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Journal articles on the topic 'TKIs resistance'

Author: Grafiati

Published: 24 May 2025

Last updated: 31 July 2025

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1

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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3

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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8

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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11

Ku, Bo Mi, Jae Yeong Heo, Jinchul Kim, et al. "ERK inhibitor ASN007 effectively overcomes acquired resistance to EGFR inhibitor in non‐small cell lung cancer." Investigational New Drugs 40, no. 2 (2022): 265–73. http://dx.doi.org/10.1007/s10637-021-01121-6.

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SummaryThe emergence of acquired resistance limits the long-term efficacy of EGFR tyrosine kinase inhibitors (EGFR TKIs). Thus, development of effective strategies to overcome resistance to EGFR TKI is urgently needed. Multiple mechanisms to reactivate ERK signaling have been successfully demonstrated in acquired resistance models. We found that in EGFR mutant non-small cell lung cancer (NSCLC) patients, acquired resistance to EGFR TKIs was accompanied by increased activation of ERK. Increased ERK activation was also found in in vitro models of acquired EGFR TKI resistance. ASN007 is a potent

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12

Zhang, Lei, John Coffin, Kim Formenti, Quincy Chu, and Iyare Izevbaye. "Application of liquid biopsy-based targeted capture sequencing analysis to improve the precision treatment of non-small cell lung cancer by tyrosine kinase inhibitors." BMJ Open Respiratory Research 9, no. 1 (2022): e001154. http://dx.doi.org/10.1136/bmjresp-2021-001154.

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BackgroundTargeted therapy of patients with non-small cell lung cancer (NSCLC) who harbour sensitising mutations by tyrosine kinase inhibitors (TKIs) has been found more effective than traditional chemotherapies. However, target genes status (eg, epidermal growth factor receptor (EGFR) TKIs sensitising and resistant mutations) need to be tested for choosing appropriate TKIs. This study is to investigate the performance of a liquid biopsy-based targeted capture sequencing assay on the molecular analysis of NSCLC.MethodsPlasma samples from patients with NSCLC who showed resistance to the first/s

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Ishida, Masaki, Tadaaki Yamada, Yuki Katayama, Kazuo Yasumoto, and Koichi Takayama. "Abstract 1721: AXL signaling promotes adaptive resistance to HER2 tyrosine kinase inhibitors in HER2 aberrant tumor cells." Cancer Research 85, no. 8_Supplement_1 (2025): 1721. https://doi.org/10.1158/1538-7445.am2025-1721.

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Abstract Introduction: Human epidermal growth factor receptor 2 (HER2) is an oncogene target in various cancers, including lung, stomach, and breast cancers. Several HER2-tyrosine kinase inhibitors (TKIs) have been developed for clinical use in patients with tumors exhibiting HER2 aberrations. However, achieving complete tumor remission remains challenging. Therefore, identifying optimal combined therapeutic approaches with HER2-TKIs is crucial for improving clinical outcomes. This study focuses on elucidating the adaptive resistance mechanisms to HER2-TKIs and the therapeutic strategies neede

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Marrocco, Ilaria, Yuya Haga, and Yosef Yarden. "Abstract 1097: First-line therapy based on kinase inhibitors and antibodies prevents resistance in EGFR-mutated lung cancer." Cancer Research 82, no. 12_Supplement (2022): 1097. http://dx.doi.org/10.1158/1538-7445.am2022-1097.

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Abstract Introduction: Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) are commonly used to treat patients with EGFR+ non-small cell lung cancer (NSCLC). Unfortunately, despite the initial response, the long-term efficacy of the five clinically approved TKIs (i.e., gefitinib, erlotinib, afatinib, dacomitinib, osimertinib) is limited by the onset of resistance. Several mechanisms of resistance have been described, including the appearance of new EGFR mutations (e.g., T790M, C797S), activation of bypass pathways (e.g., AXL, HER2, MET and IGF1R) and phenotypic alteration

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15

Polonio-Alcalá, Emma, Sònia Palomeras, Daniel Torres-Oteros, et al. "Fatty Acid Synthase Inhibitor G28 Shows Anticancer Activity in EGFR Tyrosine Kinase Inhibitor Resistant Lung Adenocarcinoma Models." Cancers 12, no. 5 (2020): 1283. http://dx.doi.org/10.3390/cancers12051283.

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Epidermal growth factor receptor (EGFR) tyrosine kinases inhibitors (TKIs) are effective therapies for non-small cell lung cancer (NSCLC) patients whose tumors harbor an EGFR activating mutation. However, this treatment is not curative due to primary and secondary resistance such as T790M mutation in exon 20. Recently, activation of transducer and activator of transcription 3 (STAT3) in NSCLC appeared as an alternative resistance mechanism allowing cancer cells to elude the EGFR signaling. Overexpression of fatty acid synthase (FASN), a multifunctional enzyme essential for endogenous lipogenes

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Miyawaki, Taichi, Hirotsugu Kenmotsu, Ryo Ko, et al. "Current Status of Multimodal Therapy for Oligometastatic Disease, Induced Oligometastatic Disease, and Oligo-Progressive Disease in EGFR-Mutated Non-Small-Cell Lung Cancer." Cancers 17, no. 13 (2025): 2202. https://doi.org/10.3390/cancers17132202.

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Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) have shown clinical activity for patients with EGFR-mutated non-small-cell lung cancer (NSCLC). However, the development of resistance to EGFR-TKIs is almost inevitable, posing a significant barrier to long-term survival. Local ablative therapy (LAT) may facilitate the prolonged survival of patients with oligometastatic NSCLC. Therapeutic combinations of EGFR-TKIs and LAT for residual disease have been suggested to be potentially effective in EGFR-mutated NSCLC with induced oligometastatic disease, wherein a few lesions

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Michels, Sebastian Yves Friedrich, Carina Heydt, Barbara Deschler-Baier, et al. "Molecular panel sequencing of pre-treatment samples to reveal mechanisms of innate resistance to 3rd generation EGFR TKI treatment in T790M-positive NSCLC patients." Journal of Clinical Oncology 35, no. 15_suppl (2017): 9041. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.9041.

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9041 Background: Resistance to early generation epidermal growth factor receptor ( EGFR) tyrosine kinase inhibitors (TKI) inevitably develops in EGFR-mutant lung cancer. The secondary EGFR p.T790M mutation is the driving factor in 60% of cases and 3rd generation EGFR TKIs have been developed to overcome T790M-mediated resistance. However, besides T790M other genetic aberrations such as amplifications of MET may contribute to resistance to EGFR inhibition in the same patient. We here report on the systematic analysis of co-occurring genetic aberrations that may influence response to 3rd generat

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Zhou, Yan, Hao Bai, Lei Cheng, Baohui Han, and Liwen Xiong. "Novel ETV1 mutation in small cell lung cancer transformation resistant to EGFR tyrosine kinase inhibitors." Journal of Clinical Oncology 39, no. 15_suppl (2021): e20568-e20568. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e20568.

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e20568 Background: Non-small cell lung cancer (NSCLC) patients harboring mutations in the epidermal growth factor receptor (EGFR) gene dramatically respond to EGFR tyrosine kinase inhibitors (TKIs). However, these patients inevitably developed acquired resistance to TKIs. Among them, small cell lung cancer (SCLC) transformation is a relatively rare mechanism of resistance. However, the mechanism of SCLC transformation is largely unclear. Methods: We performed a 639 cancer-relevant gene panel to detect genetic differences of tissues before and after TKIs resistance caused by SCLC transformation

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Lin, Kimberly, Catherine C. Smith, Sara Salerno, and Neil P. Shah. "Mutations At The FLT3 Activation Loop D835 Residue Confer Differential Resistance To Clinically Active FLT3 Inhibitors." Blood 122, no. 21 (2013): 3929. http://dx.doi.org/10.1182/blood.v122.21.3929.3929.

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Abstract Background Activating mutations in FLT3 occur in ∼30% of adult acute myeloid leukemia (AML), primarily consisting of internal tandem duplication (ITD) mutations (∼25%) and point mutations in the tyrosine kinase domain (∼5%), commonly at the activation loop residue D835. Secondary D835 mutants in FLT3-ITD are frequently associated with acquired clinical resistance to effective FLT3 TKIs. While molecular docking studies suggest that D835 mutations confer resistance by favoring an active “DFG-in” kinase conformation that is unfavorable to the binding of type II FLT3 TKIs, which bind to a

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Ta, Van Thanh. "ID3021 Acquired resistance to with EGFR tyrosine kinase inhibitors by the EGFR T790M mutation in non-small cell lung cancer." Biomedical Research and Therapy 4, S (2017): 33. http://dx.doi.org/10.15419/bmrat.v4is.243.

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Mutations in the tyrosine kinase (TK) domain of the epidermal growth factor receptor (EGFR) gene respond well to treatment with EGFR tyrosine kinase inhibitors (EGFR-TKIs) including gefitinib and erlotinib in non-small cell lung cancer (NSCLC). Detection of these mutations has an important role for therapeutic decision-making in NSCLC treatment. However, all patients who experienced marked improvements with these drugs eventually developed disease progression after 10-20 months of treatment due to the acquisition of drug resistance. Approximately half of the cases with acquired resistance to E

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Proto, Claudia, Giuseppe Lo Russo, Giulia Corrao, et al. "Treatment in EGFR-mutated Non-small Cell Lung Cancer: How to Block the Receptor and overcome Resistance Mechanisms." Tumori Journal 103, no. 4 (2017): 325–37. http://dx.doi.org/10.5301/tj.5000663.

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In non-small cell lung cancer (NSCLC), the identification of epidermal growth factor receptor (EGFR) mutations and the parallel development of EGFR tyrosine kinase inhibitors (TKIs) have radically changed the therapeutic management strategies. Currently, erlotinib, gefitinib, and afatinib are all approved as standard first-line treatment in EGFR-mutated NSCLC. However, despite the proven efficacy, some EGFR-mutated NSCLCs do not respond to EGFR TKIs, while some patients, after a favorable and prolonged response to EGFR TKIs, inevitably progress within about 10-14 months. Epidermal growth facto

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Urbanska, Edyta M., Jens B. Sørensen, Linea C. Melchior, Junia C. Costa, and Eric Santoni-Rugiu. "Changing ALK-TKI-Resistance Mechanisms in Rebiopsies of ALK-Rearranged NSCLC: ALK- and BRAF-Mutations Followed by Epithelial-Mesenchymal Transition." International Journal of Molecular Sciences 21, no. 8 (2020): 2847. http://dx.doi.org/10.3390/ijms21082847.

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Anaplastic lymphoma-kinase (ALK)-rearranged non-small cell lung cancer (NSCLC) is prone to developing heterogeneous, only partly known mechanisms of resistance to ALK-tyrosine-kinase-inhibitors (ALK-TKIs). We present a case of a 38-year old male, who never smoked with disseminated ALK-rearranged (EML4 (20) – ALK (20) fusion variant 2) lung adenocarcinoma, who received four sequentially different ALK-TKIs and two lines of chemotherapy in-between. We observed significant clinical benefit by the first three ALK-TKIs (Crizotinib, Ceritinib, Alectinib) and chemotherapy with Pemetrexed, resulting in

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Gleba, Justyna J., Aylin Alasonyalilar-Demirer, Matthew L. Pawlush, et al. "Abstract 5489: Synergistic activity of SCD1 blockade in combination with tyrosine kinase inhibitors lenvatinib and cabozantinib in hepatocellular carcinoma (HCC)." Cancer Research 83, no. 7_Supplement (2023): 5489. http://dx.doi.org/10.1158/1538-7445.am2023-5489.

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Abstract Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer. Tyrosine kinase inhibitors (TKIs) are approved as a first-line treatment for unresectable HCC. Lenvatinib and cabozantinib are two of the most used TKIs, but the therapeutic duration is limited due to the development of drug resistance. Therefore, understanding the mechanisms of resistance and combining TKIs with other drugs antagonizing resistance should lead to antitumor synergy, eliminating drug resistance. It turns out that the simultaneous use of TKIs together with an inhibitor of stearoyl-CoA desatur

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Tsubata, Yukari, Ryosuke Tanino, and Takeshi Isobe. "Current Therapeutic Strategies and Prospects for EGFR Mutation-Positive Lung Cancer Based on the Mechanisms Underlying Drug Resistance." Cells 10, no. 11 (2021): 3192. http://dx.doi.org/10.3390/cells10113192.

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The discovery of activating mutations in the epidermal growth factor receptor (EGFR) gene and the development of EGFR tyrosine kinase inhibitors (TKIs) have led to a paradigm shift in the treatment of non-small cell lung cancer (NSCLC). EGFR mutation-positive NSCLC is common in East Asia, and approximately 50% of adenocarcinomas harbor EGFR mutations. Undoubtedly, EGFR-TKIs, with their promising efficacy, are the mainstay of primary therapy. However, even if tumor shrinkage is achieved, most patients become resistant to EGFR-TKIs and relapse; hence, EGFR-TKIs do not achieve a radical cure. The

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Kang, Xiao-Hong, Zhen-Ye Xu, Ya-Bin Gong, et al. "Bufalin Reverses HGF-Induced Resistance to EGFR-TKIs in EGFR Mutant Lung Cancer Cells via Blockage of Met/PI3k/Akt Pathway and Induction of Apoptosis." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/243859.

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The epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), such as gefitinib and erlotinib, have shown promising therapeutic efficacy in nonsmall cell lung cancer (NSCLC) patients harboring epidermal growth factor receptor- (EGFR-) activating mutation. However, the inevitable recurrence resulting from acquired resistance has limited the clinical improvement in therapy outcomes. Many studies demonstrate that hepatocyte growth factor- (HGF-) Met axis plays an important role in tumor progression and drug sensitivity. HGF may induce resistance to EGFR-TKIs in EGFR mutant lung can

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Dickerson, Henry, Ahmad Diab, and Othman Al Musaimi. "Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Cancer: Current Use and Future Prospects." International Journal of Molecular Sciences 25, no. 18 (2024): 10008. http://dx.doi.org/10.3390/ijms251810008.

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Tyrosine kinase inhibitors (TKIs) have emerged as a leading targeted cancer therapy, reducing the side effects often seen with non-targeted treatments, especially the damage to healthy cells. To tackle resistance, typically caused by epidermal growth factor receptor (EGFR) mutations, four generations of TKIs have been developed. Each generation has shown improved effectiveness and fewer side effects, resulting in better patient outcomes. For example, patients on gefitinib, a first-generation TKI, experienced a progression-free survival (PFS) of 10 months compared to 5 months with conventional

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Yang, Jin-Ji, Chi Zhang, Jun Zhao, et al. "ALK resistance mutations and co-occurring genetic alterations to the ALK tyrosine kinase inhibitors in lung cancer." Journal of Clinical Oncology 37, no. 15_suppl (2019): e20675-e20675. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e20675.

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e20675 Background: Acquired ALK mutations pose a challenge in multiple ALK tyrosine kinase inhibitors (TKIs) for lung cancer. In our study, we examined the profiles of ALK resistance mutations and co-occurring genetic alterations after targeted therapy. Methods: Using targeted gene capture and next-generation sequencing technologies, we analyzed the somatic mutations from174 patients (pts) with post-TKI samples. Among them, 123 pts received first-generation TKI crizotinib only, 51 pts (34 with second-generation TKI, 17 with third-generation TKI) treated with multiple ALK-TKIs. Results: After t

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Campos-Parra, Alma D., David Sánchez-Marín, and Víctor Acevedo-Sánchez. "MicroRNAs as Sensitizers of Tyrosine Kinase Inhibitor Resistance in Cancer: Small Molecule Partnerships." Pharmaceuticals 18, no. 4 (2025): 492. https://doi.org/10.3390/ph18040492.

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Tyrosine kinase inhibitors (TKIs) have revolutionized cancer treatments by being less toxic and improving the survival of cancer patients. The greatest challenge to their success is the resistance exhibited by cancer patients. However, the potential of microRNAs (miRNAs) for sensitizing molecules to TKIs has been well recognized, with several reports publishing promising results. Nonetheless, this therapeutic window faces challenges and several often-overlooked limitations. One of the most fundamental challenges is selecting the optimal miRNA candidates for clinical trials, as miRNAs are promi

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Aldonza, Mark Borris D., Jayoung Ku, Ji-Young Hong, et al. "Prior acquired resistance to paclitaxel relays diverse EGFR-targeted therapy persistence mechanisms." Science Advances 6, no. 6 (2020): eaav7416. http://dx.doi.org/10.1126/sciadv.aav7416.

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Secondary drug resistance stems from dynamic clonal evolution during the development of a prior primary resistance. This collateral type of resistance is often a characteristic of cancer recurrence. Yet, mechanisms that drive this collateral resistance and their drug-specific trajectories are still poorly understood. Using resistance selection and small-scale pharmacological screens, we find that cancer cells with primary acquired resistance to the microtubule-stabilizing drug paclitaxel often develop tolerance to epidermal growth factor receptor–tyrosine kinase inhibitors (EGFR-TKIs), leading

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Karaca Atabay, Elif, Carmen Mecca, Qi Wang, et al. "Tyrosine phosphatases regulate resistance to ALK inhibitors in ALK+ anaplastic large cell lymphoma." Blood 139, no. 5 (2022): 717–31. http://dx.doi.org/10.1182/blood.2020008136.

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Abstract Anaplastic large cell lymphomas (ALCLs) frequently carry oncogenic fusions involving the anaplastic lymphoma kinase (ALK) gene. Targeting ALK using tyrosine kinase inhibitors (TKIs) is a therapeutic option in cases relapsed after chemotherapy, but TKI resistance may develop. By applying genomic loss-of-function screens, we identified PTPN1 and PTPN2 phosphatases as consistent top hits driving resistance to ALK TKIs in ALK+ ALCL. Loss of either PTPN1 or PTPN2 induced resistance to ALK TKIs in vitro and in vivo. Mechanistically, we demonstrated that PTPN1 and PTPN2 are phosphatases that

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Kosaka, Takayuki, Ei Yamaki, Akira Mogi, and Hiroyuki Kuwano. "Mechanisms of Resistance to EGFR TKIs and Development of a New Generation of Drugs in Non-Small-Cell Lung Cancer." Journal of Biomedicine and Biotechnology 2011 (2011): 1–7. http://dx.doi.org/10.1155/2011/165214.

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Gefitinib and erlotinib, which are epidermal growth factor receptor- (EGFR-) specific tyrosine kinase inhibitors (TKIs), are widely used as molecularly targeted drugs for non-small-cell lung cancer (NSCLC). Currently, the search forEGFRgene mutations is becoming essential for the treatment of NSCLC since these have been identified as predictive factors for drug sensitivity. On the other hand, in almost all patients responsive to EGFR-TKIs, acquired resistance is a major clinical problem. Mechanisms of acquired resistance reported in the past few years include secondary mutation of theEGFRgene,

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Izumi, Motohiro, Meghan Lee, Daisuke Shibahara, Ikei S. Kobayashi, David Plotnick, and Susumu S. Kobayashi. "Abstract 3460: Targeting the MIF-CD74 axis to overcome resistance to tyrosine kinase inhibitors in non-small cell lung cancer." Cancer Research 83, no. 7_Supplement (2023): 3460. http://dx.doi.org/10.1158/1538-7445.am2023-3460.

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Abstract Development of tyrosine kinase inhibitors (TKIs) against oncogenic drivers has significantly improved survival of patients with oncogene-mutated non-small cell lung cancer (NSCLC). However, acquired resistance to TKIs emerges over time in essentially all patients who initially respond. Recent evidence suggests that drug-tolerant persister (DTP) cells, which survive and adapt to targeted therapies during an early phase of treatment, play an important role in the emergence of drug resistance. We previously reported that CD74 expression is upregulated in EGFR-mutated lung cancer after tr

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Chang, Yu-Ting, Daniela Hernandez, Salvador Alonso, et al. "Role of CYP3A4 in bone marrow microenvironment–mediated protection of FLT3/ITD AML from tyrosine kinase inhibitors." Blood Advances 3, no. 6 (2019): 908–16. http://dx.doi.org/10.1182/bloodadvances.2018022921.

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Abstract An intriguing aspect of the clinical activity of FMS-like tyrosine kinase 3 inhibitors (FLT3 TKIs) is their apparent higher activity against peripheral blasts from FLT3/internal tandem duplication (ITD) acute myeloid leukemia than marrow disease in the same patients. Accordingly, studies showed that the bone marrow microenvironment plays a role in FLT3 TKI resistance, although the underlying mechanisms are unclear. We recently identified a previously undescribed mechanism by which the bone marrow microenvironment can contribute to drug resistance: expression of cytochrome P450 enzymes

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Li, Junnan, and Hang Kwok. "Current Strategies for Treating NSCLC: From Biological Mechanisms to Clinical Treatment." Cancers 12, no. 6 (2020): 1587. http://dx.doi.org/10.3390/cancers12061587.

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The identification of specific epidermal growth factor receptor (EGFR)-activating mutations heralded a breakthrough in non-small-cell lung cancer (NSCLC) treatments, with the subsequent development of EGFR-tyrosine kinase inhibitor (TKIs) becoming the first-line therapy for patients harboring EGFR mutations. However, acquired resistance to EGFR-TKIs inevitably occurs in patients following initial TKI treatment, leading to disease progression. Various mechanisms are behind the acquired resistance, and mainly include (1) target gene modification, (2) alternative parallel pathway activation, (3)

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Chen, Chia-Hung, Bo-Wei Wang, Yu-Chun Hsiao та ін. "PKCδ-mediated SGLT1 upregulation confers the acquired resistance of NSCLC to EGFR TKIs". Oncogene 40, № 29 (2021): 4796–808. http://dx.doi.org/10.1038/s41388-021-01889-0.

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AbstractThe tyrosine kinase inhibitors (TKIs) targeting epidermal growth factor receptor (EGFR) have been widely used for non-small cell lung cancer (NSCLC) patients, but the development of acquired resistance remains a therapeutic hurdle. The reduction of glucose uptake has been implicated in the anti-tumor activity of EGFR TKIs. In this study, the upregulation of the active sodium/glucose co-transporter 1 (SGLT1) was found to confer the development of acquired EGFR TKI resistance and was correlated with the poorer clinical outcome of the NSCLC patients who received EGFR TKI treatment. Blocka

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Trela, Ewelina, Sylwester Glowacki, and Janusz Błasiak. "Therapy of Chronic Myeloid Leukemia: Twilight of the Imatinib Era?" ISRN Oncology 2014 (January 30, 2014): 1–9. http://dx.doi.org/10.1155/2014/596483.

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Chronic myeloid leukemia (CML) results from the clonal expansion of pluripotent hematopoietic stem cells containing the active BCR/ABL fusion gene produced by a reciprocal translocation of the ABL1 gene to the BCR gene. The BCR/ABL protein displays a constitutive tyrosine kinase activity and confers on leukemic cells growth and proliferation advantage and resistance to apoptosis. Introduction of imatinib (IM) and other tyrosine kinase inhibitors (TKIs) has radically improved the outcome of patients with CML and some other diseases with BCR/ABL expression. However, a fraction of CML patients pr

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Nagano, Tatsuya, Motoko Tachihara, and Yoshihiro Nishimura. "Mechanism of Resistance to Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitors and a Potential Treatment Strategy." Cells 7, no. 11 (2018): 212. http://dx.doi.org/10.3390/cells7110212.

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Treatment with epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) improves the overall survival of patients with EGFR-mutated non-small-cell lung cancer (NSCLC). First-generation EGFR-TKIs (e.g., gefitinib and erlotinib) or second-generation EGFR-TKIs (e.g., afatinib and dacomitinib) are effective for the treatment of EGFR-mutated NSCLC, especially in patients with EGFR exon 19 deletions or an exon 21 L858R mutation. However, almost all cases experience disease recurrence after 1 to 2 years due to acquired resistance. The EGFR T790M mutation in exon 20 is the most frequent

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Chen, H., Y. Wu, X. Zhang, Z. Chen, A. Guo, and H. Cheng. "KRAS mutation in the primary or acquired resistance of Chinese NSCLC to EGFR tyrosine kinase inhibitors." Journal of Clinical Oncology 27, no. 15_suppl (2009): e19071-e19071. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e19071.

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e19071 Background: Prevalence of KRAS mutation in Asian NSCLC is different to population of white ethnicity. Data about KRAS mutation after development of resistance to EGFR tyrosine kinase inhibitors (TKIs) are rare. This study was to investigate the prevalence of KRAS mutation in Chinese NSCLC after primary or acquired resistance to EGFR TKIs. Methods: 155 EGFR TKI-naive NSCLC patients and corresponding tumor specimens were collected to establish baseline of KRAS mutation. 45 specimens from six patients with primary resistance to TKIs and twenty-nine patients with acquired resistance to TKIs

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Yao, Yu, Min Zhang, Xiuju Liu, et al. "RET fusion in first/third-generation EGFR-TKIs resistance in advanced non-small cell lung cancer." Journal of Clinical Oncology 37, no. 15_suppl (2019): e20634-e20634. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e20634.

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e20634 Background: EGFR-TKIs is the standard first/second-line treatment for EGFR-mutant advanced non-small-cell lung cancer (NSCLC). The mechanisms of EGFR-TKIs resistance are still under exploration. Acquired fusion have been reported contribute to EGFR-TKIs resistance. Here we focus on RET fusion in first/third-generation EGFR-TKIs resistant NSCLC. Methods: We retrospectively reviewed 3600 cases of EGFR-TKIs resistant NSCLC samples from 2016 to 2018 in our institute. Tumor biopsy, ctDNA or pleural effusion samples were analyzed using hybridization capture-based NGS ER-seq method, which enab

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Conlon, Neil T., Jeffrey J. Kooijman, Suzanne J. C. van Gerwen, et al. "Comparative analysis of drug response and gene profiling of HER2-targeted tyrosine kinase inhibitors." British Journal of Cancer 124, no. 7 (2021): 1249–59. http://dx.doi.org/10.1038/s41416-020-01257-x.

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Abstract Background Human epidermal growth factor 2 (HER2/ERBB2) is frequently amplified/mutated in cancer. The tyrosine kinase inhibitors (TKIs) lapatinib, neratinib, and tucatinib are FDA-approved for the treatment of HER2-positive breast cancer. Direct comparisons of the preclinical efficacy of the TKIs have been limited to small-scale studies. Novel biomarkers are required to define beneficial patient populations. Methods In this study, the anti-proliferative effects of the three TKIs were directly compared using a 115 cancer cell line panel. Novel TKI response/resistance markers were iden

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Podolski-Renić, Ana, Jelena Dinić, Tijana Stanković, et al. "New Therapeutic Strategy for Overcoming Multidrug Resistance in Cancer Cells with Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors." Cancers 13, no. 21 (2021): 5308. http://dx.doi.org/10.3390/cancers13215308.

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Tyrosine kinase inhibitors (TKIs) often interact with the multidrug resistant (MDR) phenotype of cancer cells. In some cases, TKIs increase the susceptibility of MDR cancer cells to chemotherapy. As the overexpression of membrane transporter P-glycoprotein (P-gp) is the most common alteration in MDR cancer cells, we investigated the effects of TKI pyrazolo[3,4-d]pyrimidines on P-gp inhibition in two cellular models comprising sensitive and corresponding MDR cancer cells (human non-small cell lung carcinoma and colorectal adenocarcinoma). Tested TKIs showed collateral sensitivity by inducing st

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Gawi Ermi, Ali, and Devanand Sarkar. "Resistance to Tyrosine Kinase Inhibitors in Hepatocellular Carcinoma (HCC): Clinical Implications and Potential Strategies to Overcome the Resistance." Cancers 16, no. 23 (2024): 3944. http://dx.doi.org/10.3390/cancers16233944.

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Hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths worldwide, and the development of effective treatment strategies remains a significant challenge in the management of advanced HCC patients. The emergence of tyrosine kinase inhibitors (TKIs) has been a significant advancement in the treatment of HCC, as these targeted therapies have shown promise in prolonging the survival of patients with advanced disease. Although immunotherapy is currently considered as the first line of treatment for advanced HCC patients, many such patients do not meet the clinical criteria to be

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Verdura, Sara, Jose Antonio Encinar, Eduard Teixidor, et al. "Silibinin Overcomes EMT-Driven Lung Cancer Resistance to New-Generation ALK Inhibitors." Cancers 14, no. 24 (2022): 6101. http://dx.doi.org/10.3390/cancers14246101.

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Epithelial-to-mesenchymal transition (EMT) may drive the escape of ALK-rearranged non-small-cell lung cancer (NSCLC) tumors from ALK-tyrosine kinase inhibitors (TKIs). We investigated whether first-generation ALK–TKI therapy-induced EMT promotes cross-resistance to new-generation ALK–TKIs and whether this could be circumvented by the flavonolignan silibinin, an EMT inhibitor. ALK-rearranged NSCLC cells acquiring a bona fide EMT phenotype upon chronic exposure to the first-generation ALK–TKI crizotinib exhibited increased resistance to second-generation brigatinib and were fully refractory to t

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Krchniakova, Maria, Jan Skoda, Jakub Neradil, Petr Chlapek, and Renata Veselska. "Repurposing Tyrosine Kinase Inhibitors to Overcome Multidrug Resistance in Cancer: A Focus on Transporters and Lysosomal Sequestration." International Journal of Molecular Sciences 21, no. 9 (2020): 3157. http://dx.doi.org/10.3390/ijms21093157.

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Tyrosine kinase inhibitors (TKIs) are being increasingly used to treat various malignancies. Although they were designed to target aberrant tyrosine kinases, they are also intimately linked with the mechanisms of multidrug resistance (MDR) in cancer cells. MDR-related solute carrier (SLC) and ATB-binding cassette (ABC) transporters are responsible for TKI uptake and efflux, respectively. However, the role of TKIs appears to be dual because they can act as substrates and/or inhibitors of these transporters. In addition, several TKIs have been identified to be sequestered into lysosomes either d

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Lim, Jeong Uk, Junyang Jung, Yeon Wook Kim, et al. "Targeting the Tumor Microenvironment in EGFR-Mutant Lung Cancer: Opportunities and Challenges." Biomedicines 13, no. 2 (2025): 470. https://doi.org/10.3390/biomedicines13020470.

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Tyrosine kinase inhibitors (TKIs) have transformed the treatment of epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer. However, treatment resistance remains a major challenge in clinical practice. The tumor microenvironment (TME) is a complex system composed of tumor cells, immune and non-immune cells, and non-cellular components. Evidence indicates that dynamic changes in TME during TKI treatment are associated with the development of resistance. Research has focused on identifying how each component of the TME interacts with tumors and TKIs to understand therapeutic t

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Breitenbuecher, Frank, Boyka Markova, Stefan Kasper, et al. "A novel molecular mechanism of primary resistance to FLT3-kinase inhibitors in AML." Blood 113, no. 17 (2009): 4063–73. http://dx.doi.org/10.1182/blood-2007-11-126664.

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Abstract Currently, FLT3 tyrosine kinase inhibitors (TKIs) are emerging as the most promising drug therapy to overcome the dismal prognosis of acute myelogenous leukemia (AML) patients harboring internal tandem duplications (ITDs) of FLT3. However, up-front drug resistance occurs in approximately 30% of patients, and molecular mechanisms of resistance are poorly understood. Here, we have uncovered a novel mechanism of primary resistance to FLT3 TKIs in AML: an FLT3 receptor harboring a nonjuxtamembrane ITD atypically integrating into the β-2 sheet of the first kinase domain (FLT3_ITD627E) indu

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Hirsh, Vera. "Turning EGFR mutation-positive non-small-cell lung cancer into a chronic disease: optimal sequential therapy with EGFR tyrosine kinase inhibitors." Therapeutic Advances in Medical Oncology 10 (January 2018): 175883401775333. http://dx.doi.org/10.1177/1758834017753338.

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Four epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), erlotinib, gefitinib, afatinib and osimertinib, are currently available for the management of EGFR mutation-positive non-small-cell lung cancer (NSCLC), with others in development. Although tumors are exquisitely sensitive to these agents, acquired resistance is inevitable. Furthermore, emerging data indicate that first- (erlotinib and gefitinib), second- (afatinib) and third-generation (osimertinib) EGFR TKIs differ in terms of efficacy and tolerability profiles. Therefore, there is a strong imperative to optimize

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Rocco, Danilo, Luigi Sapio, Luigi Della Gravara, Silvio Naviglio, and Cesare Gridelli. "Treatment of Advanced Non-Small Cell Lung Cancer with RET Fusions: Reality and Hopes." International Journal of Molecular Sciences 24, no. 3 (2023): 2433. http://dx.doi.org/10.3390/ijms24032433.

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RET-selective tyrosine kinase inhibitors (TKIs) selpercatinib and pralsetinib have revolutionized the landscape of RET-positive (RET+) advanced non-small cell lung cancer (NSCLC) treatment thanks to their efficacy and safety profiles. This class of medications currently represents the standard of care for both naïve and patients that have not received selective RET-TKIs in the first-line setting. However, we presently lack a satisfactory understanding of resistance mechanism developing after selective RET-TKIs usage, as well as a specific treatment for patients progressing on selpercatinib or

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Ma, Hayley S., Bao Nguyen, Mark Levis, Allen B. Williams, and Donald Small. "TTT-3002 Is Active Against Relapsed/Refractory AML Patient Bone Marrow With FLT3 TKI-Resistance Mutations At Residue D835." Blood 122, no. 21 (2013): 3818. http://dx.doi.org/10.1182/blood.v122.21.3818.3818.

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Abstract Over 35% of acute myeloid leukemia (AML) patients harbor a constitutively activating mutation in FLT3, either internal tandem duplication (ITD) or point mutations (FLT3/PM). FLT3/ITD mutations in particular confer a poor prognosis, and thus several FLT3 tyrosine kinase inhibitors (TKIs) have been developed and are currently in clinical trials. However, many have failed due to insufficient achievement of FLT3 kinase inhibition in vivo. This is thought to be due to insufficient potency, reduced activity against FLT3/PM, and/or selection for resistance-conferring point mutations in FLT3/

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Waliany, Sarah, Andrew Do, Jenn Peterson, et al. "Shifting landscape of resistance to next-generation ALK inhibitors with evolving treatment paradigm in ALK+ lung cancer." Journal of Clinical Oncology 43, no. 16_suppl (2025): 8607. https://doi.org/10.1200/jco.2025.43.16_suppl.8607.

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8607 Background: Next-generation (gen) ALK tyrosine kinase inhibitors (TKIs) are standard first-line (1L) therapy for patients (pts) with ALK -rearranged (ALK+) metastatic non-small cell lung cancer (mNSCLC), having supplanted crizotinib (criz). While past studies uncovered mechanisms of resistance to next-gen ALK TKIs, vast majority of analyzed biopsies (bx) were obtained from pts treated with next-gen TKIs after 1L criz, reflecting the outdated treatment paradigm. Limited knowledge exists on the mechanisms of resistance to second- (2G) and third-gen (3G) ALK TKIs received without 1L criz exp

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