Results 11 to 20 of about 2,201,777 (199)

Osimertinib induces paraptosis and TRIP13 confers resistance in glioblastoma cells

open access: yesCell Death Discovery, 2023
The efficacy of osimertinib, a third-generation epidermal growth factor receptor tyrosine kinase inhibitor, has been evaluated in glioblastoma (GBM) through preclinical and clinical trials.
Lulu Hu   +12 more
doaj   +4 more sources

Brief Report: Heterogeneity of Acquired Resistance Mechanisms to Osimertinib and Savolitinib [PDF]

open access: yesJTO Clinical and Research Reports, 2021
Introduction: MET amplification is a frequently observed mechanism of resistance to osimertinib, and coinhibition strategy of MET and EGFR revealed promising results in recent clinical trials. Nevertheless, acquired resistance mechanisms to combined EGFR
Sun Min Lim, MD, PhD   +4 more
doaj   +7 more sources

Mechanisms of resistance to osimertinib

open access: yesJournal of Thoracic Disease, 2020
The introduction of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) has significantly improved the prognosis of advanced non-small cell lung cancer (NSCLC) patients with EGFR mutations.
Santarpia M.   +4 more
core   +5 more sources

RETaliation - tackling rare resistance alterations to osimertinib

open access: yesClinical Cancer Research, 2023
RET fusions occur as a rare mechanism of acquired resistance to osimertinib in epidermal growth factor receptor mutation (EGFRm) positive non-small cell lung cancer (NSCLC) patients.
Sanjay Popat   +3 more
core   +4 more sources

Acquired Mechanisms of Resistance to Osimertinib—The Next Challenge

open access: yesCancers, 2022
EGFR-mutated tumors represent a significant percentage of non-small cell lung cancer. Despite the increasing use of osimertinib, a treatment that has demonstrated an outstanding clinical benefit with a tolerable toxicity profile, EGFR tumors eventually ...
Moliner Jiménez, Laura   +5 more
core   +3 more sources

Mechanisms of osimertinib resistance and emerging treatment options.

open access: yesLung Cancer, 2020
Osimertinib is an irreversible EGFR-tyrosine kinase inhibitor initially approved for treatment of EGFR-positive patients exhibiting a T790 M resistance mutation in the second line setting and now emerging as the new standard of care for all EGFR positive
Schmid S, Li JJN, Leighl NB
core   +4 more sources

MicroRNA-130a-3p regulates osimertinib resistance by targeting runt-related transcription factor 3 in lung adenocarcinoma [PDF]

open access: yesScientific Reports
Overcoming resistance to epidermal growth factor receptor tyrosine kinase inhibitors, including osimertinib, is urgent to improve lung cancer treatment outcomes.
Takuya Shintani   +9 more
doaj   +4 more sources

Clonal Evolution and Heterogeneity of Osimertinib Acquired Resistance Mechanisms in EGFR Mutant Lung Cancer [PDF]

open access: yesCell Reports Medicine, 2020
Summary: Clonal evolution of osimertinib-resistance mechanisms in EGFR mutant lung adenocarcinoma is poorly understood. Using multi-region whole-exome and RNA sequencing of prospectively collected pre- and post-osimertinib-resistant tumors, including at ...
Nitin Roper   +30 more
doaj   +3 more sources

3-Phosphoinositide-dependent kinase 1 drives acquired resistance to osimertinib [PDF]

open access: yesCommunications Biology, 2023
Osimertinib sensitive and resistant NSCLC NCI-H1975 clones are used to model osimertinib acquired resistance in humanized and non-humanized mice and delineate potential resistance mechanisms.
Ismail M. Meraz   +20 more
doaj   +2 more sources

Trastuzumab emtansine delays and overcomes resistance to the third-generation EGFR-TKI osimertinib in NSCLC EGFR mutated cell lines [PDF]

open access: yesJournal of Experimental & Clinical Cancer Research, 2017
Background Osimertinib is a third-generation EGFR-TKI with a high selective potency against T790M-mutant NSCLC patients. Considering that osimertinib can lead to enhanced HER-2 expression on cell surface and HER-2 overexpression is a mechanism of ...
Silvia La Monica   +12 more
doaj   +2 more sources

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