Results 61 to 70 of about 3,492,883 (216)

Aurora kinase A drives the evolution of resistance to third-generation EGFR inhibitors in lung cancer. [PDF]

open access: yes, 2019
Although targeted therapies often elicit profound initial patient responses, these effects are transient due to residual disease leading to acquired resistance.
A Hübner   +66 more
core   +1 more source

Mitochondrial-Targeting MET Kinase Inhibitor Kills Erlotinib-Resistant Lung Cancer Cells [PDF]

open access: yesACS Medicinal Chemistry Letters, 2016
Lung cancer cells harboring activating EGFR mutations acquire resistance to EGFR tyrosine kinase inhibitors (TKIs) by activating several bypass mechanisms, including MET amplification and overexpression. We show that a significant proportion of activated MET protein in EGFR TKI-resistant HCC827 lung cancer cells resides within the mitochondria ...
Tianming, Yang   +6 more
openaire   +2 more sources

Loss of activating EGFR mutant gene contributes to acquired resistance to EGFR tyrosine kinase inhibitors in lung cancer cells. [PDF]

open access: yesPLoS ONE, 2012
Non-small-cell lung cancer harboring epidermal growth factor receptor (EGFR) mutations attains a meaningful response to EGFR-tyrosine kinase inhibitors (TKIs).
Keisuke Tabara   +16 more
doaj   +1 more source

Effective osimertinib treatment in a patient with discordant T790 M mutation detection between liquid biopsy and tissue biopsy. [PDF]

open access: yes, 2018
BACKGROUND:We report the successful treatment of the patient with osimertinib 80 mg/day following disease progression and a discordance in the detection of a mechanism of resistance epithelial growth factor receptor (EGFR) T790 M between liquid biopsy ...
Mambetsariev, Isa   +3 more
core   +1 more source

Identification of LDH-A as a therapeutic target for cancer cell killing via (i) p53/NAD(H)-dependent and (ii) p53 independent pathways [PDF]

open access: yes, 2014
Most cancer cells use aerobic glycolysis to fuel their growth. The enzyme lactate dehydrogenase-A (LDH-A) is key to cancer’s glycolytic phenotype, catalysing the regeneration of nicotinamide adenine dinucleotide (NAD þ ) from reduced nicotinamide adenine
Allison, Simon J.   +6 more
core   +1 more source

Partial Response to Platinum Doublets in Refractory EGFR-Positive Non-Small Cell Lung Cancer Patients after RRx-001: Evidence of Episensitization. [PDF]

open access: yes, 2016
RRx-001, an experimental systemically non-toxic epi-immunotherapeutic agent, which potentiates the resensitization of resistant cancer cells to formerly effective therapies, is under active investigation in several clinical trials that are based on ...
Brzezniak, Christina   +8 more
core   +3 more sources

Molecular Mechanism of Erlotinib Resistance in Epidermal Growth Factor Receptor 
Mutant Non-small cell Lung Cancer Cell Line H1650

open access: yesChinese Journal of Lung Cancer, 2012
Background and objective Epidermal growth factor receptor (EGFR) overexpression and mutations were existed in more than 40% of the lung cancer, and it’s the one of molecular targets in clinical treatment.
Ruili HAN   +7 more
doaj   +1 more source

GBM heterogeneity as a function of variable epidermal growth factor receptor variant III activity. [PDF]

open access: yes, 2016
Abnormal activation of the epidermal growth factor receptor (EGFR) due to a deletion of exons 2-7 of EGFR (EGFRvIII) is a common alteration in glioblastoma (GBM). While this alteration can drive gliomagenesis, tumors harboring EGFRvIII are heterogeneous.
David James, C   +11 more
core   +1 more source

Crizotinib sensitizes the erlotinib resistant HCC827GR5 cell line by influencing lysosomal function [PDF]

open access: yesJournal of Cellular Physiology, 2020
AbstractIn non‐small cell lung cancer, sensitizing mutations in epidermal growth factor receptor (EGFR) or cMET amplification serve as good biomarkers for targeted therapies against EGFR or cMET, respectively. Here we aimed to determine how this different genetic background would affect the interaction between the EGFR‐inhibitor erlotinib and the cMET ...
Nele Van Der Steen   +14 more
openaire   +7 more sources

Subsequent chemotherapy reverses acquired tyrosine kinase inhibitor resistance and restores response to tyrosine kinase inhibitor in advanced non-small-cell lung cancer

open access: yesBMC Cancer, 2011
Background Patients with advanced or metastatic non-small cell lung cancer (NSCLC) can develop acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors (TKIs) erlotinib and gefitinib.
Sun Jin   +5 more
doaj   +1 more source

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