Relevant bibliographies by topics / NPM1 mutation

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  2. Dissertations / Theses
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Academic literature on the topic 'NPM1 mutation'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 February 2022

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Journal articles on the topic "NPM1 mutation"

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Huang, Min, Xinran Li, and Beverly S. Mitchell. "Cysteine 288 Regulates NPMc+ Cytoplasmic Localization and Sensitizes Leukemic Cells to Bortezomib-Induced Apoptosis Through a Redox-Sensitive Mechanism." Blood 120, no. 21 (2012): 532. http://dx.doi.org/10.1182/blood.v120.21.532.532.

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Abstract Abstract 532 Increasing evidence points to NPM1 mutations in exon 12 of the NPM1 gene (NPMc+) as a founder genetic event that defines a distinct leukemia entity accounting for approximately one-third of all AML. Unlike wild type NPM1, which resides predominantly in the nucleoli, NPMc+ mutants localize aberrantly in the leukemic-cell cytoplasm due to mutations at the C-terminus of NPM1. We have found that expression of NPMc+ in K562 and 32D cells sensitizes these cells to Bortezomib-induced apoptosis. Conversely, inducible small interfering RNA (shRNA)-induced knockdown of NPM1 in OCI-
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Lit, Benny Man Wai, Yok Lam Kwong, and Kit Fai Wong. "Immunohistochemical detection of cytoplasmic nucleophosmin in formalin-fixed paraffin-embedded marrow trephine biopsies in acute myeloid leukaemia." Journal of Clinical Pathology 69, no. 5 (2015): 409–14. http://dx.doi.org/10.1136/jclinpath-2015-203175.

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AimsNucleophosmin (NPM1) gene mutations resulting in cytoplasmic delocalisation of nucleophosmin (NPMc+) are the most common genetic abnormality in acute myeloid leukaemia (AML). In this study, we tested whether immunohistochemical (IHC) detection of cytoplasmic NPM1 (cNPM1) in formalin-fixed bone marrow trephine biopsies correlated with NPM1 mutations and the prognostic impact of NPM1 and fms-related tyrosine kinase 3-internal tandem duplication (FLT3-ITD) gene mutations was also assessed.MethodsA total of 71 Chinese adult de novo AML cases were evaluated for cNPM1 by IHC where the bone marro
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Chou, Wen-Chien, Shiu-Huey Chou, Ji-Shain Chiou, et al. "A “canonical” Npm1 mutation Knock-in Mouse Model Revealed Subtle but Definitive Myeloid Expansion with Poor HSC Niche Interaction." Blood 118, no. 21 (2011): 762. http://dx.doi.org/10.1182/blood.v118.21.762.762.

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Abstract Abstract 762 Nucleophosmin (NPM1) is a ubiquitous multifunctional phosphoprotein, which has nucleocytoplasmic shuttling activity. Somatic mutations in NPM1 gene result in cytoplasmic dislocation of NPM1 (NPM1c) and are frequently associated with acute myeloid leukemia (AML). The pathogenetic effects of mutated NPM1 protein have been explored by animal models including transgenic or “humanized” knock-in mouse models. Here, we demonstrate the first “canonical” mouse Npm1 mutant knock-in model. Different from the previously report of humanized NPM1 mutant knock-in model, we inserted TCTG
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Schnittger, Susanne, Wolfgang Kern, Claudia Tschulik, et al. "Minimal residual disease levels assessed by NPM1 mutation–specific RQ-PCR provide important prognostic information in AML." Blood 114, no. 11 (2009): 2220–31. http://dx.doi.org/10.1182/blood-2009-03-213389.

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Abstract Nucleophosmin (NPM1)–mutated acute myeloid leukemia (AML), which is recognized as a provisional entity in the World Health Organization 2008 classification of myeloid neoplasms, accounts for 30% of AML. We analyzed 1227 diagnostic and follow-up samples in 252 NPM1-mutated AML patients with 17 different NPM1 mutation–specific real-time quantitative polymerase chain reaction (RQ-PCR) assays. Paired diagnostic/relapse samples of 84 patients revealed stable NPM1 mutations in all cases, suggesting that they are pathogenetically early events and thus applicable for minimal residual disease
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Liso, Arcangelo, Filippo Castiglione, Antonio Cappuccio, et al. "One-Mutation Model Can Explain Age Incidence in AML Carrying Nucleophosmin (NPM1) Mutations." Blood 110, no. 11 (2007): 4312. http://dx.doi.org/10.1182/blood.v110.11.4312.4312.

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Abstract Acute myeloid leukemia (AML) carrying nucleophosmin (NPM1) mutations and cytoplasmic NPM (NPMc+ AML) accounts for about one-third of all AML patients, and exhibits distinctive biological and clinical features. The role of NPM1 mutations in leukemogenesis remains elusive. Mathematical models have been developed that, starting from cancer incidence data, allow to infer the somatic mutation rate, or the number of genetic events required to cause cancer. We collected data on age at diagnosis of AML patients from four centers in three different countries, and calculated age-specific rates
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Velu, Priya D., Chris C. S. Hsiung, Kiarash Salafian, Adam Bagg, Jennifer J. D. Morrissette, and Selina Luger. "Mutational Shift in FLT3 and NPM1-Positive Acute Myeloid Leukemia (AML) Relative to Therapy and Disease Progression." Blood 128, no. 22 (2016): 2866. http://dx.doi.org/10.1182/blood.v128.22.2866.2866.

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Abstract Introduction: Clonal myeloid malignancies such as AML are often characterized and treated based on specific mutation profiles identified at diagnosis. Routine use of clinical cancer next-generation sequencing (NGS) in diagnosis and disease monitoring has resulted in sequential mutation profiles of individual patients. On NGS profiling at interval follow-ups, mutations identified at diagnosis may change, or shift, through disease course. Here we track FLT3 and NPM1 mutations in the context of therapy, disease progression, clinical course, and pathology. Methods: Patients with AML or MD
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Zhang, Su-Jiang, Jianyong Li, and Yangli Han. "The Analysis of FLT3 and NPM1 Gene Mutations in Chinese Patients with Acute Myeloid Leukemia." Blood 114, no. 22 (2009): 4136. http://dx.doi.org/10.1182/blood.v114.22.4136.4136.

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Abstract Abstract 4136 Objective To investigate the frequency of nucleophosmin(NPM1) gene mutations and FLT3 mutations in Chinese patients with acute myeloid leukemia (AML) and its correlation with clinical feature and prognosis. Methods 123 first diagnosed AML patients were involved in our study. Polymerase chain reaction (PCR) combined with electrophoresis was directly used to detect FLT3-ITD mutations, PCR combined with EcoRV digestion was used to detect FLT3-TKD mutation, and PCR combined with directly sequencing was used to detect NPM1 mutations. Results (1) In the 123 first diagnosed AML
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Xu, Jie, Wu Zhang, Xiaojing Yan, et al. "NPM1 Mutation Contributes to Hematological Dysfunction By Disrupting H3K79 Methylation." Blood 128, no. 22 (2016): 2702. http://dx.doi.org/10.1182/blood.v128.22.2702.2702.

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Abstract NPM1 is one of the most frequent acquired mutated genes in acute myeloid leukemia (AML). Previous studies have shown that NPM1 mutation (NPMc+) established the distinctive gene expression signatures, which were associated with mixed lineage leukemia (MLL)-target genes, like MEIS1 and HOXA cluster. In AML carrying MLL fusion-oncoproteins, DOT1L-mediated histone 3 lysine 79 (H3K79) methylation is implicated in the regulation of MLL-target genes. Compared with MLL abnormalities, NPM1 variants preserve the similar transcriptional characteristics. However, whether NPM1 mutation could affec
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Oelschlaegel, Uta, Sina Koch, Markus Schaich, et al. "A Rapid Flow Cytometric Method for the Detection of NPM1 Mutated Patients with Acute Myeloid Leukemia (AML)." Blood 112, no. 11 (2008): 1490. http://dx.doi.org/10.1182/blood.v112.11.1490.1490.

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Abstract In about 30% of patients with AML the predominantly nucleolar protein nucleophosmin (NPM1) is dislocated into the cytoplasm (NPM1c), caused by mutations in exon 12 of the NPM1 gene. NPM1-mutations are associated with a specific subgroup of AML with particular clinical, cytogenetic, and prognostic characteristics, and NPM1-mutations are part of the new WHO classification, which makes the detection an important diagnostic aspect. Thus far, NPM1 mutations can be detected either using molecular techniques or immunocyto- or histochemistry. We reasoned that by the cytoplasmic dislocation, t
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Chauhan, Pradeep Singh, Rakhshan Ihsan, L. C. Singh, Dipendra Kumar Gupta, Vishakha Mittal, and Sujala Kapur. "Mutation of NPM1 and FLT3 Genes in Acute Myeloid Leukemia and Their Association with Clinical and Immunophenotypic Features." Disease Markers 35 (2013): 581–88. http://dx.doi.org/10.1155/2013/582569.

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Background.Mutations in NPM1 and FLT3 genes represent the most frequent genetic alterations and important diagnostic and prognostic indicators in patients with acute myeloid leukemia (AML).Objective.We investigated the prevalence and clinical characteristics of NPM1 and FLT3 mutations in 161 patients of de novo AML including adults and children.Results.NPM1 mutation was found in 21% and FLT3 mutation in 25% of the AML patients. Thirteen (8%) samples were positive for both NPM1 and FLT3/ITD mutations. Adult patients had significantly higher frequency of NPM1 mutation than children (25.8% versus
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Dissertations / Theses on the topic "NPM1 mutation"

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Seibl, Marlene. "Quantifizierung von minimaler Resterkrankung bei akuter myeloischer Leukämie mit NPM1 Mutation mittels Real-Time-PCR." Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-126943.

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Gille, Christine [Verfasser], and Karsten [Akademischer Betreuer] Spiekermann. "MRD-Monitoring bei AML-Patienten mittels Hochdurchsatz-Amplikonsequenzierung (NPM1 Mutation A) / Christine Gille ; Betreuer: Karsten Spiekermann." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2021. http://d-nb.info/1229835466/34.

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Jensen, Kai-Ole [Verfasser]. "Monitoring minimaler Resterkrankung (MRD) bei der akuten myeloischen Leukämie (AML) mit NPM1 Mutation / Kai-Ole Jensen." Ulm : Universität Ulm, 2016. http://d-nb.info/1110969465/34.

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Gourvest, Morgane. "Etude des longs ARNs non codants dans les leucémies aiguës myéloïdes : relevance clinique et caractérisation fonctionnelle." Thesis, Toulouse 3, 2020. http://www.theses.fr/2020TOU30117.

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Les longs ARNs non codants (lncRNAs) sont définis comme des transcrits ayant une taille supérieure à 200 nucléotides et dépourvus de potentiel codant. Longtemps considérés comme inutiles, leur étude récente a démontré qu’ils jouent un rôle important dans l’expression de nos gènes. On compte d’ailleurs de plus en plus d’exemples de ces lncRNAs dérégulés dans les cancers. Notre étude visait à évaluer l’existence de profils d’expression particuliers de lncRNAs au sein des leucémies aiguës myéloïdes à caryotype normal (LAM-CN), dont l’implication dans cette pathologie n’est que peu décrite. Le séq
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Lüker, Jakob [Verfasser]. "Nachweis von NPM1- und FLT3-Mutationen bei Patienten mit AML / Jakob Lüker." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2011. http://d-nb.info/1009752928/34.

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Leung, Siu-yung, and 梁小容. "NPM1 and FLT3-ITD mutations in cytogenetically normal acute myeloid leukaemia patients of Hong Kong." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44671143.

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Graul, Katja [Verfasser]. "Untersuchungen von NPM1-Mutationen bei Patienten mit akuter myeloischer Leukämie bei Diagnosestellung und im Verlauf / Katja Graul." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2014. http://d-nb.info/1057869686/34.

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Aydin, Isabella [Verfasser]. "Inzidenz und prognostische Bedeutung von NPM1-Mutationen bei der akuten myeloischen Leukämie des Erwachsenen: Analysen im Rahmen der AML HD98-A Studie / Isabella Aydin." Ulm : Universität Ulm. Medizinische Fakultät, 2014. http://d-nb.info/1052585922/34.

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Krebs, Bernhard Peter [Verfasser]. "Inzidenz und prognostische Bedeutung von Mutationen des Nucleophosmin (NPM1) Gens bei der akuten myeloischen Leukämie (AML) des älteren Patienten (> 60 Jahre) / Bernhard Peter Krebs." Ulm : Universität Ulm. Medizinische Fakultät, 2012. http://d-nb.info/1023728656/34.

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Dörr, Alexandra [Verfasser]. "Molekulargenetische Analysen zur Inzidenz von NPM1- und FLT3-Mutationen bei der akuten myeloischen Leukämie des älteren Patienten und Evaluation ihrer Bedeutung als prognostische Marker / Alexandra Dörr." Ulm : Universität Ulm, 2018. http://d-nb.info/1161008578/34.

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Books on the topic "NPM1 mutation"

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Sedel, Frédéric. Niemann-Pick Disease Type C. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0053.

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Niemann-Pick disease type C (NPC) is a fatal neurovisceral lipid storage disease of autosomal inheritance resulting from mutations in either the NPC1 (95% of families) or NPC2 gene. The encoded proteins appear to be involved in lysosomal/late endosomal transport of cholesterol, glycolipids, and other molecules, but their exact function is still unknown. The clinical spectrum of the disease ranges from a neonatal rapidly fatal disorder to an adult-onset chronic neurodegenerative disease characterized prominently by psychiatric disorders, cerebellar ataxia, cognitive decline, and vertical supran
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Book chapters on the topic "NPM1 mutation"

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Robetorye, Ryan S. "Acute Myeloid Leukemia with Recurrent Genetic Abnormalities, Part II: Mutations Involving CEBPA, NPM1, and RUNX1." In Molecular Pathology Library. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-62146-3_2.

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Zampieri, Stefania, Bruno Bembi, Natalia Rosso, Mirella Filocamo, and Andrea Dardis. "Treatment of Human Fibroblasts Carrying NPC1 Missense Mutations with MG132 Leads to an Improvement of Intracellular Cholesterol Trafficking." In JIMD Reports. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/8904_2011_49.

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"FLT3, NPM1, and CEBPA Mutations." In Diagnostic Pathology: Molecular Oncology. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-323-37678-5.50022-0.

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Bendari, Mounia, Nisrine Khoubila, Siham Cherkaoui, et al. "Current Cytogenetic Abnormalities in Acute Myeloid Leukemia." In Chromosomal Abnormalities. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.91425.

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Cytogenetic abnormalities are frequently reported in the literature describing the presence of chromosomal rearrangements in important cases of acute myeloid leukemia (AML); the rate can reach 50–60% of cases of AML. Cytogenetic abnormalities represent an important prognosis factor, their analysis is crucial for AML; cytogenetic study permits to classify prognostic groups and indicate the treatment strategy and helps to improve the outcome of these patients and to increase their chances of cure. Hundreds of uncommon chromosomal aberrations from AML exist. This chapter summarizes chromosomal abnormalities that are common and classifies AML according to the World Health Organization (WHO) classifications from 2008 to 2016; we will discuss briefly gene mutations detected in normal karyotype (NK) AML by cutting-edge next-generation sequencing technology, like FLT3-ITD, nucleophosmin (NPM1), CCAAT/enhancer-binding protein alpha (CEBPA), and other additional mutations.
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Conference papers on the topic "NPM1 mutation"

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Ragon, Brittany Knick, Issam S. Hamadeh, C. Greer Vestal, et al. "Abstract 1920: Response to hypomethylating agents based on cytidine deaminase expression, genetic polymorphisms, and NPM1 mutation status in acute myeloid leukemia." 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.am2020-1920.

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Li, Yanrong, Kai Wang, and Jingdong Zhang. "Abstract 1818: Activation of IGF-1R pathway and NPM-ALK G1269A mutation confer resistance to crizotinib in NPM-ALK positive lymphoma." 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.am2018-1818.

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Clara, Etienne De, Hanjing Ma, François Vergez, et al. "Abstract A27: Long noncoding RNA expression in cytogenetically normal acute myeloid leukemia identifies a distinct signature associated with NPM1 mutations." In Abstracts: AACR Special Conference on Noncoding RNAs and Cancer: Mechanisms to Medicines; December 4-7, 2015; Boston, MA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.nonrna15-a27.

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Ferrari, Anna, Cristina Papayannidis, Elisa Zuffa, et al. "Abstract 4906: TP53 mutations are mutually exclusive with FLT3 and NPM mutations in AML patients and are strongly associated with complex karyotype and poor outcome." 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.am2015-4906.

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Merlo, ME Boggio, M. Mallardo, G. De Conti, et al. "PO-272 Leukemia-associated NPM mutations promote quiescence of hematopoietic stem cells and prevent their functional exhaustion upon oncogene-induced hyper-proliferation." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.303.

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