrum of mutational changes can be used to identify chemical mutagens and to explore the molecular mechanisms of mutagenesis. In this article, we propose a Bayesian hierarchical modeling approach for the analysis of mutational spectra. We assume that the total number of independent mutations and the numbers of mutations falling into different response categories, defined by location within a gene and/or type of alteration, follow binomial and multinomial sampling distributions, respectively. We use prior distributions to summarize past information about the overall mutation frequency and the probabilities corresponding to the different mutational categories. These priors can be chosen on the basis of data from previous studies using an approach that accounts for heterogeneity among studies. Inferences about the overall mutation frequency, the proportions of mutations in each response category, and the category-specific mutation frequencies can be based on posterior distributions, which incorporate past and current data on the mutant frequency and on DNA sequence alterations. Methods are described for comparing groups and for assessing doserelated trends. We illustrate our approach using data from the literature.
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Rainey, P., and R. Moxon. "Unusual mutational mechanisms and evolution." Science 260, no. 5116 (June 25, 1993): 1958–60. http://dx.doi.org/10.1126/science.8316837.

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Hurst, L., and A. Grafen. "Unusual mutational mechanisms and evolution." Science 260, no. 5116 (June 25, 1993): 1959–60. http://dx.doi.org/10.1126/science.8316838.

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Watson, D. "Unusual mutational mechanisms and evolution." Science 260, no. 5116 (June 25, 1993): 1958–59. http://dx.doi.org/10.1126/science.8391167.

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Auerbach, Scott S., Miaofei Xu, B. Alex Merrick, Mark J. Hoenerhoff, Dhiral Phadke, Debra J. Taxman, Ruchir Shah, et al. "Exome Sequencing of Fresh-frozen or Formalin-fixed Paraffin-embedded B6C3F1/N Mouse Hepatocellular Carcinomas Arising Either Spontaneously or due to Chronic Chemical Exposure." Toxicologic Pathology 46, no. 6 (July 25, 2018): 706–18. http://dx.doi.org/10.1177/0192623318789398.

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Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide; however, the mutational properties of HCC-associated carcinogens remain largely uncharacterized. We hypothesized that mechanisms underlying chemical-induced HCC can be characterized by evaluating the mutational spectra of these tumors. To test this hypothesis, we performed exome sequencing of B6C3F1/N HCCs that arose either spontaneously in vehicle controls ( n = 3) or due to chronic exposure to gingko biloba extract (GBE; n = 4) or methyleugenol (MEG; n = 3). Most archived tumor samples are available as formalin-fixed paraffin-embedded (FFPE) blocks, rather than fresh-frozen (FF) samples; hence, exome sequencing from paired FF and FFPE samples was compared. FF and FFPE samples showed 63% to 70% mutation concordance. Multiple known (e.g., Ctnnb1T41A, BrafV637E) and novel (e.g., Erbb4C559S, Card10A700V, and Klf11P358L) mutations in cancer-related genes were identified. The overall mutational burden was greater for MEG than for GBE or spontaneous HCC samples. To characterize the mutagenic mechanisms, we analyzed the mutational spectra in the HCCs according to their trinucleotide motifs. The MEG tumors clustered closest to Catalogue of Somatic Mutations in Cancer signatures 4 and 24, which are, respectively, associated with benzo(a)pyrene- and aflatoxin-induced HCCs in humans. These results establish a novel approach for classifying liver carcinogens and understanding the mechanisms of hepatocellular carcinogenesis.
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Balamurugan, Kuppareddi, Martin L. Tracey, Uwe Heine, George C. Maha, and George T. Duncan. "Mutation at the Human D1S80 Minisatellite Locus." Scientific World Journal 2012 (2012): 1–8. http://dx.doi.org/10.1100/2012/917235.

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Little is known about the general biology of minisatellites. The purpose of this study is to examine repeat mutations from the D1S80 minisatellite locus by sequence analysis to elucidate the mutational process at this locus. This is a highly polymorphic minisatellite locus, located in the subtelomeric region of chromosome 1. We have analyzed 90,000 human germline transmission events and found seven (7) mutations at this locus. The D1S80 alleles of the parentage trio, the child, mother, and the alleged father were sequenced and the origin of the mutation was determined. Using American Association of Blood Banks (AABB) guidelines, we found a male mutation rate of1.04×10-4and a female mutation rate of5.18×10-5with an overall mutation rate of approximately7.77×10-5. Also, in this study, we found that the identified mutations are in close proximity to the center of the repeat array rather than at the ends of the repeat array. Several studies have examined the mutational mechanisms of the minisatellites according to infinite allele model (IAM) and the one-step stepwise mutation model (SMM). In this study, we found that this locus fits into the one-step mutation model (SMM) mechanism in six out of seven instances similar to STR loci.
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Pálinkás, Hajnalka Laura, Lőrinc Pongor, Máté Balajti, Ádám Nagy, Kinga Nagy, Angéla Békési, Giampaolo Bianchini, Beáta G. Vértessy, and Balázs Győrffy. "Primary Founder Mutations in the PRKDC Gene Increase Tumor Mutation Load in Colorectal Cancer." International Journal of Molecular Sciences 23, no. 2 (January 6, 2022): 633. http://dx.doi.org/10.3390/ijms23020633.

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The clonal composition of a malignant tumor strongly depends on cellular dynamics influenced by the asynchronized loss of DNA repair mechanisms. Here, our aim was to identify founder mutations leading to subsequent boosts in mutation load. The overall mutation burden in 591 colorectal cancer tumors was analyzed, including the mutation status of DNA-repair genes. The number of mutations was first determined across all patients and the proportion of genes having mutation in each percentile was ranked. Early mutations in DNA repair genes preceding a mutational expansion were designated as founder mutations. Survival analysis for gene expression was performed using microarray data with available relapse-free survival. Of the 180 genes involved in DNA repair, the top five founder mutations were in PRKDC (n = 31), ATM (n = 26), POLE (n = 18), SRCAP (n = 18), and BRCA2 (n = 15). PRKDC expression was 6.4-fold higher in tumors compared to normal samples, and higher expression led to longer relapse-free survival in 1211 patients (HR = 0.72, p = 4.4 × 10−3). In an experimental setting, the mutational load resulting from UV radiation combined with inhibition of PRKDC was analyzed. Upon treatments, the mutational load exposed a significant two-fold increase. Our results suggest PRKDC as a new key gene driving tumor heterogeneity.
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Walker, Brian A., Christopher P. Wardell, Lorenzo Melchor, Sanna Hulkki, Nicola E. Potter, David C. Johnson, Kerry Fenwick, et al. "Intraclonal heterogeneity and distinct molecular mechanisms characterize the development of t(4;14) and t(11;14) myeloma." Blood 120, no. 5 (August 2, 2012): 1077–86. http://dx.doi.org/10.1182/blood-2012-03-412981.

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Abstract We have used whole exome sequencing to compare a group of presentation t(4;14) with t(11;14) cases of myeloma to define the mutational landscape. Each case was characterized by a median of 24.5 exonic nonsynonymous single-nucleotide variations, and there was a consistently higher number of mutations in the t(4;14) group, but this number did not reach statistical significance. We show that the transition and transversion rates in the 2 subgroups are similar, suggesting that there was no specific mechanism leading to mutation differentiating the 2 groups. Only 3% of mutations were seen in both groups, and recurrently mutated genes include NRAS, KRAS, BRAF, and DIS3 as well as DNAH5, a member of the axonemal dynein family. The pattern of mutation in each group was distinct, with the t(4;14) group being characterized by deregulation of chromatin organization, actin filament, and microfilament movement. Recurrent RAS pathway mutations identified subclonal heterogeneity at a mutational level in both groups, with mutations being present as either dominant or minor subclones. The presence of subclonal diversity was confirmed at a single-cell level using other tumor-acquired mutations. These results are consistent with a distinct molecular pathogenesis underlying each subgroup and have important impacts on targeted treatment strategies. The Medical Research Council Myeloma IX trial is registered under ISRCTN68454111.
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Dissertations / Theses on the topic "Mutational mechanisms"

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Robertson, Scott C. "Mechanisms of protein kinase activation determined by molecular modeling and mutational analysis /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1999. http://wwwlib.umi.com/cr/ucsd/fullcit?p9938596.

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Legler, Patricia Marie. "Kinetic, magnetic, resonance, and mutational studies of the mechanisms of GDP-mannose mannosyl hydrolase, an unusual nudix enzyme." Available to US Hopkins community, 2002. http://wwwlib.umi.com/dissertations/dlnow/3046492.

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Kennouche, Paul. "New insights into meningococcal pathogenesis : exploring the role of the major pilin PilE in the functions of type IV pili Mechanisms of meningococcal type IV pili multiple functions revealed by deep mutational scanning." Thesis, Sorbonne Paris Cité, 2018. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=1972&f=12515.

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Les pili de type IV (PT4) sont des filaments micrométriques qui exercent de multiples fonctions à la surface de nombreux procaryotes. Chez Neisseria meningitidis, les PT4 sont des homopolymères de la piline majeure PilE. Leur implication dans l'agrégation interbactérienne et l'adhésion aux cellules humaines les rend centraux dans la virulence du méningocoque. Cependant, les mécanismes permettant aux PT4 d'exercer ces diverses fonctions restent trop élusifs. Durant ce doctorat, nous avons simultanément déterminé les régions de PilE impliquées dans l'assemblage des pili, l'auto-agrégation, l'adhésion aux cellules humaines et la compétence à la transformation en utilisant la technique de deep mutational scanning. L'analyse approfondie de cette carte fonctionnelle de la séquence de la piline offre de nouvelles perspectives sur les mécanismes de fonctionnement des PT4 : tout d'abord, le domaine hyperconservé 1 de PilE est impliqué dans la régulation de la balance entre la longueur et le nombre des pili ; par ailleurs, nous avons identifié un groupe d'acides aminés électropositifs autour de la lysine 140 requis pour l'agrégation ; enfin, nous montrons l'importance de l'extrémité distale des PT4 dans l'adhésion. En résumé, ces résultats sont en faveur d'un rôle direct de PilE dans l'agrégation et l'adhésion bactérienne et identifient les domaines spécifiquement impliqués dans ces fonctions. Ces travaux ouvrent aussi de nouvelles perspectives sur la pathogénicité de Neisseria meningitidis et pourraient participer au développement de nouvelles thérapies pour combattre les pathologies provoquées par le méningocoque
Type IV pili (TFP) are multifunctional micrometer-long filaments expressed at the surface of many prokaryotes. In Neisseria meningitidis, TFP are homopolymers of the major pilin PilE. They are crucial for virulence as they mediate interbacterial aggregation and adhesion to host cells although the mechanisms behind these functions remain unclear. During this doctoral work, we simultaneously determined the regions of PilE involved in pili display, auto-aggregation and adhesion to human cells by using deep mutational scanning. Mining of this extensive functional map of the pilin sequence provides new mechanistic insights: first, the hyperconserved 1-domain of PilE was found to be involved in the balance between pili length and number; moreover, we identified an electropositive cluster of residues centered around Lysine 140 necessary for aggregation; finally, we show the importance of the tip of TFP in adhesion. Overall, these results support a direct role of PilE in aggregation and adhesion to host cells and identify these specific functional domains. This doctoral work opens up new perspectives on the pathogenicity mechanisms of Neisseria meningitidis and could help design new therapies to fight meningococcal disease
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Kugelberg, Elisabeth. "Mechanisms of adaptive mutations in bacteria /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-446-5/.

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Kitzenmaier, Alexandra [Verfasser], Carmen [Gutachter] Villmann, and Erhard [Gutachter] Wischmeyer. "GlyT2-Mutationen als zweithäufigste Ursache bei Hyperekplexie – Pathologischer Mechanismus der Mutation P429L / Alexandra Kitzenmaier ; Gutachter: Carmen Villmann, Erhard Wischmeyer." Würzburg : Universität Würzburg, 2020. http://d-nb.info/1208629344/34.

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Sahlin, Charlotte. "Pathogenic Mechanisms of the Arctic Alzheimer Mutation." Doctoral thesis, Uppsala University, Department of Public Health and Caring Sciences, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7582.

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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, neuropathologically characterized by neurofibrillay tangles and deposition of amyloid-β (Aβ) peptides. Several mutations in the gene for amyloid precursor protein (APP) cause familial AD and affect APP processing leading to increased levels of Aβ42. However, the Arctic Alzheimer mutation (APP E693G) reduces Aβ levels. Instead, the increased tendency of Arctic Aβ peptides to form Aβ protofibrils is thought to contribute to the pathogenesis.

In this thesis, the pathogenic mechanisms of the Arctic mutation were further investigated, specifically addressing if and how the mutation affects APP processing. Evidence of a shift towards β-secretase cleavage of Arctic APP was demonstrated. Arctic APP did not appear to be an inferior substrate for α-secretase, but the availability of Arctic APP for α-secretase cleavage was reduced, with diminished levels of cell surface APP in Arctic cells. Interestingly, administration of the fatty acid docosahexaenoic acid (DHA) stimulated α-secretase cleavage and partly reversed the effects of the Arctic mutation on APP processing.

In contrast to previous findings, the Arctic mutation generated enhanced total Aβ levels suggesting increased Aβ production. Importantly, this thesis illustrates and explains why measures of both Arctic and wild type Aβ levels are highly dependent upon the Aβ assay used, with enzyme-linked immunosorbent assay (ELISA) and Western blot generating different results. It was shown that these differences were due to inefficient detection of Aβ oligomers by ELISA leading to an underestimation of total Aβ levels.

In conclusion, the Arctic APP mutation leads to AD by multiple mechanisms. It facilitates protofibril formation, but it also alters trafficking and processing of APP which leads to increased steady state levels of total Aβ, in particular at intracellular locations. Importantly, these studies highlight mechanisms, other than enhanced production of Aβ peptide monomers, which could be implicated in sporadic AD.

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Segditsas, Stefania. "Mechanisms of intestinal tumorigenesis resulting from APC mutations." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/15923/.

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Colorectal cancer typically arises through the sequential accumulation of mutations in different genes. Mutations in the adenomatous polyposis coli (APC) gene are thought to be the initiating step in this sequence of events and are found in the majority of early colorectal tumours. Investigation of these lesions has revealed that selection of 'optimal' combinations of mutations at the APC locus is in place, but the roles of such selected combinations have never been clarified. In the work presented in this thesis, I have demonstrated that similar constraints on APC mutations are active in tumours from attenuated FAP (AFAP) patients and that given the sub-optimal location of the germline APC mutation in these patients, additional somatic mutations are often required, especially in patients with germline mutations in the alternatively spliced region of exon 9. I have also shown that APC promoter hypermethylation does not appear to play a fundamental role in the selection of optimal APC genotypes. I have shown that the optimum combinations of mutations at APC are those that allow retention of some APC activity with respect to β-catenin degradation and that this has effects on the resulting activation of the Wnt signalling pathway. Optimal combinations of APC mutations result in intermediate nuclear β-catenin levels, which surprisingly highly activate a selection of Wnt targets. In an attempt to identify novel Wnt targets that are important for tumorigenesis and could serve as therapeutic targets, I have validated results from a cross-species comparison that identified a set of genes showing consistent differential expression between early tumour samples carrying APC mutations and normal tissue. In addition, I have investigated the biological function of one such-identified molecule, the serum/glucocorticoid-regulated kinase (SGK1), and I have revealed its potential role as a key regulator of intestinal cell differentiation and apoptosis.
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Williams, Louise Jane. "Recombinational mechanisms in human genetic diversity." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342483.

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Robinson, Alexis Anne. "Molecular Mechanisms of DJ-1 Mutations in Parkinson's Disease." Thesis, University College London (University of London), 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487292.

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Mutations in PARK7 - the human chromosome Ip36 locus which harbours the DJ-J gene have been shown to be responsible for the onset of autosomal recessive Parkinson's disease. The exact function of DJ-I is unknown due to its diverse role in numerous biological processes including oncogenesis, transcriptional regulation and oxidative stress. This study focuses on the reported missense mutations ofDJ-1 in an attempt to elucidate their pathogenic mechanisms. Effects on DJ-I dimerisation and DJ-I interaction with known protein partners were initially assessed using the yeast two-hybrid system. Results were confinned in a mammalian cell system using af9nity purification methods. This study demonstrated that dlmerisation of DJ-I is required for all DJ-I binding protein interactions, and only mutation Ll66P had an effect on protein dimerisation. DJ-I mutations were found to have a specific disruptive effect on DJ-I interaction with DJ-I binding proteins. Mutation M261 abolished interactions with SUMO-I, a small ubiquitin-like modifier, by an unknown mechanism. Of particular interest was the finding that three distinct DJ-I missense mutations (A104T, Dl49A and E163K) selectively abolished interaction with the so-called DJ-I binding protein (DJBP). Further investigation of DJBP, involving peR amplification from human brain eDNA, revealed the existence of multiple isofonns of DJBP, generated by alternative splicing. Sequence analysis indicated the potential of DJBP to function as a mitochondrially-Iocated calcium-binding protein, due to the identification of EF-hand motifs and an N-tenninal mitochondrial targeting sequence... Disruption of the DJ-I/DJBP interaction may provide a molecular explanation for the underlying cause of DJ-I-related Parkinson's disease. The predicted role of DJBP as a mitochondrially-Iocated calcium-binding protein supports the involvement ofDJ-1 and DJBP in a pathway which exerts a protective effect on the cell under conditions of oxidative stress. Mutations which abolish DJ-I/DJBP interaction may abrogate the protective effect, resulting in increased susceptibility to cellular stress, providing a link between mitochondria and the pathogenesis of Parkinson's disease. These results also suggest that the gene encoding DJBP on human chromosome 22ql3 is a suitable candidate for genetic analysis in Parkinson's disease.
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Rutherford, Jodie. "Germline p53 mutations : characterisation and mechanisms of P53 dysfunction." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252278.

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Books on the topic "Mutational mechanisms"

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Elduque, Alberto. Mutations of Alternative Algebras. Dordrecht: Springer Netherlands, 1994.

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Gershenson, S. M. Molecular mechanisms of mutagenicity of DNA and other natural and synthetic polynucleotides. Kiev: National Academy of Science of Ukraine, Institute of Plant Physiology and Genetics, 1997.

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Hughes, Alis, and Lesley Jones. Pathogenic Mechanisms. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0013.

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Huntington’s disease (HD) pathogenesis is complex. In the two decades since the gene and its mutation were discovered, there has been extensive exploration of how the expanded CAG repeat in HTT leads to neurodegeneration in HD. This chapter focuses on the mechanisms that potentially contribute to the dysfunction and death of cells in HD. These include repeat instability and RNA toxicity and the production, processing, modification, and degradation of mutant huntingtin. The effects of mutant HTT on cellular processes such as transcription, transport, neurotransmission, and protein clearance are also described. The interdependence and individual importance of these mechanisms in disease etiology remains to be clarified; however, consideration of each could be important for the development of therapeutic interventions in HD.
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Mendelsohn, Mortimer L. Mutation & The Environment Pt.a: BASIC MECHANISMS (DISCONTINUED (Progress in Clinical and Biological Research)). Edited by Mortimer Mendelsohn. John Wiley & Sons, 1990.

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Grant, Seth G. N. Synaptic Mechanisms of Psychotic Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0017.

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Synapses are the hallmark of the neuroanatomy of the brain. The million billion synapses of the human brain connect the nerve cells into the networks that underpin all behavior. The molecular anatomy of synapses is also remarkably complicated with ~2000 proteins in the synapse proteome. The proteins are physically organized into a hierarchy of molecular machines that control synapse biology. These proteins integrate and compute the information in patterns of nerve cell activity. Mutations in hundreds of genes that encode synaptic proteins contribute to over one hundred brain diseases, including common mental disorders. The synapse proteome is of fundamental importance to mental illness.
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Cazeneuve, Cécile, and Alexandra Durr. Genetic and Molecular Studies. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0006.

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Huntington’s disease (HD) is a rare inherited neurologic disorder due to a single mutational mechanism in a large gene (HTT). The mutation is an abnormal CAG repeat expansion, which is translated to a polyglutamine stretch in the huntingtin protein. The growing field of repeat expansion disorders benefits greatly from the lessons learned from the role of the CAG repeat expansion in HD and its resulting phenotype–genotype correlations. The molecular diagnosis can be difficult, and there are some pitfalls for accurate sizing of the CAG repeat, especially in juvenile HD and for intermediate alleles. Correlation between CAG length and age of onset accounts for up to 72% of the variance in different populations, but the search for genes modifying age of onset or progression of HD is still ongoing.
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Sun, Warren Da-Ren. Structural, mutational and kinetic analyses of Aquifex aeolicus prephenate dehydrogenase: Elucidation of the catalytic mechanism. 2006.

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Pocheville, Arnaud, and Étienne Danchin. Genetic Assimilation and the Paradox of Blind Variation. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199377176.003.0003.

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This chapter confronts the neo-Darwinian core tenet of blind variation, or random mutation, with classical and recent models of genetic assimilation. We first argue that all the mechanisms proposed so far rely on blind genetic variation fueling natural selection. Then, we examine a new hypothetical mechanism of genetic assimilation, relying on nonblind genetic variation. Yet, we show that such a model still relies on blind variation of some sort to explain adaptation. Last, we discuss the very meaning of the tenet of blind variation. We propose a formal characterization of the tenet and argue that it should not be understood solely as an empirical claim, but also as a core explanatory principle.
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Mechanisms in B-cell neoplasia 1994. Berlin: Springer-Verlag, 1995.

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Potter, M., and Michael Potter. Mechanisms in B-Cell Neoplasia 1994. SPRINGER-VERLAG, 1995.

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Book chapters on the topic "Mutational mechanisms"

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Barrett, J. Carl. "Asbestos Carcinogenicity: A Mutational Hypothesis." In Mechanisms in Fibre Carcinogenesis, 309–18. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-1363-2_25.

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Reatégui, Ricardo, Wade Johnson, Wu Xu, Boris Zybailov, Ilya Vassiliev, Gaozhong Shen, John H. Golbeck, and Parag R. Chitnis. "Mutational Analysis of Photosystem I." In Photosynthesis: Mechanisms and Effects, 515–20. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-3953-3_121.

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Kehrer-Sawatzki, Hildegard, and David N. Cooper. "NF1 Microdeletions and Their Underlying Mutational Mechanisms." In Neurofibromatosis Type 1, 187–209. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-32864-0_14.

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Glickman, Barry W., Douglas F. Fix, Fumio Yatagai, Philip A. Burns, and Roel M. Schaaper. "Mechanisms of Spontaneous Mutagenesis: Clues from Mutational Specificity." In Mechanisms of DNA Damage and Repair, 425–37. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-9462-8_45.

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Asano, Shinji, Tohru Kimura, and Takeguchi Noriaki. "Mutational Analysis of Gastric Proton Pump, α- and β-Subunits." In Mechanisms and Consequences of Proton Transport, 59–70. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0971-4_6.

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Glickman, Barry W., Philip A. Burns, and Douglas F. Fix. "Mechanisms of Spontaneous Mutagenesis: Clues from Altered Mutational Specificity in DNA Repair-Defective Strains." In Antimutagenesis and Anticarcinogenesis Mechanisms, 259–81. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5182-5_23.

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Hartman, Philip E., and Sharon Lea Aukerman. "Salmonella Tester Strains: Mutational Targets and Correlation with Animal Carcinogenicity and Teratogenicity." In Mechanisms of DNA Damage and Repair, 407–24. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-9462-8_44.

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Cariello, Neal F., and William G. Thilly. "Use of Gradient Denaturing Gels to Determine Mutational Spectrum in Human Cells." In Mechanisms of DNA Damage and Repair, 439–52. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-9462-8_46.

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Martinko, John, and Khaled Girgis. "Evidence for Multiple Mutational Mechanisms which Generate Polymorphism at H-2K." In Molecular Evolution of the Major Histocompatibility Complex, 155–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84622-9_12.

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Burnouf, Dominique, Patrice Koehl, and Robert P. P. Fuchs. "Position of a Single Acetylaminofluorene Adduct Within a Mutational Hot Spot is Critical for the Related Mutagenic Event." In Antimutagenesis and Anticarcinogenesis Mechanisms II, 277–87. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-9561-8_23.

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Conference papers on the topic "Mutational mechanisms"

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Nik-Zainal, Serena. "Abstract IA01: Advancing the field of mutational signatures: Mechanisms and clinical applications." In Abstracts: AACR Special Conference on DNA Repair: Tumor Development and Therapeutic Response; November 2-5, 2016; Montreal, QC, Canada. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3125.dnarepair16-ia01.

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Sherborne, Amy, Philip Davidson, Katharine Yu, Alice Nakamura, Mamunur Rashid, and Jean Nakamura. "Abstract A50: Mutational analysis of a mouse model of second malignant neoplasms." In Abstracts: AACR Special Conference: Advances in Pediatric Cancer Research: From Mechanisms and Models to Treatment and Survivorship; November 9-12, 2015; Fort Lauderdale, Florida. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.pedca15-a50.

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Jegg, A., TM Ward, E. Iorns, M. Gallas, SA Aparicio, and MD Pegram. "PD01-09: Identifying Novel Mechanisms of Resistance to Lapatinib in ERBB2+ Breast Cancer Cells through Whole Genome Mutational Analysis." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-pd01-09.

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Pitt, Jason J., Toshio F. Yoshimatsu, Yonglan Zheng, Jason Grundstad, Jigyasa Tuteja, Jiebiao Wang, Abayomi Odetunde, et al. "Abstract 4494: Whole genome sequencing reveals different patterns of mutational mechanisms in breast tumors between women of African and European descent." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4494.

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Gautieri, Alfonso, Sebastien Uzel, Simone Vesentini, Alberto Redaelli, and Markus J. Buehler. "Osteogenesis Imperfecta: Molecular and Mesoscale Disease Mechanisms." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204530.

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Osteogenesis Imperfecta (OI) is a genetic disorder in collagen characterized by mechanically weakened tendon and fragile bones that affects more than 1 in 10,000 individuals. Even though many studies have attempted to associate specific mutation types with phenotypic severity, the mechanisms by which a single point mutation influences the mechanical behavior of tissues at multiple length-scales remain unknown. Here we show by a hierarchy of full atomistic and mesoscale simulation that OI mutations severely compromise the mechanical properties of collagenous tissues at multiple scales, from single molecules to collagen fibrils.
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Echeverria, Gloria Vittone, Sahil Seth, Zhongqi Ge, Alessandro Carugo, Christopher Bristow, Prabjhot Mundi, Sabrina Jeter-Jones, et al. "Abstract 212: High-resolution barcoding in patient-derived xenografts of triple-negative breast cancer reveals reversible chemoresistance conferred by non-mutational mechanisms." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-212.

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Woo, Janghee, Teppei Morikawa, Shuji Ogino, D. Gary Gilliland, and Ramesh A. Shivdasani. "Abstract 3106: Intestinal mesenchymal fibroblasts promote early epithelial tumorigenesis through activation of integrin beta4 and receptor tyrosine kinases, bypassing common mutational mechanisms." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3106.

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Montesion, Meagan, Ethan S. Sokol, Todd C. Knepper, Andrew S. Brohl, Garrett M. Frampton, Phil J. Stephens, James A. DeCaprio, Kenneth Y. Tsai, and Lee A. Albacker. "Abstract 4003: Comprehensive genomic profiling of Merkel cell carcinoma samples reveals bimodal distribution of tumor mutational burden and two mutually exclusive candidate mechanisms of malignant transformation." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4003.

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Mukhopadhyay, Asima, Nicola Curtin, and Richard Edmondson. "Evaluation of different methods to assess homologous recombination status and sensitivity to PARP inhibitors in ovarian cancer." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685289.

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Methods: Matched samples of ascites and tumor tissue were taken from patients undergoing surgery for epithelial ovarian cancer. Tumor samples were formalin fixed and paraffin embedded (FFPE); ascites samples were used to generate primary cultures (PC). HR status was determined in PCs as previously described.[1] IC50 for the PARP inhibitor Rucaparib was estimated using SRB assays. DNA was extracted from the FFPE tissue. The following techniques were evaluated in PCs or paired FFPE samples: DR-GFP reporter assay, PARP activity assay, BRCA1 expression on immunohistochemistry, BRCA1 methylation status and BRCA1/2 mutation analysis. A next generation sequencing based assay was used to detect mutations and other genomic alterations in a large panel of cancer-associated genes, including BRCA1/2. Results: Paired samples were collected from 64 patients and characterized for HR function. 47/64 (76%) were high grade serous. 44% (28/64)) were HR defective (HRD) by Rad51 assay and correlated with Rucaparib sensitivity (PPV-92%, NPV-100%). Molecular analysis revealed that all mutations and other genomic alterations detected in ascites derived PCs were also found in matched FFPE tumor tissues. All tumors with serous histology contained p53 mutations, whilst the remaining tumors without p53 mutations were non-serous in histology. DR-GFP assay was unreliable in PC due to poor transfection. In a subset of 50 cancers there was reduced BRCA1 expression in the HRD vs. HRC tumours (34.8% vs. 22.7%, ns) whilst in a further subset of 30 cases there was no difference in endogenous or stimulated PARP activity between HRD and HRC tumours. Deleterious BRCA2 mutations were identified in 7 tumors, 6 of which were HRD. Only 1 deleterious BRCA1 mutation was detected but methylation of BRCA1 was identified in 13 of 64 (20%) tumors, 7 of which were HRD. Mutation of BRCA2 was mutually exclusive to methylation of BRCA1. HRD vs. HRC tumours showed BRCA1 methylation (25% vs. 17%) and BRCA1/2 mutation (21% vs. 0.3%). 14/28 (50%) HR defective tumors do not have BRCA1/2 mutations or BRCA1 methylation, suggesting other mechanisms can also result in a HR defective phenotype. 28/64 (43%) of samples demonstrated the HR defective phenotype. In all cases HR status correlated with sensitivity to Rucaparib. Conclusion: As expected, deleterious BRCA2 mutations conferred a HRD phenotype in cells but methylation of BRCA1 was not universally associated with HRD. This may be as a result of only partial silencing of the gene by methylation and further work is required to identify thresholds of methylation which may predict HR status. The use of BRCA1/2 mutation testing alone is unlikely to identify the majority of HR defective ovarian tumors. Assessment of functional status of HRD is the preferred option and further technologies should be developed to simplify the Rad51 assay.
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Youssoufiän, H., A. Patel, D. Phillips, H. H. Kazazian, and S. E. Antonarakis. "RECURRENT MUTATIONS AND AN UNUSUAL DELETION IN HEMOPHILIA A." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644014.

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We have identified 15 mutations of the factor VIII (F8) gene from a panel of 107 patients with hemophilia A and have characterized these gene defects byrestriction analysis, oligonucleotide hybridization, cloning and DNA sequencing. Recurrent point mutations that involve CG to TG transitions were identified in exon 18, exon 22, and exon 24; a single CG to TG transition was identified in exon 23; and a CG to CA transition was identified in exon 24. In addition, a Taq I site alteration in intron 4 was identified in a patient with mild hemophilia, which arose dg. S23&in a grandpaternal germ cell. Cloning and sequencing of this region suggests the generation of a newsplice donor site. These data suggest that CG to TG transition is a prominent mechanism of mutation in hemophilia A. Six different deletions were also characterized. In one family, the deletion involved exon 26. However, the deletion endpoints in the male proband were different from those in his carrier mother, suggesting either gonadal mosaicism or a second deletion event in maternal meiosis.Of the 15 mutations, 6 occurred de novo within 2 generations: 4 in males and 2 in females. In these djg.novo mutations paternal age at conception was 35 (range = 32-38) and maternal age was 24 and 27. The ability to discover a sizable number of mutations in the F8 gene producing hemophilia A enables us to determine the frequency and nature of de novo mutations in man.
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Reports on the topic "Mutational mechanisms"

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Walsh, Tomas, and Mary-Claire King. WholeGenome Sequencing of High-Risk Families to Identify New Mutational Mechanisms of Breast Cancer Predisposition. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613308.

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Walsh, Tom, and Mary-Claire King. Whole Genome Sequencing of High-Risk Families to Identify New Mutational Mechanisms of Breast Cancer Predisposition. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613072.

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Petrosino, Joseph F. Mechanisms of Mutation in Non-Dividing Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada406067.

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Petrosino, Joseph F., and Susan Rosenberg. Mechanisms of Mutation in Non-Dividing Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada416708.

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Ponder, Rebecca, and Susan Rosenberg. Mechanism of Mutation in Non-Dividing Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396622.

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Ponder, Rebecca G., and Susan Rosenberg. Mechanism of Mutation in Non-Dividing Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada408728.

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Ponder, Rebecca G., and Susan Rosenberg. Mechanism of Mutation in Non-Dividing Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada418965.

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Splitter, Gary, and Menachem Banai. Microarray Analysis of Brucella melitensis Pathogenesis. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7709884.bard.

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Original Objectives 1. To determine the Brucella genes that lead to chronic macrophage infection. 2. To identify Brucella genes that contribute to infection. 3. To confirm the importance of Brucella genes in macrophages and placental cells by mutational analysis. Background Brucella spp. is a Gram-negative facultative intracellular bacterium that infects ruminants causing abortion or birth of severely debilitated animals. Brucellosis continues in Israel, caused by B. melitensis despite an intensive eradication campaign. Problems with the Rev1 vaccine emphasize the need for a greater understanding of Brucella pathogenesis that could improve vaccine designs. Virulent Brucella has developed a successful strategy for survival in its host and transmission to other hosts. To invade the host, virulent Brucella establishes an intracellular niche within macrophages avoiding macrophage killing, ensuring its long-term survival. Then, to exit the host, Brucella uses placenta where it replicates to high numbers resulting in abortion. Also, Brucella traffics to the mammary gland where it is secreted in milk. Missing from our understanding of brucellosis is the surprisingly lillie basic information detailing the mechanisms that permit bacterial persistence in infected macrophages (chronic infection) and dissemination to other animals from infected placental cells and milk (acute infection). Microarray analysis is a powerful approach to determine global gene expression in bacteria. The close genomic similarities of Brucella species and our recent comparative genomic studies of Brucella species using our B. melitensis microarray, suqqests that the data obtained from studying B. melitensis 16M would enable understanding the pathogenicity of other Brucella organisms, particularly the diverse B. melitensis variants that confound Brucella eradication in Israel. Conclusions Results from our BARD studies have identified previously unknown mechanisms of Brucella melitensis pathogenesis- i.e., response to blue light, quorum sensing, second messenger signaling by cyclic di-GMP, the importance of genomic island 2 for lipopolysaccharide in the outer bacterial membrane, and the role of a TIR domain containing protein that mimics a host intracellular signaling molecule. Each one of these pathogenic mechanisms offers major steps in our understanding of Brucella pathogenesis. Strikingly, our molecular results have correlated well to the pathognomonic profile of the disease. We have shown that infected cattle do not elicit antibodies to the organisms at the onset of infection, in correlation to the stealth pathogenesis shown by a molecular approach. Moreover, our field studies have shown that Brucella exploit this time frame to transmit in nature by synchronizing their life cycle to the gestation cycle of their host succumbing to abortion in the last trimester of pregnancy that spreads massive numbers of organisms in the environment. Knowing the bacterial mechanisms that contribute to the virulence of Brucella in its host has initiated the agricultural opportunities for developing new vaccines and diagnostic assays as well as improving control and eradication campaigns based on herd management and linking diagnosis to the pregnancy status of the animals. Scientific and Agricultural Implications Our BARD funded studies have revealed important Brucella virulence mechanisms of pathogenesis. Our publication in Science has identified a highly novel concept where Brucella utilizes blue light to increase its virulence similar to some plant bacterial pathogens. Further, our studies have revealed bacterial second messengers that regulate virulence, quorum sensing mechanisms permitting bacteria to evaluate their environment, and a genomic island that controls synthesis of its lipopolysaccharide surface. Discussions are ongoing with a vaccine company for application of this genomic island knowledge in a Brucella vaccine by the U.S. lab. Also, our new technology of bioengineering bioluminescent Brucella has resulted in a spin-off application for diagnosis of Brucella infected animals by the Israeli lab by prioritizing bacterial diagnosis over serological diagnosis.
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Dubeau, Louis. Mechanism of Ovarian Epithelial Tumor Predispostion in Individuals Carrying Germline BRCA1 Mutations. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada433994.

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Dubeau, Louis. Mechanism of Ovarian Epithelial Tumor Predisposition in Individuals Carrying Germline BRCA1 Mutations. Fort Belvoir, VA: Defense Technical Information Center, January 2006. http://dx.doi.org/10.21236/ada462015.

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