Relevant bibliographies by topics / TKIs resistance

Contents

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

Academic literature on the topic 'TKIs resistance'

Author: Grafiati
Published: 24 May 2025
Last updated: 31 July 2025

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Journal articles on the topic "TKIs resistance"

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Ji, Xing-Zu, Zhong-Da Liu, Yi-Ping Ye, et al. "Advanced Lung Adenocarcinoma with EGFR 19-del Mutation Transformed into SCC after EGFR-tyrosine Kinase inhibitors Treatment: A Case report." World Journal of Clinical Cases 12, no. 20 (2024): 4405–11. http://dx.doi.org/10.12998/wjcc.v12.i20.4405.

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BACKGROUND Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) significantly improve the survival of patients with Epidermal growth factor receptor (EGFR) sensitive mutations in non-small cell lung cancer (NSCLC). CASE SUMMARY A 67-year-old female patient in advanced lung adenocarcinoma suffered from drug resistance after EGFR-TKIs treatment. Secondary pathological tissue biopsy confirmed squamous cell carcinoma (SCC) transformation. Patients inevitably encountered drug resistance issues after receiving EGFR-TKIs treatment for a certain period of time, while EGFR-TKIs can s
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Koulouris, Andreas, Christos Tsagkaris, Anna Chiara Corriero, Giulio Metro, and Giannis Mountzios. "Resistance to TKIs in EGFR-Mutated Non-Small Cell Lung Cancer: From Mechanisms to New Therapeutic Strategies." Cancers 14, no. 14 (2022): 3337. http://dx.doi.org/10.3390/cancers14143337.

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Resistance to tyrosine kinase inhibitors (TKIs) of the epidermal growth factor receptor (EGFR) in advanced mutant Non-Small Cell Lung Cancer (NSCLC) constitutes a therapeutic challenge. This review intends to summarize the existing knowledge about the mechanisms of resistance to TKIs in the context of EGFR mutant NSCLC and discuss its clinical and therapeutic implications. EGFR-dependent and independent molecular pathways have the potential to overcome or circumvent the activity of EGFR-targeted agents including the third-generation TKI, osimertinib, negatively impacting clinical outcomes. CNS
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Khaddour, Karam, Sushma Jonna, Alexander Deneka, et al. "Targeting the Epidermal Growth Factor Receptor in EGFR-Mutated Lung Cancer: Current and Emerging Therapies." Cancers 13, no. 13 (2021): 3164. http://dx.doi.org/10.3390/cancers13133164.

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Epidermal growth factor receptor-targeting tyrosine kinase inhibitors (EGFR TKIs) are the standard of care for patients with EGFR-mutated metastatic lung cancer. While EGFR TKIs have initially high response rates, inherent and acquired resistance constitute a major challenge to the longitudinal treatment. Ongoing work is aimed at understanding the molecular basis of these resistance mechanisms, with exciting new studies evaluating novel agents and combination therapies to improve control of tumors with all forms of EGFR mutation. In this review, we first provide a discussion of EGFR-mutated lu
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Fukuda, Shota, Kenichi Suda, Akira Hamada, et al. "Potential Utility of a 4th-Generation EGFR-TKI and Exploration of Resistance Mechanisms—An In Vitro Study." Biomedicines 12, no. 7 (2024): 1412. http://dx.doi.org/10.3390/biomedicines12071412.

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The emergence of acquired resistance to EGFR-tyrosine kinase inhibitors (TKIs) is almost inevitable even after a remarkable clinical response. Secondary mutations such as T790M and C797S are responsible for the resistance to 1st/2nd-generation (1/2G) TKIs and 3G TKIs, respectively. To overcome both the T790M and C797S mutations, novel 4G EGFR-TKIs are now under early clinical development. In this study, we evaluated the efficacy of a 4G EGFR-TKI in the treatment of lung cancer with EGFR mutation as well as explored resistance mechanisms to a 4G TKI. First, we compared the efficacies of seven T
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Ruzickova, Eliska, Nikola Skoupa, Petr Dolezel, Dennis A. Smith, and Petr Mlejnek. "The Lysosomal Sequestration of Tyrosine Kinase Inhibitors and Drug Resistance." Biomolecules 9, no. 11 (2019): 675. http://dx.doi.org/10.3390/biom9110675.

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The Lysosomal sequestration of weak-base anticancer drugs is one putative mechanism for resistance to chemotherapy but it has never been directly proven. We addressed the question of whether the lysosomal sequestration of tyrosine kinase inhibitors (TKIs) itself contributes to the drug resistance in vitro. Our analysis indicates that lysosomal sequestration of an anticancer drug can significantly reduce the concentration at target sites, only when it simultaneously decreases its extracellular concentration due to equilibrium, since uncharged forms of weak-base drugs freely diffuse across cellu
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Gazzeri, Sylvie, Nadiia Zubchuk, Elodie Montaudon, et al. "PPP3CB overexpression mediates EGFR TKI resistance in lung tumors via calcineurin/MEK/ERK signaling." Life Science Alliance 7, no. 12 (2024): e202402873. http://dx.doi.org/10.26508/lsa.202402873.

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Despite initial high response rates to first-line EGFR TKI, all non–small-cell lung cancer (NSCLC) with EGFR-activating mutation will ultimately develop resistance to treatment. Identification of resistance mechanisms is critical to adapt treatment and improve patient outcomes. Here, we show that aPPP3CBtranscript that encodes full-length catalytic subunit 2B of calcineurin accumulates in EGFR-mutant NSCLC cells with acquired resistance against different EGFR TKIs and in post-progression biopsies of NSCLC patients treated with EGFR TKIs. Neutralization ofPPP3CBby siRNA or inactivation of calci
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Zhu, Yu, Jianyong Li, Chun Qiao, et al. "PFKFB3 Is a Crucial Target in the Treatment of Tyrosine Kinase Inhibitor Resistant Chronic Myelogenous Leukemia." Blood 128, no. 22 (2016): 3936. http://dx.doi.org/10.1182/blood.v128.22.3936.3936.

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Abstract Resistance to the BCR-ABL tyrosine kinase inhibitor (TKI) imatinib mesylate (IM) remains challenge for the treatment of chronic myeloid leukemia (CML). IM resistance often results from unknown mechanisms with wild type BCR-ABL that have no effects on TKIs binding to ABL kinase domain. The basis of such BCR-ABL-independent IM resistance remains to be elucidated. To gain insight into BCR-ABL-independent IM resistance mechanisms, we performed an initial bioinformatics screen on over represented CML genes, followed by a quantitative PCR screen of genes that were elevated in TKIs resistant
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Laface, Carmelo, Felicia Maria Maselli, Anna Natalizia Santoro, et al. "The Resistance to EGFR-TKIs in Non-Small Cell Lung Cancer: From Molecular Mechanisms to Clinical Application of New Therapeutic Strategies." Pharmaceutics 15, no. 6 (2023): 1604. http://dx.doi.org/10.3390/pharmaceutics15061604.

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Almost 17% of Western patients affected by non-small cell lung cancer (NSCLC) have an activating epidermal growth factor receptor (EGFR) gene mutation. Del19 and L858R are the most-common ones; they are positive predictive factors for EGFR tyrosine kinase inhibitors (TKIs). Currently, osimertinib, a third-generation TKI, is the standard first-line therapy for advanced NSCLC patients with common EGFR mutations. This drug is also administered as a second-line treatment for those patients with the T790M EGFR mutation and previously treated with first- (erlotinib, gefitinib) or second- (afatinib)
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Li, Dongyu, Jingnan Wang, Chengming Liu, et al. "Making the Best Use of Available Weapons for the Inevitable Rivalry-Resistance to EGFR-TKIs." Biomedicines 11, no. 4 (2023): 1141. http://dx.doi.org/10.3390/biomedicines11041141.

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The emergence of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) revolutionized the treatment of advanced-stage non-small cell lung cancer (NSCLC). Detected in more than 50% of late-stage lung adenocarcinoma in Asian patients, the EGFR mutation was regarded as a golden mutation for Asians. However, resistance to TKIs seems inevitable and severely hinders patients from getting further benefits from treatment. Even though resistance caused by EGFR T790M could be effectively managed by third-generation EGFR-TKIs currently, resistance to third-generation EGFR-TKIs is still
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Zhou, Caicun, and Weijing Cai. "Intratumoral heterogeneity and EGFR-TKIs resistance." Journal of Thoracic Oncology 11, no. 2 (2016): S15. http://dx.doi.org/10.1016/j.jtho.2015.12.025.

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Dissertations / Theses on the topic "TKIs resistance"

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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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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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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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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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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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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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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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Books on the topic "TKIs resistance"

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Wong, Han Hsi, Basma Greef, and Tim Eisen. Treatment of metastatic renal cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0089.

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Metastatic renal cancer is resistant to standard chemotherapy. Although some patients with indolent disease can be initially managed with observation, the majority of patients will require aggressive treatment soon after diagnosis. Options include cytoreductive nephrectomy, resection of a solitary metastasis in highly selected cases, or systemic therapy options. The TKIs sunitinib and pazopanib are currently the first-line treatments of choice. Whilst axitinib and cabozantinib have important roles in the second line the PD-1 checkpoint inhibitor, nivolumab, is now established as standard secon
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Book chapters on the topic "TKIs resistance"

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Cappuzzo, Federico. "Resistance to EGFR TKIs." In Guide to Targeted Therapies: Treatment Resistance in Lung Cancer. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20741-4_3.

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Cappuzzo, Federico. "Overcoming EGFR-TKI Resistance." In Guide to Targeted Therapies: Treatment Resistance in Lung Cancer. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20741-4_4.

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Than, Hein, Charles Chuah, and S. Tiong Ong. "Molecular Mechanism of TKI Resistance and Potential Approaches to Overcome Resistance." In Molecular Pathogenesis and Treatment of Chronic Myelogenous Leukemia. Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55714-2_11.

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Anthony Othieno-Abinya, Nicholas, and Pier Paolo Piccaluga. "Modern Therapy of Chronic Myeloid Leukaemia." In Advances in Hematological Malignancies [Working Title]. IntechOpen, 2024. http://dx.doi.org/10.5772/intechopen.115458.

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The advent of tyrosine kinase inhibitors (TKIs) has transformed CML from a fatal disease into a manageable chronic condition. This review aims to provide a comprehensive overview of the current therapeutic landscape for CML and discuss the unique challenges in the treatment of CML, particularly in resource-limited settings such as Kenya. The introduction of TKIs marked a paradigm shift in the management of CML. Imatinib, the first-generation TKI, demonstrated remarkable efficacy in inducing durable cytogenetic and molecular responses, establishing it as the gold standard for first-line therapy
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Mologni, Luca. "Resistance mechanisms to ALK TKIs in tumors other than lung cancer." In Therapeutic Strategies to Overcome ALK Resistance in Cancer. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-821774-0.00005-x.

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Adachi, Yuta, and Hiromichi Ebi. "Role of epithelial to mesenchymal transition in the resistant mechanism of EGFR-TKIs." In Overcoming Resistance to EGFR Inhibitors in EGFR Mutant NSCLC. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-12-822833-3.00005-x.

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Katayama, Ryohei. "Resistance to anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors (TKIs) in patients with lung cancer: Single mutations, compound mutations, and other mechanisms of drug resistance." In Therapeutic Strategies to Overcome ALK Resistance in Cancer. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-821774-0.00015-2.

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Pacheco, Pedro Espinhosa, and João Antonio Piffer Bini. "USE OF OSIMERTINIB 160mg FOR TREATMENT OF NSCLC: CASE REPORT." In Developing Health: The Intersection of Science and Practice. Seven Editora, 2025. https://doi.org/10.56238/sevened2024.039-026.

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Introduction: Lung cancer is the most prevalent cancer in the world, and it is also the cancer with the highest mortality. Non-small cell lung cancer (NSCLC) accounts for 85% of cases, and is related to bone metastases in the central nervous system (CNS), and liver. It is known that a large part of the mutations involved in the development of NSCLC is the mutation in the epidermal growth factor receptor (EGFR) gene, leading to the production of EGFR with permanent activation, and thus, generating a lack of control over cell growth pathways. Thus, drugs capable of blocking the mutated EGFR rece
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Bhuyan, Biswajit, Somanath Padhi, Probodha Kumar Das, and Chinmayee Panigrahi. "Chronic Myeloid Leukemia: Biology, Diagnosis, and Management." In Leukemia - From Biology to Diagnosis and Treatment [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108334.

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Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasm characterized by florid myelo-megakaryocytic proliferation involving peripheral blood, bone marrow, and spleen. These results are due to balanced reciprocal translocation between long arm of chromosome 9 and 22 that produces a truncated chromosome 22 (Philadelphia chromosome) leading to fusion of BCR-ABL1 genes causing enhanced autonomous activation of tyrosine kinase and downstream cellular proliferation pathway. While targeted therapy with novel tyrosine kinase inhibitors (TKI) has revolutionized the outcome in such patie
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Collazo-Lorduy, Ana, Beatriz Jiménez, María Castro-Henriques, and Jordi Remon. "ALK rearranged lung cancer: TKI treatment and outcome." In Therapeutic Strategies to Overcome ALK Resistance in Cancer. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-821774-0.00013-9.

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Conference papers on the topic "TKIs resistance"

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Rho, Jin Kyung, Yun Jung Choi, Su Jin Choi, et al. "Abstract 620: Addition of silibinin to EGFR-TKIs overcomes T790M-mediated drug resistance." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-620.

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Paul, Sarah M., Xioafen Ye, Zora Modrusan, Somasekar Seshagiri, Robert Yauch, and David S. Shames. "Abstract B25: A comparison of resistance mechanisms to 1st, 2nd, and 3rd generation EGFR TKIs in NSCLC." In Abstracts: AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; June 18-21, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-b25.

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Chmielecki, Juliann, Maria C. Pietanza, Mark Kris, Vincent Miller, Thomas Stout, and William Pao. "Abstract 1774: Selection for the EGFR T790M gatekeeper resistance mutation may vary among different small molecule EGFR TKIs." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1774.

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Knebel, Franciele, Fabiana Bettoni, Andrea Shimada, et al. "Abstract B168: Monitoring acquired resistance to EGFR-TKIs and clonal evolution in metastatic NSCLC patients using liquid biopsies." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-b168.

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Ware, Katie E., and Lynn E. Heasley. "Abstract B70: Participation of fibroblast growth factor receptors (FGFRs) in acquired resistance to EGFR-specific TKIs in NSCLC." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-b70.

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Yano, Seiji, Ivan S. Donev, Wei Wang, Qi Li, Shinji Takeuchi, and Tadaaki Yamada. "Abstract 1730: Transient PI3K inhibition induces apoptosis and overcomes HGF-mediated resistance to EGFR-TKIs inEGFRmutant lung cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1730.

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Honarnejad, Saman. "Abstract C53: Fractional response to small-molecule TKIs in single cancer cells: A combination rational to overcome adaptive drug resistance." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c53.

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Cascone, Tina, Matthew H. Herynk, Li Xu, et al. "Abstract 376: Increased HGF is associated with resistance to VEGFR tyrosine kinase inhibitors (TKIs) in non-small cell lung cancer (NSCLC)." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-376.

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Bertran-Alamillo, Jordi, Jon Travers, Ana Giménez-Capitán, et al. "Abstract 1020: Amplification of 22q11 is associated with hypersensitivity to AURKB inhibition in cell line models of resistance to EGFR TKIs." 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.am2021-1020.

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Yan, Dan, Xiaodong Wang, Stephen V. Frye, Shelton H. Earp, Deborah DeRyckere, and Douglas K. Graham. "Abstract 1082: MerTK promotes resistance to irreversible EGFR TKIs by activation of the PI3K-AKT pathway in NSCLCs expressing wild-type EGFR." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1082.

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Reports on the topic "TKIs resistance"

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Song, Yaowen, Shuiyu Lin, Jun Chen, Silu Ding, and Jun Dang. First-line treatment with TKI plus brain radiotherapy vs TKI alone in EGFR-mutated non-small-cell lung cancer with brain metastases: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.1.0013.

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Review question / Objective: It remains uncertain whether first-line treatment with upfront brain radiotherapy (RT) in combination with epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) is superior to EGFR-TKIs alone in EGFR-mutated non-small-cell lung cancer with newly diagnosed brain metastases (BMs). We performed a meta-analysis to address this issue. Condition being studied: Brain radiotherapy (RT) has been shown to damage the blood-brain barrier (BBB) and improve the concentration of EGFR-TKIs in the CSF. Additionally, RT can result in a reduction of EGFR-TKIs resist
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Guan, Guohui, Yujia Chi, Yiliang Liu, et al. Treatment strategy for advanced or metastatic NSCLC patients with EGFR mutations after TKI-resistance: A scoping review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2025. https://doi.org/10.37766/inplasy2025.5.0089.

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wan, zhiling, yaru Guo, xiaojin Wu, zexian Wang, xiaohan Qin, and Chen Liu. Efficacy of immunotherapy combined with chemotherapy in NSCLC patients with EGFR-TKI resistance: a meta-analysis of randomized clinical trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2024. http://dx.doi.org/10.37766/inplasy2024.2.0075.

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