Relevant bibliographies by topics / Tyrosine kinom

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  1. Journal articles
  2. Dissertations / Theses
  3. Conference papers

Academic literature on the topic 'Tyrosine kinom'

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

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Journal articles on the topic "Tyrosine kinom"

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Bardelli, A. "Mutational Analysis of the Tyrosine Kinome in Colorectal Cancers." Science 300, no. 5621 (2003): 949. http://dx.doi.org/10.1126/science.1082596.

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Creeden, Justin F., Khaled Alganem, Ali S. Imami, et al. "Kinome Array Profiling of Patient-Derived Pancreatic Ductal Adenocarcinoma Identifies Differentially Active Protein Tyrosine Kinases." International Journal of Molecular Sciences 21, no. 22 (2020): 8679. http://dx.doi.org/10.3390/ijms21228679.

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Pancreatic cancer remains one of the most difficult malignancies to treat. Minimal improvements in patient outcomes and persistently abysmal patient survival rates underscore the great need for new treatment strategies. Currently, there is intense interest in therapeutic strategies that target tyrosine protein kinases. Here, we employed kinome arrays and bioinformatic pipelines capable of identifying differentially active protein tyrosine kinases in different patient-derived pancreatic ductal adenocarcinoma (PDAC) cell lines and wild-type pancreatic tissue to investigate the unique kinomic net
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Loriaux, Marc, Ross Levine, Jeffrey Tyner, et al. "High-Throughput Sequence Analysis of the Tyrosine Kinome in Acute Myeloid Leukemia." Blood 110, no. 11 (2007): 886. http://dx.doi.org/10.1182/blood.v110.11.886.886.

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Abstract Mutations that result in constitutive tyrosine kinase activation occur in a wide spectrum of human malignancies, including acute myeloid leukemia (AML). Although activating mutations in the tyrosine kinases FLT3 and c-KIT occur in a significant proportion of patients with AML, the genomic events responsible for oncogenic signaling in most patients with AML have not been identified. To determine whether other aberrantly activated tyrosine kinases contribute to the pathogenesis of AML, we employed high throughput (HT) DNA sequence analysis to screen the exons encoding domains implicated
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Tyner, Jeffrey W., Denise K. Walters, Stephanie G. Willis, et al. "RNAi screening of the tyrosine kinome identifies therapeutic targets in acute myeloid leukemia." Blood 111, no. 4 (2008): 2238–45. http://dx.doi.org/10.1182/blood-2007-06-097253.

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Despite vast improvements in our understanding of cancer genetics, a large percentage of cancer cases present without knowledge of the causative genetic events. Tyrosine kinases are frequently implicated in the pathogenesis of numerous types of cancer, but identification and validation of tyrosine kinase targets in cancer can be a time-consuming process. We report the establishment of an efficient, functional screening assay using RNAi technology to directly assess and compare the effect of individually targeting each member of the tyrosine kinase family. We demonstrate that siRNA screening ca
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Angus, Steven P., Timothy Stuhlmiller, Noah Sciaky, et al. "TBCRC 036: Window of opportunity clinical trial reveals adaptive kinome reprogramming in single and combination HER2-targeting in breast cancer (BrCa)." Journal of Clinical Oncology 35, no. 15_suppl (2017): 1027. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.1027.

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1027 Background: HER2 targeting is challenging due to heterogeneity in response and resistance. Adaptive kinome reprogramming (AKRP) is a resistance mechanism to kinase-targeted therapy (Rx) in TNBC ( Cancer Discovery2017). We studied AKRP in HER2+ BrCa by comparing transcriptome and kinome profiles before and after Rx with FDA-approved anti-HER2 drugs and combinations: trastuzumab (T), pertuzumab (P), T+P, or T+ lapatinib (T+L). Profiling was by RNA sequencing (RNAseq) and multiplexed inhibitor beads coupled with mass spectrometry (MIB/MS). MIB affinity-purification selectively enriches the f
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Ha, Jacqueline R., Peter M. Siegel, and Josie Ursini-Siegel. "The Tyrosine Kinome Dictates Breast Cancer Heterogeneity and Therapeutic Responsiveness." Journal of Cellular Biochemistry 117, no. 9 (2016): 1971–90. http://dx.doi.org/10.1002/jcb.25561.

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Tong, Jiefei, Mohamed Helmy, Florence M. G. Cavalli, et al. "Integrated analysis of proteome, phosphotyrosine-proteome, tyrosine-kinome, and tyrosine-phosphatome in acute myeloid leukemia." PROTEOMICS 17, no. 6 (2017): 1600361. http://dx.doi.org/10.1002/pmic.201600361.

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Tyner, Jeffrey W., Marc Loriaux, Stephanie G. Willis, et al. "RNAi Screening of the Tyrosine Kinome Identifies Therapeutic Targets in Leukemia Patients." Blood 112, no. 11 (2008): 758. http://dx.doi.org/10.1182/blood.v112.11.758.758.

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Abstract A large percentage of cancer cases present without knowledge of the causative genetic events. Tyrosine kinases are frequently implicated in the pathogenesis of cancer, but identification of specific tyrosine kinases as cancer targets has been a slow process. In the near future, whole-genome sequencing will enable vast amounts of sequence data to be collected, however clinical application of this information will require a detailed understanding of the functional consequences of each sequence change. Here, we present an RNAi-assisted protein target identification (RAPID) assay by which
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Tyner, Jeffrey W., Stephanie Willis, Michael W. N. Deininger, and Brian J. Druker. "RNAi Functional Screening of the Tyrosine Kinome Identifies Therapeutic Targets in Acute Myeloid Leukemia Patients." Blood 110, no. 11 (2007): 208. http://dx.doi.org/10.1182/blood.v110.11.208.208.

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Abstract A large percentage of cancer cases present without knowledge of the causative genetic events. Tyrosine kinases are frequently implicated in the pathogenesis of cancer, but identification of specific tyrosine kinases as cancer targets has been a slow process. Tyrosine kinases are thought to play a causative role in acute myeloid leukemia (AML), based in part on the high percentage of cases with phosphorylation of STAT5—a marker for activity of tyrosine kinase signaling. However, known abnormalities in tyrosine kinases in AML are restricted to internal tandem duplications of FLT3 or gen
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Loriaux, Marc M., Ross L. Levine, Jeffrey W. Tyner, et al. "High-throughput sequence analysis of the tyrosine kinome in acute myeloid leukemia." Blood 111, no. 9 (2008): 4788–96. http://dx.doi.org/10.1182/blood-2007-07-101394.

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Abstract To determine whether aberrantly activated tyrosine kinases other than FLT3 and c-KIT contribute to acute myeloid leukemia (AML) pathogenesis, we used high-throughput (HT) DNA sequence ana-lysis to screen exons encoding the activation loop and juxtamembrane domains of 85 tyrosine kinase genes in 188 AML patients without FLT3 or c-KIT mutations. The screen identified 30 nonsynonymous sequence variations in 22 different kinases not previously reported in single-nucleotide polymorphism (SNP) databases. These included a novel FLT3 activating allele and a previously described activating mut
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Dissertations / Theses on the topic "Tyrosine kinom"

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Schmachtenberg, Anna-Juliane. "Differentielle Expression des Tyrosin-Kinoms bei akuter lymphatischer Leukämie des erwachsenen Alters." Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19369.

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Tyrosinkinasen (TK) sind Schlüsselregulatoren der zellulären Signaltransduktion und beeinflussen Zellzyklus, Zellüberleben, Apoptose, Proliferation und Differenzierung. Die Dysregulation der TK-Aktivität trägt zur Entwicklung von Leukämie und anderen malignen Erkrankungen bei. So sind 25% der akuten lymphatischen Leukämien bei Erwachsenen (ALL) durch die BCR-ABL1-Translokation bedingt. Trotz intensiver Therapie beträgt das 5-Jahres-Überleben von erwachsenen Patienten mit ALL nur etwa 50 %. Als Alternative zu herkömmlichen Chemotherapeutika bietet der Einsatz von spezifisch wirkenden TK-Inhibit
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Hazen, Amy L. "Inositol phospholipid and tyrosine phosphorylation signaling in the biology of hematopoietic stem cells." [Tampa, Fla] : University of South Florida, 2009. http://digital.lib.usf.edu/?e14.2829.

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Schmachtenberg, Anna-Juliane [Verfasser], Kai [Gutachter] Matuschewski, Thomas [Gutachter] Burmeister, and Michael [Gutachter] Hummel. "Differentielle Expression des Tyrosin-Kinoms bei akuter lymphatischer Leukämie des erwachsenen Alters / Anna-Juliane Schmachtenberg ; Gutachter: Kai Matuschewski, Thomas Burmeister, Michael Hummel." Berlin : Humboldt-Universität zu Berlin, 2018. http://d-nb.info/1185578285/34.

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Mazed, Fetta. "Etude des mécanismes de résistance aux inhibiteurs de FLT3 dans les leucémies aigues myéloïdes." Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCC089.

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Les leucémies aiguës myéloïdes (LAM) constituent un groupe hétérogène d’hémopathies malignes résultant de la prolifération clonale d’un progéniteur myéloïde bloqué dans sa différenciation. De pronostic globalement défavorable, dépend de l’âge et de facteurs cytogénétiques et moléculaires. La mutation du gène FLT3 de type duplication en tandem du domaine juxta-membranaire (ITD : internal tandem duplication) est détectée dans 30% des échantillons de LAM, corrèle à une fréquence accrue de rechutes et à un pronostic défavorable. La mutation ITD conduit à une activation dérégulée et constitutive de
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Conference papers on the topic "Tyrosine kinom"

1

Bußmann, L., A. Münscher, K. Rothkamm, and K. Hoffer. "Kinom profiling of tyrosine kinases identifies Src-family kinases to be highly activated in HNSCC." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1639995.

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Puco, Katarina, Andliena Tahiri, Faris Naji, et al. "Abstract 2292: Tyrosine kinome profiling of renal cell carcinoma (RCC)." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2292.

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Rudd, Meghan L., Hassan Mohamed, Jessica C. Price, et al. "Abstract 5312: Mutational analysis of the tyrosine kinome in serous and clear cell endometrial cancers." 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.am2013-5312.

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Shelton, Abby, Erin Smithberger, Madison Butler, et al. "Abstract 331: Dynamic kinome targeting reveals kinases involved in acquired resistance to tyrosine kinase inhibitors in EGFR-driven glioblastomas." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-331.

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Shelton, Abby, Erin Smithberger, Madison Butler, et al. "Abstract 331: Dynamic kinome targeting reveals kinases involved in acquired resistance to tyrosine kinase inhibitors in EGFR-driven glioblastomas." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-331.

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Ichihara, Eiki, Joshua A. Bauer, Pengcheng Lu, et al. "Abstract 768: A kinome-wide siRNA screen identifies modifiers of sensitivity to the EGFR T790M-targeted tyrosine kinase inhibitor (TKI), AZD9291, in EGFR mutant lung adenocarcinoma." 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.am2015-768.

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