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Dissertations / Theses on the topic 'TKIs resistance'

Author: Grafiati

Published: 24 May 2025

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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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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3

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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4

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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Mitchell, Rebecca. "Exploring BCR-ABL-independent mechanisms of TKI-resistance in chronic myeloid leukaemia." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/7977/.

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As the prevalence of Chronic Myeloid Leukaemia (CML) grows, due to the therapeutic success of tyrosine kinase inhibitors (TKI), we are witnessing increased incidences of drug resistance. Some of these patients have failed all currently licensed TKIs and have no mutational changes in the kinase domain that may explain the cause of TKI resistance. This poses a major clinical challenge as there are currently no other drug treatment options available for these patients. Therefore, our aim was to identify and target alternative survival pathways against BCR-ABL in order to eradicate TKI-resistant c

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Tarantino, Giuseppe <1991&gt. "NGS and medically-driven integrative bioinformatics applications in gastrointestinal stromal tumors to overcome the TKI resistance." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2020. http://amsdottorato.unibo.it/9270/1/tesi_GT.pdf.

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The complex molecular biology involved in gastrointestinal stromal tumors (GIST) progressive disease led to a growing urgency and interest in developing new strategies to overcome TKI resistance. In this study, we have used Next generation sequencing data and several bioinformatics approaches to investigate the GITS infiltrating immune-cell subpopulations and to perform an integrated molecular characterization of D842V mutant GIST, with the aim evaluating the potential of an anti-PD-L1 treatment in combination with tyrosine kinase inhibitors (TKI) and to identify new possible target. Gene expr

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7

Amin, Amit Dipak, Lingxiao Li, Soumya S. Rajan, et al. "TKI sensitivity patterns of novel kinase-domain mutations suggest therapeutic opportunities for patients with resistant ALK+ tumors." IMPACT JOURNALS LLC, 2016. http://hdl.handle.net/10150/617186.

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The anaplastic lymphoma kinase (ALK) protein drives tumorigenesis in subsets of several tumors through chromosomal rearrangements that express and activate its C-terminal kinase domain. In addition, germline predisposition alleles and acquired mutations are found in the full-length protein in the pediatric tumor neuroblastoma. ALK-specific tyrosine kinase inhibitors (TKIs) have become important new drugs for ALK-driven lung cancer, but acquired resistance via multiple mechanisms including kinase-domain mutations eventually develops, limiting median progression-free survival to less than a year

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8

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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9

Guérard, Marie. "Signalisation nucléaire de l'IGF-1R et résistance aux thérapies anti-EGFR dans les cancers du poumon." Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAV085/document.

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Responsable de 1,6 million de décès par an dans le monde, le cancer du poumon constitue aujourd’hui la première cause de mortalité par cancer. Les cancers bronchiques non-à-petites cellules représentent 85% des cancers du poumon et ont un pronostic vital très mauvais. Les EGFR-TKI (inhibiteurs de l’activité tyrosine kinase de l’EGFR, gefitinib) constituent un réel progrès thérapeutique pour le traitement des cancers du poumon. Cependant, ces traitements ne sont efficaces que dans un petit sous-groupe de patients. Un des enjeux actuels est donc d’identifier les mécanismes de résistance primaire

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10

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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11

Castelain, Lauriane. "Sphingosine kinase 1, transition épithélio-mésenchymateuse et résistance primaire aux inhibiteurs pharmacologiques de l'EGFR." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066595.

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Une transition épithélio-mésenchymateuse (TEM) et une expression élevée de la sphingosine kinase 1 (SPHK1) sont souvent observées dans les cancers. Notre étude du génome et du transcriptome d'adénocarcinomes pulmonaires (AP) montre que l'expression élevée de SPHK1 est en rapport, d'une part, avec des gains de la région incluant le locus SPHK1 et, d'autre part, avec une signature d'expression génique de TEM dans des tumeurs invasives. L'expression de SPHK1 est restreinte aux cellules tumorales. La surexpression de SPHK1 dans des cellules d'AP et l'exposition à son produit, la sphingosine-1-phos

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12

Castelain, Lauriane. "Sphingosine kinase 1, transition épithélio-mésenchymateuse et résistance primaire aux inhibiteurs pharmacologiques de l'EGFR." Electronic Thesis or Diss., Paris 6, 2016. http://www.theses.fr/2016PA066595.

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Une transition épithélio-mésenchymateuse (TEM) et une expression élevée de la sphingosine kinase 1 (SPHK1) sont souvent observées dans les cancers. Notre étude du génome et du transcriptome d'adénocarcinomes pulmonaires (AP) montre que l'expression élevée de SPHK1 est en rapport, d'une part, avec des gains de la région incluant le locus SPHK1 et, d'autre part, avec une signature d'expression génique de TEM dans des tumeurs invasives. L'expression de SPHK1 est restreinte aux cellules tumorales. La surexpression de SPHK1 dans des cellules d'AP et l'exposition à son produit, la sphingosine-1-phos

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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

Hernandez, Charlotte. "Contribution de la polarité cholinergique du système nerveux autonome à la pathogenèse de l’hépatocarcinome : implications en pharmacologie." Electronic Thesis or Diss., Lyon 1, 2024. http://www.theses.fr/2024LYO10175.

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Les fonctions du système nerveux autonome sont décrites depuis plusieurs décennies. Cependant, son rôle dans la biologie cellulaire des tissus innervés n’a fait que plus récemment l’objet d’un intérêt soutenu, en particulier en cancérologie. Les fibres afférentes et efférentes de ce système innervent les organes périphériques et contribuent au maintien de l’homéostasie de l’organisme. Elles sont impliquées dans les processus de développement, de réparation et de régénération. Tous ces phénomènes sont, de leur côté, documentés depuis longtemps comme étant associés au cancer. De nouvelles preuve

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15

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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16

Chen, Yi-Hung, and 陳依鴻. "The role of YTHDF3, a RNA m6A modification reader, in EGFR-TKIs resistance of lung adenocarcinoma." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/zpb5g5.

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17

Yun, Hsu, and 徐昀. "Crosstalk of EGFR-TKI resistance with stem cell signalling in lung cancer." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/xgwuf2.

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18

Hsu, Chia-Ying, and 徐嘉盈. "Identification of tumor suppressors and EGFR-TKI resistance genes by systemic approaches." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/13106465776843743598.

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博士<br>國立臺灣大學<br>醫學檢驗暨生物技術學研究所<br>104<br>Metastasis is a major cause of cancer-related death. Here, we identify a novel tumor suppressor gene, FAM198B, which has never been characterized in humans previously, by comparing the transcriptional profiles of a high metastatic lung adenocarcinoma cell line and its isogenic low metastatic cell line. The high expression of FAM198B was associated with favorable survival in lung adenocarcinoma patients. Enforced expression of FAM198B suppressed cell invasion, migration, mobility, proliferation and anchorage-independent growth in vitro and reduced tumor g

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19

Huang, Shih-Hsiang, and 黃士翔. "Role of AKT3 in EGFR-TKI Resistance of Non-Small Cell Lung Cancer." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/4z6m6t.

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碩士<br>國立臺灣大學<br>藥理學研究所<br>106<br>Lung cancer is the leading cause of cancer deaths worldwide, and EGFR-TKI is the first-line treatment for non-small cell lung cancer (NSCLC) harbouring EGFR activation mutation. However, most patients develop acquired resistance within 9–14 months. Therefore, it is critical to explore the mechanisms of drug resistance to improve treatment efficacy. Two resistant cells, HCC827/IR (IRESSA resistance) and H1975/AR (AZD9291 resistance) exhibiting EMT phenotypes were generated to investigate the molecular and cellular characteristics of the EGFR-TKI acquired resista

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20

Huang, Jheng-Cheng, and 黃正誠. "Investigation of the Wnt5a function in lung cancer and the correlation between Wnt5a and TKI-resistance." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/58314758765001959546.

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碩士<br>國立臺灣大學<br>病理學研究所<br>103<br>Lung cancer is the leading cause of cancer death. Some studies indicate that epidermal growth factor receptor (EGFR) mutation in Asian lung cancer cell of a substantial percentage. EGFR is a receptor tyrosine kinase that correlates with cell proliferation, growth, metastasis and survival in lung cancer. Currently, EGFR-TKI target therapy is specific for patients with exon 19 deletion or/and L858R mutations. EGFR-TKIs include the drugs Gefitinib (Iressa), Erlotinib (Tarceva) and Afatinib (Gilotrif). Gefitinib and Erlotinib are the first-generation reversible EGF

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21

Luo, Ping, and 羅平. "The role of HMGCR in colorectal cancer and the study of lncRNA in lung cancer TKI-resistance." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/16834146712359097988.

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22

Leow, Benjamin Chia Sing. "Multiple Molecular Mechanisms Contribute Towards In Vitro Resistance to Tyrosine Kinase Inhibitors in Chronic Myeloid Leukaemia." Thesis, 2019. http://hdl.handle.net/2440/121613.

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Resistance to therapeutic drugs is detrimental to treatment efficacy in chronic myeloid leukaemia (CML). CML is driven by the constitutive activity of the tyrosine kinase, Bcr-Abl, and has been treated effectively, in the majority of patients, using tyrosine kinase inhibitor (TKI) therapy. However, therapeutic TKI resistance often results in suboptimal treatment response. The molecular mechanisms of TKI resistance include: overexpression of Bcr-Abl; perturbed activity of cell membrane influx/efflux transporters; amino acid substitutions in the Bcr-Abl kinase domain precluding TKI binding (know

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23

Hsieh, Jia-Juan, and 謝佳娟. "Study of Mechanisms of Resistance to EGFR-TKI in Non-small Cell Lung Cancer with EGFR L858R Mutation." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/4q4af5.

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博士<br>國立臺灣海洋大學<br>生命科學暨生物科技學系<br>107<br>Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) are effective therapies for patients with non-small cell lung cancer (NSCLC) bearing EGFR mutations. It is reported that the response rate is 60-80% in Taiwan. Despite bearing EGFR active mutations, 20-40% of patients did not respond to TKIs. Moreover, in certain patients responding to TKIs initially, drug resistance will develop in 8-12 months after treatment. An acquired T790M mutation was detected in half of TKI-resistant tumors and the third-generation EGFR inhibitors, osimerti

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24

Huang, Kuo-Yen, and 黃國彥. "Characterization of the Small Compounds -T315 on EGFR Degradation in EGFR-TKI Resistant Lung Adenocarcinoma." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/cw66dg.

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博士<br>國防醫學院<br>生命科學研究所<br>104<br>ABSTRACT Several nature or synthetic small compounds can be helpful in improving the symptoms of diseases and treating patients. Post-translational modification (PTM) plays a vital role in various biological processes and disease progression such as cellular differentiation, signaling transduction, and protein stability and localization. Aberrant epidermal growth factor receptor (EGFR) signaling is one of the most critical oncogenic pathways in non-small-cell lung carcinoma (NSCLC) that triggers the tumor progression. However, suppression of the EGFR downstream

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25

Karasová, Dominika. "Molekulární mechanismy mutageneze a rezistence u buněčných linií CML." Master's thesis, 2018. http://www.nusl.cz/ntk/nusl-388488.

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Chronic myeloid leukemia is a clonal haematopoietic disease, with characteristic BCR-ABL1 fusion gene. Despite the significant improvement in patient treated with tyrosine kinase inhibitors (TKI), 20-30 % of patients develop resistance. One of the main causes of treatment failure are mutations in the BCR-ABL1 kinase domain (KD). The aim of this work was to elucidate the molecular mechanisms of resistance and mutagenesis development in CML using an in vitro CML model KCL-22. The main part of this work was focused on the identification of genes involved in DNA damage response and repair, that co

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"New insight of EGFR-TKI therapy in NSCLC: a novel treatment strategy and the mechanistic study of acquired resistance." 2015. http://repository.lib.cuhk.edu.hk/en/item/cuhk-1291849.

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Cheong, Hio Teng.<br>Thesis M.Phil. Chinese University of Hong Kong 2015.<br>Includes bibliographical references (leaves 127-139).<br>Abstracts also in Chinese.<br>Title from PDF title page (viewed on 16, November, 2016).

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Chen, Hsiao-Wei Tina. "Analysis of Signalling Network Consequent to FLT3 in AML Patients." Thesis, 2011. http://hdl.handle.net/1807/30545.

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The FMS-like tyrosine kinase 3- internal tandem duplication (FLT3/ITD) aberration is common in acute myeloid leukemia (AML) and associated with poor patient outcome. Inhibitors targeting FLT3/ITD are in development, but clinical responses are transient. This project focussed on elucidating molecular signalling consequences of FLT3/ITD inhibition, to identify rational drug combinations for future development. A Multicolour Phospho Flow Cytometry (MPFC) assay was developed to assess signalling events downstream of FLT3/ITD in primary patient samples, focusing on alterations in ERK, STAT5, Akt, a

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28

Caruso, Simona. "The pluripotency transcription factor Nanog plays a potential role as a BCR/ABL independent mechanism of TKI resistance in Chronic Myeloid Leukemia." Tesi di dottorato, 2017. http://www.fedoa.unina.it/11817/1/Tesi%20Simona%20Caruso%20Dottorato%20di%20ricerca%2029%C2%B0ciclo.pdf.

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Chronic Myeloid Leukemia (CML) is a clonal myeloproliferative disease characterized by a specific chromosomal translocation t(9;22) that gives rise to a fusion gene BCR-ABL1. The oncogenic product BCR-ABL1 is a constitutively active tyrosine kinase that promotes cell proliferation and inhibits apoptosis of the leukemic clone. In the era of target therapy, the treatment of CML patients in chronic phase (CML-CP) with tyrosine kinase inhibitors (TKIs) showed a substantially life expectancy improving. However, a large number of them develop drug intolerance or resistance and relapse after TKIs tre

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29

"Toward an Improved Chronic Myelogenous Leukemia Treatment: Blocking the Stem Cell Factor–Mediated Innate Resistance With Anti–c-Kit Synthetic-Antibody Inhibitors." Thesis, 2015. http://hdl.handle.net/10388/ETD-2015-03-1990.

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Chronic Myelogenous Leukemia (CML) is a blood cancer that arises when hematopoietic cells acquire an abnormal protein known as BCR-ABL. Current therapies for CML include drugs that inhibit BCR-ABL. However, these drugs only suppress the disease and do not cure it. One reason is that BCR-ABL drugs fail to kill the primitive population of CML cells, referred to as leukemia stem cells (LSCs), which are responsible for initiating and propagating CML. Since LSCs are not killed, the cancer is not cured and many affected patients eventually relapse. Recent studies suggest that LSCs are protected from

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