Relevant bibliographies by topics / Mutation-specific

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Mutation-specific'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Mutation-specific"

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Erdem-Eraslan, Lale, Ya Gao, Nanne K. Kloosterhof, et al. "Mutation specific functions of EGFR result in a mutation-specific downstream pathway activation." European Journal of Cancer 51, no. 7 (2015): 893–903. http://dx.doi.org/10.1016/j.ejca.2015.02.006.

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Kerem, Eitan. "Mutation specific therapy in CF." Paediatric Respiratory Reviews 7 (January 2006): S166—S169. http://dx.doi.org/10.1016/j.prrv.2006.04.213.

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Alderton, Gemma K. "Cancer mutation-specific immune responses." Nature Reviews Cancer 14, no. 6 (2014): 387. http://dx.doi.org/10.1038/nrc3763.

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Erdem-Eraslan, L., Y. Gao, N. Kloosterhof, et al. "CS-05 * MUTATION SPECIFIC FUNCTIONS OF EGFR RESULT IN A MUTATION-SPECIFIC DOWNSTREAM PATHWAY ACTIVATION." Neuro-Oncology 16, suppl 5 (2014): v52. http://dx.doi.org/10.1093/neuonc/nou242.5.

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Harper, P. S. "A specific mutation for Huntington's disease." Journal of Medical Genetics 30, no. 12 (1993): 975–77. http://dx.doi.org/10.1136/jmg.30.12.975.

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Schmid, Fabian, Esther Glaus, Frans P. M. Cremers, Barbara Kloeckener-Gruissem, Wolfgang Berger, and John Neidhardt. "Mutation- and Tissue-Specific Alterations ofRPGRTranscripts." Investigative Opthalmology & Visual Science 51, no. 3 (2010): 1628. http://dx.doi.org/10.1167/iovs.09-4031.

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von Deimling, Andreas, Felix Sahm, and David Capper. "Mutation specific antibodies: tool or dinosaur?" Oncotarget 3, no. 9 (2012): 907–8. http://dx.doi.org/10.18632/oncotarget.633.

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Heinen, Charlotte A., Aldo Jongejan, Peter J. Watson, et al. "A specific mutation inTBL1XR1causes Pierpont syndrome." Journal of Medical Genetics 53, no. 5 (2016): 330–37. http://dx.doi.org/10.1136/jmedgenet-2015-103233.

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Turchini, John, Juliana Andrici, Loretta Sioson, et al. "NRASQ61R Mutation-specific Immunohistochemistry is Highly Specific for Either NRASQ61R or KRASQ61R Mutation in Colorectal Carcinoma." Applied Immunohistochemistry & Molecular Morphology 25, no. 7 (2017): 475–80. http://dx.doi.org/10.1097/pai.0000000000000333.

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Ardicli, D., B. Konuskan, G. Haliloglu, M. Alikasifoglu, and H. Topaloğlu. "Nonsense mutation dystrophinopathy: How mutation-specific treatments changed our clinical practice?" Neuromuscular Disorders 25 (October 2015): S253. http://dx.doi.org/10.1016/j.nmd.2015.06.247.

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Dissertations / Theses on the topic "Mutation-specific"

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Lehman, Sarah, and Sarah Lehman. "Mutation-Specific Calcium Dysregulation in Hypertrophic Cardiomyopathy." Diss., The University of Arizona, 2018. http://hdl.handle.net/10150/626641.

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As the genetic causes of Hypertrophic Cardiomyopathy (HCM) have become widely recognized, considerable lag in the development of targeted therapeutics has limited interventions to symptom palliation. This is in part due to an oft-noted finding that similar point mutations within myofilament proteins are known to cause differential disease severity, highlighting the need to understand disease progression at the molecular level. One commonly described pathway in HCM progression is calcium homeostasis dysregulation, albeit little is understood about disruption of the pathway. This dissertation in
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Ibrahim, Daniel Murad. "ChIP-seq reveals mutation-specific pathomechanisms of HOXD13 missense mutations." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2015. http://dx.doi.org/10.18452/17102.

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Mutationen von Transkriptionsfaktoren (TF) betreffen nicht nur die Funktion des TFs, sondern auch die Expression seiner Zielgene und liegen häufig angeborenen Entwicklungsdefekten zugrunde. Über 20 Mutationen in HOXD13, einem TF der die Entwicklung der Extremitäten kontrolliert, sind bisher als Ursache verschiedenartiger Extremitätenfehlbildungen entdeckt worden. Eine molekularbiologische Grundlage für die Vielgestaltigkeit der HOXD13-Mutationen ist jedoch unbekannt. Die bisherigen Methoden zur funktionellen Charakterisierung von TF-Mutationen ermöglichten eine lediglich eingeschränkte Inte
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Kay, Christopher. "Population genetics and allele-specific silencing of the Huntington disease mutation." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/61761.

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Huntington disease (HD) is a devastating neurodegenerative disorder caused by an expanded CAG trinucleotide repeat in the huntingtin gene (HTT). A repeat of ≥36 CAG defines the HD mutation and is diagnostic in the presence of motor or psychiatric phenotypes. All patients have an expanded CAG repeat, usually inherited from an affected parent and heterozygous with a normal (≤35) CAG repeat allele. This thesis addresses numerous gaps in our understanding of the HD mutation at the population level, including heterozygote frequency, penetrance, ancestry, the de novo mutation rate, and haplotypes us
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Matsuo, Takashi. "Strain-Specific Manifestation of Lupus-like Systemic Autoimmunity Caused by Zap70 Mutation." Kyoto University, 2019. http://hdl.handle.net/2433/244498.

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Nowacki, Piotr Marek. "Design, development, and deployment of a locus specific mutation database : the PAHdb example." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0004/MQ44234.pdf.

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Willis, Brandon S. "Cell-type specific activation of a Protein Kinase A inhibitory mutation in mice /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/5053.

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King, Kathleen. "The Effect of R382W Mutation on Citrus paradisi Flavonol Specific 3-O-Glucosyltransferase." Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/honors/355.

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Flavonoids are a class of plant metabolites with C6-C3-C6 structure responsible for many biological functions, including coloration and defense. Citrus paradisi, grapefruit, contains a wide variety of flavonoids which are grouped by the extent of modification, examples of which are flavonols, flavones, and flavanones. A major modification is the addition of glucose by glucosyltransferases (GTs) to stabilize the structure and provide ease of transport. Glucosyltransferases can be highly substrate and regiospecific. With Cp3OGT, glucose is added at the 3-hydroxy position. This 3GT only accepts f
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King, Kathleen, Devaiah P. Shivakumar, and Cecelia A. McIntosh. "The Effect of R382W Mutation on C. paradisi Flavonol-Specific 3-O-Glucosyltransferase." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/358.

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Flavonoids are a class of plant metabolites with C6-C3-C6 structure responsible for many biological functions, including coloration and defense. Citrus paradisi, grapefruit, contains a wide variety of flavonoids which are grouped by the extent of modification, examples of which are flavonols, flavones, and flavanones. A major modification is the addition of glucose by glucosyltransferases (GTs) to stabilize the structure and provide ease of transport. This process can be highly substrate and regiospecific. With Cp3OGT, glucose is added at the 3-hydroxy position. This 3GT only accepts flavonols
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King, Kathleen, Devaiah P. Shivakumar, and Cecelia A. McIntosh. "Analysis of Impact of R382W Mutation on Substrate Specificity of Grapefruit Flavonol Specific 3-Glucosyltransferase." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/351.

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Flavonoids are a class of plant metabolites with a C6-C3-C6 structure. They are responsible for a large range of biological functions including UV protection, pigmentation, and anti-microbial properties. Citrus paradisi, the grapefruit, contains a wide variety of flavonoids, including the target flavonols which are characterized by a hydroxyl group at the C3 position. A glucose molecule is added to flavonols by 3-Oglucosyltransferases (3-O-GTs). C. paradisi F3-O-GT only glucosylates flavonols; however, Vitis vinifera (grape) 3-O-GT can accept both flavonols and anthocyanidins. The two enzymes
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Hung, Chun-hin, and 孔進軒. "Effect of novel Chinese specific presenilin-1 V97L mutation on intracellular calcium homeostasis in human neuroblastoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193533.

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Presenilin-1 (PS1) mutations caused by the PSEN1 gene mutations are the major cause of early onset familial Alzheimer’s disease (EOFAD). Two Chinesespecific EOFAD related PS1 mutations, V97L and A136G, have been found. Studies suggested that V97L mutation lead to the overexpression of Aβ42 and tau hyperphosphorylation, which are the major hallmarks of Alzheimer’s disease (AD), while properties of A136G were unclear. Since calcium dysregulation was suggested to play an important role in AD, the research project investigated if V97L and A136G mutations also lead to altered endoplasmic reticulum
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Books on the topic "Mutation-specific"

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Popova, Elmira, David Morton, Paul Damien, and Tim Hanson. Paternity testing allowing for uncertain mutation rates. Edited by Anthony O'Hagan and Mike West. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780198703174.013.8.

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This article discusses the use of probabilistic reasoning to analyse a disputed paternity case, where the DNA genotypes are compatible on all markers but one, allowing for the possibility of mutation, when the mutation rate is itself uncertain. It first describes the construction and Bayesian analysis of a suitable model for paternity testing, taking into account the potentially misleading effect of genetic mutation and allowing for mutation rate uncertainty, before introducing the simplest type of disputed paternity case. It then considers a specific disputed paternity case, in which an appar
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McPherson, M. J. Directed Mutagenesis: A Practical Approach (The Practical Approach Series). Oxford University Press, USA, 1991.

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McPherson, M. J. Directed Mutagenesis: A Practical Approach (Practical Approach Series). Oxford University Press, USA, 1991.

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J, McPherson M., ed. Directed mutagenesis: A practical approach. IRL Press, 1991.

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McPherson, M.J., (Ed.), ed. Directed Mutagenesis: A Practical Approach. I.R.L. P., 1991.

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Kerr, Bradley J. The link between an Nav1.7 mutation and erythromelalgia. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0081.

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The landmark paper discussed in this chapter is ‘Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons’, published by Dib-Hajj et al. in 2005. The voltage-dependent sodium channels Nav1.7, Nav1.8, and Nav1.9 have a restricted pattern of expression in sensory neurons in the periphery and are concentrated in small nociceptive neurons of the dorsal root ganglion, the trigeminal ganglion, and the nodose ganglion. In this paper, Dib-Hajj and colleagues studied a family with erythromelalgia (Weir Mitchell disease), an autosomal-dominant, inherited pain d
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Horsley, Alex. Genetics and pathophysiology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0001.

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This chapter describes the genetics and inheritance of CF. Different mutations have different effects on the CFTR protein, some leading to no CFTR being expressed at all and others to a poorly functioning variant. In the new era of mutation-specific therapies, the specific mutation expressed in a patient has important implications for their treatment.
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Kay, Chris, Emily Fisher, and Michael R. Hayden. Epidemiology. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0007.

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The prevalence and persistence of Huntington’s disease (HD) is crucially informed by the causative mutation. Diagnostic and predictive testing has enabled a new era of epidemiologic study of HD, whereby only those who carry an expanded CAG repeat are included in such measures. In Western populations, estimated prevalence of the disease is higher following the introduction of genetic testing, and prevalence may also be increasing in absolute terms. There are worldwide differences in the prevalence of HD by ethnicity and population, which may be accounted for in part by genetic diversity of the
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Simmonds, Nicholas, and Elaine Dhouieb. Management of stable CF lung disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0004.

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This chapter addresses the nuts and bolts of everyday management of CF lung disease. It outlines the most up-to-date recommendations to ensure lung function is optimised and remains as stable as possible, including all the latest specialist CF drugs and advancements in respiratory physiotherapy techniques. Topics covered include clinical and radiological assessments of lung disease; airway clearance techniques; inhaler device selection; inhaled therapies (including the new antibiotics and drugs targeting mucus production and clearance); oral antibiotics, including azithromycin; fungal treatmen
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Bosch, Annet M., and Elaine Murphy. Galactosemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0002.

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There are three known inherited disorders of galactose metabolism: classic galactosemia (galactose-1-phosphate uridyltransferase deficiency), galactokinase deficiency, and uridine diphosphate galactose 4-epimerase deficiency. Classic galactosemia presents in the newborn period with liver and renal impairment and failure to thrive. Acute symptoms resolve when lactose is excluded from the diet, but long-term complications are frequent and include neurocognitive and social difficulties, speech and language problems, motor problems, and premature ovarian insufficiency. Patients with galactokinase
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Book chapters on the topic "Mutation-specific"

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Zhang, Daqing, and Ling Wang. "Specific Dimension Stagnation Optimal Mutation of Particle Swarm Optimization Algorithm." In Recent Advances in Computer Science and Information Engineering. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-25789-6_4.

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Hane, James K., Angela H. Williams, Adam P. Taranto, Peter S. Solomon, and Richard P. Oliver. "Repeat-Induced Point Mutation: A Fungal-Specific, Endogenous Mutagenesis Process." In Fungal Biology. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-10503-1_4.

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Makita, Naomasa. "Phenotypic Overlap of Lethal Arrhythmias Associated with Cardiac Sodium Mutations: Individual-Specific or Mutation-Specific?" In Genes and Cardiovascular Function. Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-7207-1_18.

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Hofinger, Bernhard J., Owen A. Huynh, Joanna Jankowicz-Cieslak, and Bradley J. Till. "A Protocol for Benchtop Extraction of Single-Strand-Specific Nucleases for Mutation Discovery." In Biotechnologies for Plant Mutation Breeding. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45021-6_15.

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Aonuma, Hiroka, Athanase Badolo, Kiyoshi Okado, and Hirotaka Kanuka. "Detection of Mutation by Allele-Specific Loop-Mediated Isothermal Amplification (AS-LAMP)." In Methods in Molecular Biology. Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-535-4_10.

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Roque, Ashley M., and Antonio Omuro. "Emerging Meningioma Therapies I: Precision Medicine, Targeted Therapies, and Mutation-Specific Approaches." In Meningiomas. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-59558-6_14.

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Rosenthal, Susanne, Nail El-Sourani, and Markus Borschbach. "Impact of Different Recombination Methods in a Mutation-Specific MOEA for a Biochemical Application." In Evolutionary Computation, Machine Learning and Data Mining in Bioinformatics. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-37189-9_17.

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Rosenthal, Susanne, Nail El-Sourani, and Markus Borschbach. "Introduction of a Mutation Specific Fast Non-dominated Sorting GA Evolved for Biochemical Optimizations." In Lecture Notes in Computer Science. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-34859-4_16.

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Makanga, Juliet O., Antonius Christianto, and Tetsuya Inazu. "Allele-Specific Real-Time Polymerase Chain Reaction as a Tool for Urate Transporter 1 Mutation Detection." In Methods in Molecular Biology. Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2365-6_8.

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Wiseman, Daniel H., and Tim C. P. Somervaille. "Nanofluidic Allele-Specific Digital PCR Method for Quantifying IDH1 and IDH2 Mutation Burden in Acute Myeloid Leukemia." In Methods in Molecular Biology. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7142-8_15.

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Conference papers on the topic "Mutation-specific"

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Kämpjärvi, Kati, Nam Hee Kim, Min Ju Park, et al. "Abstract 4961: Functional analysis of prostate cancer-specific MED12 mutation." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4961.

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Tan, Lit Yeen, Elisa Mokany, Samantha Walker, Tina Lonergan, and Alison Todd. "Abstract 4910: Sensitive, specific and highly multiplexed mutation detection for cancer management." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4910.

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ENGIN, H. BILLUR, MATAN HOFREE, and HANNAH CARTER. "IDENTIFYING MUTATION SPECIFIC CANCER PATHWAYS USING A STRUCTURALLY RESOLVED PROTEIN INTERACTION NETWORK." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2014. http://dx.doi.org/10.1142/9789814644730_0010.

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Mao, Yong, Han Chen, Han Liang, Funda Meric-Bernstam, Gordon Mills, and Ken Chen. "Abstract 5148: CanDrA: Cancer-specific driver missense mutation annotation with optimized features." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5148.

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Tanaka, Hiroki, Masahiro Yamamoto, Kosuke Yamazaki, Keiko Shimizu, and Katsuhiro Ogawa. "Abstract 661: Establishment of transgenic mice with liver-specific BRAF V600E mutation." 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.am2016-661.

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Engin, H. Billur, Matan Hofree, and Hannah Carter. "ERRATUM: "Identifying Mutation Specific Cancer Pathways Using a Structurally Resolved Protein Interaction Network"." In Pacific Symposium on Biocomputing 2018. WORLD SCIENTIFIC, 2017. http://dx.doi.org/10.1142/9789813235533_errata01.

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Woodrick, Jordan, Suhani Gupta, Sanchita Sarangi, Sanjay Adhikari, and Rabindra Roy. "Abstract 1282: Sequence-specific repair of etheno-adenine at mutation hotspots in p53." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1282.

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Srivastava, Nishi, Alison Kurimchak, Carlos Montavez, Jonathan Chernoff, and James Duncan. "Abstract A34: Defining KRAS mutation-specific kinome signatures and vulnerabilities in colorectal cancer." In Abstracts: AACR Special Conference on Targeting RAS-Driven Cancers; December 9-12, 2018; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.ras18-a34.

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Litterst, CM, HB Tran, S. Chien, X. Chen, W. Wen, and A. Begovich. "Abstract P6-07-20: Allele-specific PCR assay for estrogen receptor (ESR1) mutation detection." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p6-07-20.

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Utro, Filippo, Kahn Rhrissorrakrai, Chaya Levovitz, et al. "Abstract 1509: Estimation of lesion-specific mutation shedding in cfDNA from rapid autopsy study." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1509.

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Reports on the topic "Mutation-specific"

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Puck, T. T. Measurement of mutation and repair in mammalian cells/action of specific mutagens and antimutagens/genome exposure reaction in cancer and other disease conditions. Final subcontract report, April 1, 1996- March 31, 1996. Office of Scientific and Technical Information (OSTI), 1996. http://dx.doi.org/10.2172/378934.

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