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Dissertations / Theses on the topic 'Tyrosine Kinase Inhibitors (TKIs)'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

Recondo, Gonzalo. "Resistance Mechanisms to ALK Tyrosine Kinase Inhibitors (TKIs) in NSCLC." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS248/document.

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Les analyses moléculaires et la classification des adénocarcinomes bronchiques ont conduit au développement de thérapies ciblées sélectives visant à améliorer le contrôle de la maladie et la survie des patients. ALK (anaplastic lymphoma kinase) est un récepteur tyrosine kinase de la famille des récepteurs de l'insuline. Des réarrangements chromosomiques impliquant le domaine kinase d’ALK sont présents dans environ 3 à 6% des patients atteints d'un adénocarcinome bronchique. La protéine de fusion provoque une activation du domaine kinase de manière constitutive et indépendante du ligand. Lorlat

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2

Grassi, Susanna. "BCR/ABL1-independent markers of resistance in patients affected by chronic myeloid leukemia (CML) receiving tyrosine kinase inhibitors (TKIs)." Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1073133.

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Chronic Myeloid Leukemia (CML) is a chronic myeloproliferative neoplasm derived from the neoplastic transformation of the pluripotent stem cell characterized by the reciprocal translocation between chromosome 9 (9q) and 22 (22q) t (9; 22) (q34; q11), which leads to the formation of a new BCR-ABL1 gene that causes expansion of the pathological clone. The introduction of tyrosine kinase inhibitor drugs (TKIs) has revolutionized the treatment of this neoplasm. However, about a third of patients have to suspend treatment for resistance or intolerance to TKIs. The aim of our study was to identify t

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3

SARONNI, DAVIDE. "TYROSINE KINASE INHIBITORS IN NEUROENDOCRINE TUMORS: FROM IN VITRO TO ZEBRAFISH MODEL." Doctoral thesis, Università degli Studi di Milano, 2022. http://hdl.handle.net/2434/917967.

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(1) Background: Neuroendocrine neoplasms (NENs) are a group of tumors that arise from neuroendocrine cells throughout the body, with the lungs and gastrointestinal tract being the most common sites of origin. In patients with NENs and distant metastases, surgery is generally not curative. Although well-differentiated and low-grade NENs, classified as neuroendocrine tumors (NETs), are usually less aggressive than poorly-differentiated NENs, they can develop distant metastases in about 15% of cases. These patients require chronic medical management. However, the clinical efficacy of these treatm

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4

DAMELE, LAURA. "Effect of tyrosine kinase inhibitors on NK cell and ILC3 dvelopment and function." Doctoral thesis, Università degli studi di Genova, 2020. http://hdl.handle.net/11567/996010.

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Tyrosin kinase inhibitors (TKI) sharply improved the prognosis of Chronic Myeloid Leukemia (CML) and of Philadelphia+ Acute Lymphoblastic Leukemia (Ph+ALL) patients. However, TKI are not curative because of the development of resistance and lack of complete molecular remission in the majority of patients. Clinical evidences would support the notion that patient’s immune system may play a key role in preventing relapses. In particular, increased proportions of terminally differentiated CD56+CD16+CD57+ NK cells have been reported to be associated with successful Imatinib therapy discontin

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5

Kangboonruang, Kitsada. "Neoplastic mast cells from patients with mastocytosis express AXL : effects on proliferation, apoptosis, and resistance to tyrosine kinase inhibitors." Electronic Thesis or Diss., Université Paris Cité, 2024. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=6722&f=79753.

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La mastocytose est une maladie rare et hétérogène, caractérisée par l'accumulation de mastocytes (MC) néoplasiques dans un ou plusieurs organes. L'Organisation Mondiale de la Santé (OMS) a classé la mastocytose en plusieurs variantes, dont la mastocytose cutanée (CM), limitée à la peau, la mastocytose systémique (MS), qui affecte la moelle osseuse et divers organes, ainsi que le sarcome mastocytaire (MCS), une tumeur localisée rare et agressive. La MS est ensuite subdivisée en MS non avancée (comprenant la MS indolente (ISM) et la MS à évolution lente (SSM)) et en MS avancées (AdvSM). L'AdvSM

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6

Aljohani, Hashim M. B. S. "Signaling Pathways Associated with Gefitinib Resistance in Glioblastoma Multiforme (GBM)." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406900804.

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7

Tonus, Francesca. "Sintesi e studio di sistemi polieterociclici a potenziale attività biologica." Doctoral thesis, Università degli studi di Padova, 2012. http://hdl.handle.net/11577/3425459.

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In the last decade, some progresses have been reached in the cancer treatment, mainly through the approval of novel key drugs based on the targeted therapy. In this respect, tyrosine kinases constitute one of the most relevant class of targets. Tyrosine kinases are key enzymes involved in the intracellular signal transduction and their up-regulation is often associated with cancer onset and progression. The tyrosine kinase inhibitors act mainly as ATP-mimic compounds. Despite the initial relevant clinical successes obtained through kinase inhibitor use, rapid drug resistance phenomena onset ha

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8

Russell, Kathy, Marion Slack, Janet Cooley, and Kelly Mathews. "Impact of a Specialty Pharmacy-Based Oral Chemotherapy Adherence Program on Patient Adherence." The University of Arizona, 2016. http://hdl.handle.net/10150/614015.

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Class of 2016 Abstract<br>Objectives: Patient medication adherence is a basic requirement for treating chronic myelogenous leukemia (CML) with oral tyrosine kinase inhibitors (TKIs). When imatinib adherence rates are less than 80 or 90 percent, major and complete molecular responses, respectively, do not happen. The purpose of this study was to determine the effect of a real-time medication monitoring (RTMM) reminder system adherence program on the medication possession ratio (MPR). Methods: This analytic study was a retrospective cohort study and used data extracted from chart reviews for pa

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9

Choi, Ho-ying, and 蔡可盈. "Review of clinical benefits and cost effectiveness of epidermal growthfactor receptor-tyrosine kinase inhibitor (EGFR-TKI) as first linetreatment for patients with advanced non-small cell lung cancer(NSCLC)." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46935320.

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10

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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11

Glauche, Ingmar, Matthias Kuhn, Christoph Baldow, et al. "Quantitative prediction of long-term molecular response in TKI-treated CML – Lessons from an imatinib versus dasatinib comparison." Macmillan Publishers Limited, part of Springer Nature, 2018. https://tud.qucosa.de/id/qucosa%3A32495.

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Longitudinal monitoring of BCR-ABL transcript levels in peripheral blood of CML patients treated with tyrosine kinase inhibitors (TKI) revealed a typical biphasic response. Although second generation TKIs like dasatinib proved more efficient in achieving molecular remission compared to first generation TKI imatinib, it is unclear how individual responses differ between the drugs and whether mechanisms of drug action can be deduced from the dynamic data. We use time courses from the DASISION trial to address statistical differences in the dynamic response between first line imatinib vs. dasatin

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12

Sørum, Christopher. "Synthesis of new tyrosine kinase inhibitors." Thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for kjemi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-6863.

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13

Sahin, Katherine B. "Evaluation of cell division cycle associated protein 3 (CDCA3) as a novel prognostic/therapeutic target for EGFR-mutant non-small cell lung cancer." Thesis, Queensland University of Technology, 2022. https://eprints.qut.edu.au/231468/1/Katherine_Sahin_Thesis.pdf.

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This thesis defined a unique role for the protein cell division cycle associated protein-3 (CDCA3) in epidermal growth factor receptor (EGFR) mutant non-small cell lung cancer (NSCLC). This thesis has established an association between the levels of CDCA3 expression and the tumour response to tyrosine kinase inhibitors (TKI), which are the front-line therapy for EGFR-mutant NSCLC. In this disease, CDCA3 functions to modulate cellular growth pathways to impact sensitivity towards TKI therapy. Future work might enable development of a clinical stratification tool to discern TKI responsive from n

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14

Rothe, Tino. "Anwendung mathematischer Modelle zur Vorhersage des Therapieverlaufs von CML-Patienten." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2018. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-231508.

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Hintergrund Die chronische myeloische Leukämie (CML) ist eine myeloproliferative Er- krankung, die aufgrund ihres Modellcharakters unter der Behandlung mit Tyrosin-Kinase- Inhibitoren (TKI) gut für eine Beschreibung mittels computerbasierter Modelle geeignet ist. Grundlage für die Entstehung einer CML ist die Bildung eines Philadelphia-Chromosoms durch eine Translokation der Chromosomen 9 und 22. Es resultiert das Onkogen BCR- ABL1, welches für eine konstitutiv aktive Tyrosinkinase codiert. Diese führt zu ungeregelter Proliferation der betroffen Zellen und zur Verdrängung der gesunden Blutbild

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15

McHugh, Lynsey A. "Tyrosine kinase inhibitors as adjuncts to chemotherapy in bladder cancer." Thesis, University of Leicester, 2007. http://hdl.handle.net/2381/29860.

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16

Walter, Harriet Sarah. "Studies of Bruton's tyrosine kinase inhibitors in B-cell malignancies." Thesis, University of Leicester, 2018. http://hdl.handle.net/2381/42887.

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Despite significant advances, the prognosis in relapsed/refractory (R/R) B-cell malignancies remains poor. In the Phase I study of the selective Bruton’s Tyrosine Kinase inhibitor (BTKi) tirabrutinib in R/R B-cell malignancies, I showed that targeting BTK demonstrated remarkable clinical responses and tolerability in Chronic Lymphocytic Leukaemia and Mantle Cell Lymphoma. Targeted DNA sequencing demonstrated that no mutations were associated with a lack of response in CLL. However, in activated B-cell like diffuse large B-cell lymphoma (ABC DLBCL), only 35% of patients responded to treatment a

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17

Jeannot, Victor. "Identification et vectorisation de combinaisons de traitements pour la thérapie des tumeurs pulmonaires résistantes aux inhibiteurs de tyrosine kinase de l'EGFR." Thesis, Université Grenoble Alpes (ComUE), 2015. http://www.theses.fr/2015GREAV061/document.

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Responsable d'environ 30000 décès/an en France, le cancer du poumon est un problème de santé publique majeur. Un des enjeux actuels est d'adapter le traitement du cancer du poumon pour proposer des thérapeutiques ciblées plus efficaces et moins agressives. Les inhibiteurs de l'activité tyrosine kinase du récepteur de l'EGF (EGFR-TKI, gefitinib et erlotinib) constituent un réel progrès pour le traitement des cancers du poumon. Cependant, des mécanismes de résistance ont été décrits et des traitements combinés de thérapies ciblées avec des EGFR-TKI pourraient permettre de surmonter les résistanc

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18

Luzac, Michal Leonie. "Small Molecules as Potential Inhibitors of the Met Tyrosine Kinase Receptor." Thesis, University College London (University of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498510.

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19

Myers, Samuel Harry. "Development of novel receptor tyrosine kinase inhibitors by a chemocentric approach." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28769.

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In recent years, there has been a major movement in the pharmaceutical industry towards the development of molecules that selectivity inhibit a previously-validated specific target. This is referred to as target-based drug discovery. It was hoped that adopting this approach would usher in a new golden age of drug discovery. However, this has not been the case, with issues arising such as the target’s mechanism of action being poorly understood, with it not playing the expected role in the disease progression, or feedback resistance mechanisms causing the target to lose its role in the disease.

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20

Cooper, Margaret S. "Anti-cancer peptides containing modified tyrosine residues." Thesis, University of Nottingham, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246193.

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21

Dominguez-Escrig, J. L. "Tyrosine kinase and prenyl transferase inhibitors as potential therapeutics in urothelial carcinoma." Thesis, University of Newcastle upon Tyne, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427275.

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22

Francis, Sebastian. "Factors affecting the response to tyrosine kinase inhibitors in chronic myeloid leukaemia." Thesis, University of Liverpool, 2015. http://livrepository.liverpool.ac.uk/2050461/.

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Chronic myeloid leukaemia (CML) is a clonal stem cell disorder characterised by the Philadelphia chromosome. The treatment and outcomes of CML patients have improved with the introduction of tyrosine kinase inhibitors (TKI). Imatinib is associated with complete cytogenetic response (CCR) rate of 71% at 12 months, as documented by large phase 3 clinical trials. I carried out a large population study in the Merseyside, Cheshire and North Wales area, which showed a maximal CCR rate of 65% over 5 years of observation. This suggests there is a higher rate of imatinib failure in a general unselected

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23

Reiff, Sean. "Utilizing Reversible Bruton’s Tyrosine Kinase Inhibitors to Circumvent Acquired Resistance to Ibrutinib." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1523372591057698.

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24

D'Cunha, Ronilda Raymond. "Treatment strategies to reverse efflux transporter-mediated resistance to Tyrosine kinase inhibitors." Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6563.

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Multidrug resistance (MDR), a phenomenon in which tumors that were initially sensitive, recur and start showing resistance not only to the initial chemotherapeutic agent but also to various anticancer drugs that are structurally and functionally different from the initial drug, constitutes one of the main reasons for the failure of chemotherapy. An important mechanism of MDR is the enhanced cellular efflux of anticancer agents due to an overexpression of ATP-binding cassette (ABC) transporters (i.e. efflux transporters), especially P-glycoprotein (Pgp), Multidrug Resistance-associated Protein

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25

Bibi, Siham. "Nouvelles approches thérapeutiques au cours des mastocytoses systémiques avancées KIT D816V+ résistantes aux inhibiteurs de tyrosine kinases." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS551.

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Les mastocytoses systémiques (SM) constituent un groupe hétérogène de maladies rares, caractérisées par l’accumulation anormale de mastocytes malins dans la moelle osseuse et dans d’autres organes extra-cutanés. La majorité des patients avec SM ont une mutation activatrice du gène KIT, le plus souvent la mutation KIT D816V, retrouvée chez plus de 90% de tous les patients. Cette mutation induit l’activation constitutive du récepteur KIT en déclenchant de façon aberrante une cascade de voies de signalisation, dont la voie PI3K/AKT et JAK/STAT5, aboutissant à l’inhibition de l’apoptose et à l’aug

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26

Dillon, Anne M. R. "An investigation of protein tyrosine phosphorylation in equine blood platelets." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390250.

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27

Knights, Victoria E. E. "Tumour cell responses to novel fibroblast growth factor receptor (FGFR) tyrosine kinase inhibitors." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608393.

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28

Filho, Pedro Aurio Maia. "Genotoxicity and mutagenicity in patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors." Universidade Federal do CearÃ, 2017. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=19044.

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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico<br>Chronic myelogenous leukemia (CML) is a myeloproliferative disease of hematopoietic stem cells, characterized by the presence of the Philadelphia (Ph) chromosome, originating from a reciprocal translocation between the long arms of chromosomes 9 and 22, forming the gene BCR-ABL, which encodes a BCR-ABL oncoprotein with constitutive tyrosine kinase activity. The clinical course of CML is often divided into three phases: chronic, accelerated, and blast. The treatment of choice for the chronic phase is the first-generation tyrosine

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Gregory, T., and John Bossaer. "Pharmacogenomics Guided Dosing of Tyrosine Kinase Inhibitors in a Patient with Renal Cell Carcinoma." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/7796.

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Cytochrome P450 (CYP) enzymes play a crucial role in the human body. These enzymes are responsible for the synthesis of steroid hormones and cholesterol, as well as the metabolism of external substances such as medications. While more than 50 CYP enzymes have been identified, just 6 are credited with metabolizing most drugs. Of note is CYP 3A4, which metabolizes ~34% of medications that use the CYP enzyme system. CYP enzymes are polymorphic, meaning there are different versions of the same enzyme; therefore there is variability from individual to individual in their ability to metabolize medic

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30

Johnston, Rosie Arwen. "Implications of interactions between tyrosine kinase inhibitors and human solute carriers in cancer therapy." Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/10522.

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Members of the solute carrier (SLC) family of transporters govern the cellular influx of a multitude of endogenous compounds, xenobiotics and drugs. SLCs including organic anion transporting polypeptide (OATP) 1A2 (SLCO1A2), OATP1B3 (SLCO1B3) and organic cation transporter (OCT) 1 (SLC22A1) participate in the disposition of several anticancer drugs, such as the tyrosine kinase inhibitor (TKI) imatinib. Some of these agents may elicit drug-drug interactions (DDIs) during therapy, so the accumulation of pharmacokinetic data concerning TKIs is of clinical interest. In this project, the impact o

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Contini, A. "Synthesis, in silico and pharmacological evaluation of 2-pyridin-acetamides as tyrosine kinase inhibitors." Doctoral thesis, Università degli Studi di Milano, 2003. http://hdl.handle.net/2434/174341.

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A new synthesis of 2-pyridineacetamides was developed starting from pyran-2-one N-functionalized amidines. Secondary amines reacted in a sealed tube with the above-mentioned amidines and, by nucleophilic attack on pyran-2-one nucleus and thermal rearrangement, afforded exclusively the desired 2-pyridineacetamide derivatives. Such compounds have been pharmacologically tested on smooth muscular cells proliferation and resulted active with an IC50 ranging from 40 to 0.7 µM. With the aid of molecular modeling tools a potential mechanism of action has been proposed. The pharmacological acti

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32

Junker, Bernd. "Lokale Therapie der Sauerstoff-induzierten angioproliferativen Retinopathie im Mausmodell small molecule receptor tyrosine kinase inhibitors /." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=971428387.

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33

Abe, Mineo. "Development of peptide inhibitors of the receptor tyrosine kinase activity in a novel inhibitory mechanism." 京都大学 (Kyoto University), 2010. http://hdl.handle.net/2433/120515.

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34

Nuseibeh, Samir. "Modulation of mucin expression in respiratory epithelial cells : effect of ErbB receptor tyrosine kinase inhibitors." Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/8229.

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Secretion of mucins (e.g. MUC5AC) by the airway epithelium into the respiratory tract mucus layer is an important homeostatic mechanism which safeguards the lung from invasive pathogens and harmful particles. Airway mucus hypersecretion features in the pathophysiology of inflammatory-based airway diseases such as chronic obstructive pulmonary disease (COPD) and asthma. Signalling of the ErbB receptor tyrosine kinase subfamily, particularly the ErbB1 and ErbB2 receptor subtypes, has been implicated in the process of airway mucus hypersecretion, and upregulation of ErbB1 receptor occurs in the l

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Hähnel, Tom, Christoph Baldow, Joëlle Guilhot, et al. "Model-based inference and classification of immunological control mechanisms from TKI cessation and dose reduction in CML patients." American Association for Cancer Research (AACR), 2020. https://tud.qucosa.de/id/qucosa%3A74320.

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Recent clinical findings in chronic myeloid leukemia (CML) patients suggest that the risk of molecular recurrence after stopping tyrosine kinase inhibitor (TKI) treatment substantially depends on an individual’s leukemia-specific immune response. However, it is still not possible to prospectively identify patients that will remain in treatment-free remission (TFR). Here, we used an ordinary differential equation (ODE) model for CML, which explicitly includes an anti-leukemic immunological effect and applied it to 21 CML patients for whom BCR-ABL1/ABL1 time courses had been quantified before an

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Aljohani, Hashim M. "Targeting Tyrosine Kinase Drug Resistance Mechanisms and Metastatic Pathways in Brain Tumors." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1595846160285645.

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Lella, Divya Jyothi. "Functionalization and Modification of Naphthaquinone Analogs as HER2 Kinase Inhibitors." TopSCHOLAR®, 2014. http://digitalcommons.wku.edu/theses/1325.

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HER2 overexpression in breast cancer tumors predicts lower overall survival. Because of the aggressive nature of HER2 tumors and the association with metastatic disease, the HER2 receptor holds great promise as a therapeutic target in metastatic breast cancer. We are developing small molecule inhibitors that bind to the ATP binding site of the tyrosine kinase domain in order to inhibit tyrosine auto-phosphorylation. This process controls biological pathways that mediate the cell growth. In normal cells this process is highly controlled. We are targeting the modification of the side chain of th

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Broadbridge, Robert James. "Design and synthesis of novel inhibitors to the SH2 domain of the protein tyrosine kinase p56lck." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.494712.

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Grockowiak, Élodie. "Role of the Bone Morphogenetic Proteins pathway in tyrosine kinase inhibitors resistance in Chronic Myeloid Leukemia." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1253.

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La leucémie Myéloïde Chronique est un néoplasme myéloprolifératif causé par l'expression de la kinase oncogène BCR-ABL. Les Inhibiteurs de Tyrosine Kinase (ITK) spécifiques de BCR-ABL ont révolutionné la prise en charge de la maladie. Les ITK ne sont cependant pas curatifs ; en effet, certaines cellules souches leucémiques (CSL) sont résistantes aux ITK, et persistent dans la moelle osseuse des patients même en rémission prolongée. Ces CSL sont probablement responsables de la rechute chez 60% de ces patients après arrêt des ITK. 30% des patients développent une résistance aux ITK via des mécan

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40

Šramel, Peter. "A synthesis and biological screening of predicted inhibitors of Tyrosine Kinases, e.g. KDR, designed in silico." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAF064.

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Les protéines kinases représentent le groupe d'enzymes qui servent d'intermédiaire pour la phosphorylation de protéines - le transfert d'un groupe phosphate de l'adénosine triphosphate(ATP) sur des chaînes latérales correspondantes de tyrosine, de serine ou de thréonine des acides aminées. La phosphorylation de protéines est un des outils les plus importants pour la régulation de l'activité cellulaire. La « signalisation » cellulaire par le récepteur de tyrosine kinase VEGFR2 (KDR) appartient aux réactions biochimiques clés influençant la croissance de tumeurs. L'inhibition thérapeutique de ce

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Atatreh, Noor Aldeen S. A. "Design, synthesis and evaluation of inhibitors for Src tyrosine kinase and their impact on colorectal cancer cells." Thesis, University of Manchester, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492836.

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Colorectal cancer is the highest cause of cancer-related death in the West. c-Src protein levels are elevated in colon cancer cells compared to non-malignant cells, In addition, Src signalling and transduction are directly involved in cell growth, cell cycle, malignant transformation and cell migration, providing opportunities for inhibition of Src.

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Rogers, Susanne Jane. "Towards the Mechanistic Effects of Tyrosine Kinase Inhibitors in Squamous Cell Carcinoma of the Head and Neck." Thesis, Institute of Cancer Research (University Of London), 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516267.

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Bhosle, J. "Modulation of DNA strand break induction and repair by tyrosine kinase inhibitors targeted against EGFR and HER2." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1344180/.

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Purpose: The human epidermal growth factor receptors EGFR (erbB1) and HER2 (erbB2/neu) are involved in mediating resistance to chemotherapy and ionising radiation (IR). In vitro studies demonstrate that small molecule tyrosine kinase inhibitors (TKIs) which target these receptors can increase the effectiveness of DNA damaging agents. However, these combinations have failed to produce the clinical results anticipated and one potential explanation is that the inhibition of EGFR and HER2 cell signalling pathways by TKIs is short lived, with cells able to switch to alternative mechanisms of signal

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44

Kolli, Kaouther. "Rôle de la protéine FAK (Focal Adhésion Kinase) dans les mécanismes d'invasion cellulaire." Thesis, Strasbourg, 2012. http://www.theses.fr/2012STRAJ003.

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Cette thèse traite du rôle de la protéine FAK (Focal Adhésion Kinase) dans les mécanismes d'invasion cellulaire<br>This thesis is about the role of the protein FAK (Focal Adhesion Kinase) in the cellular mechanisms of invasion

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Roos, Kelly. "The effect of sunitinib on neuroblastoma and glioblastoma cell growth." University of the Western Cape, 2020. http://hdl.handle.net/11394/7952.

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Magister Scientiae (Medical Bioscience) - MSc(MBS)<br>Cancer is a global health catastrophe, with neuroblastoma, the most common solid childhood tumor, and glioblastoma, a deadly brain tumor, being aggressive and unresponsive to current treatment modalities. These tumors are known to utilize uncontrollable cell proliferative capabilities as a mechanism for tumor survival. Therefore, malignant cell growth can be mitigated by targeting the essential proteins that regulate cell growth, such as receptor tyrosine kinases (RTKs). Under normal physiological conditions, RTKs bind with varying affinity

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Saleem, Mohammed Umer. "Preclinical evaluation of pharmacological strategies designed to enhance the activity of established and novel anti-cancer drugs : synopsis - evaluation of pharmacological strategies designed to modulate the Warburg effect, enhance the activity of tyrosine kinase inhibitors and novel analogues of Temozolomide." Thesis, University of Bradford, 2014. http://hdl.handle.net/10454/13842.

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Whilst progress has been made in reducing mortality in some cancers, mortality rates remain high in many cancers and there is a need to develop novel therapeutic strategies. In this thesis, various pharmacological strategies designed to enhance the activity of existing therapeutic drugs were evaluated. Cancer cells are dependent upon aerobic glycolysis (the Warburg effect) and glutamine uptake. Using clinically approved tyrosine kinase inhibitors and Bortezomib, significant enhancement of chemosensitivity was observed when used in combination with inhibitors of lactate dehydrogenase (Gossypol)

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Shor, Audrey Cathryn. "Src kinase inhibitors for the treatment of sarcomas : cellular and molecular mechanisms of action." [Tampa, Fla] : University of South Florida, 2007. http://purl.fcla.edu/usf/dc/et/SFE0001906.

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Graf, Michael Georg Eduard. "Inhibition of ErbB2 by receptor tyrosine kinase inhibitors causes myofibrillarstructural damage without cell death in adult rat cardiomyocytes /." [S.l.] : [s.n.], 2009. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Skoglund, Karin. "Influence of CYP3A enzymes and ABC transporters on the activity of tyrosine kinase inhibitors in chronic myeloid leukemia." Doctoral thesis, Linköpings universitet, Avdelningen för läkemedelsforskning, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-97427.

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The introduction of imatinib, a tyrosine kinase inhibitor (TKI), in the treatment of chronic myeloid leukemia (CML) was a major break-through and the first drug that was successfully designed to target the specific mechanism of a malignant disease. Imatinib still remains as the standard treatment of newly diagnosed CML patients although a second generation of TKIs has also been approved for first-line CML treatment. Most patients achieve a good therapeutic effect with imatinib, but some patients are resistant to the drug and are at greater risk of disease progression. In order to further impro

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Lou, Qiang 1962. "Identification of peptide substrates and development of pseudosubstrate-based peptide inhibitors for p60(C-SRC) protein tyrosine kinase." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/282230.

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Protein tyrosine kinases (PTKs) mediate important signaling events associated with cellular growth, differentiation, and mitogenesis. The p60c-src protein is the first described cellular protein tyrosine kinase. Human p60c-src PTK has been implicated in the development of colon and breast cancer, and leukemia. However, the exact physiological role of p60c-src PTK or its physiological target proteins are not well known, and the mechanism by which the p60c-src PTK activity is regulated is not completely understood. Peptide substrates can be used to determine the substrate specificity and kinetic

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