Results 41 to 50 of about 2,223,573 (201)

LncRNA UCA1 Induces Acquired Resistance to Gefitinib by Epigenetically Silencing CDKN1A Expression in Non-small-Cell Lung Cancer

open access: yesFrontiers in Oncology, 2020
Lung cancer is the most common cancer globally and is associated with high morbidity and mortality. Gefitinib has been widely used for treating advanced non-small-cell lung cancer (NSCLC).
Tianwei Xu   +9 more
doaj   +1 more source

Long noncoding RNA ZMIZ1‐AS1 promotes gefitinib resistance via binding to hnRNPA1

open access: yesPrecision Medical Sciences, 2021
To gain an insight into the molecular mechanisms of gefitinib resistance in nonsmall cell lung cancer, we screened out the long noncoding RNA related to gefitinib resistance through microarray data in gefitinib‐sensitive and resistant cells. lncRNA ZMIZ1‐
Changwen Jing   +6 more
doaj   +1 more source

m6A methyltransferase METTL3-induced lncRNA SNHG17 promotes lung adenocarcinoma gefitinib resistance by epigenetically repressing LATS2 expression

open access: yesCell Death and Disease, 2022
Gefitinib has been widely applied for the treatment of lung adenocarcinoma (LUAD). However, the long-term application of gefitinib usually leads to acquired drug resistance in tumour patients, resulting in clinical treatment failure. Small nucleolar host
Heng Zhang   +9 more
doaj   +1 more source

miR-196a Upregulation Contributes to Gefitinib Resistance through Inhibiting GLTP Expression. [PDF]

open access: yesInt J Mol Sci, 2022
Tyrosine kinase inhibitor (TKI) therapy has greatly improved lung cancer survival in patients with epidermal growth factor receptor (EGFR) mutations. However, the development of TKI-acquired resistance is the major problem to be overcome.
Liu BJ   +6 more
europepmc   +3 more sources

Inhibition of the mitochondria-shaping protein Opa1 restores sensitivity to Gefitinib in a lung adenocarcinomaresistant cell line

open access: yesCell Death and Disease, 2023
Drug resistance limits the efficacy of chemotherapy and targeted cancer treatments, calling for the identification of druggable targets to overcome it.
Masafumi Noguchi   +11 more
doaj   +1 more source

miR-19a contributes to gefitinib resistance and epithelial mesenchymal transition in non-small cell lung cancer cells by targeting c-Met

open access: yesScientific Reports, 2017
Gefitinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, is used as a first-line treatment for advanced non-small cell lung cancer (NSCLC).
Xiaonian Cao   +7 more
doaj   +1 more source

FGL1 regulates acquired resistance to Gefitinib by inhibiting apoptosis in non-small cell lung cancer

open access: yesRespiratory Research, 2020
Background This study investigated the role of fibrinogen-like protein 1 (FGL1) in regulating gefitinib resistance of PC9/GR non-small cell lung cancer (NSCLC).
Cuilan Sun   +4 more
doaj   +1 more source

Sijunzi Tang improves gefitinib resistance by regulating glutamine metabolism

open access: yesBiomedicine & Pharmacotherapy, 2023
Lung cancer is a major health concern and significant barrier to human well-being and social development. Although targeted therapy has shown remarkable progress in the treatment of lung cancer, the emergence of drug resistance has limited its clinical efficacy.
Zhihong Wang   +7 more
openaire   +2 more sources

USP8 Is a Novel Target for Overcoming Gefitinib Resistance in Lung Cancer [PDF]

open access: yesClinical Cancer Research, 2013
Abstract Purpose: Common treatment modalities for non–small cell lung cancer (NSCLC) involve the EGF receptor-tyrosine kinase inhibitors (EGFR-TKIs) like gefitinib and erlotinib. However, the vast majority of treated patients acquire resistance to EGFR-TKIs, due, in large part, to secondary mutations in EGFR or amplification of the ...
Sanguine, Byun   +12 more
openaire   +2 more sources

ROS1 amplification mediates resistance to gefitinib in glioblastoma cells

open access: yesOncotarget, 2015
Glioblastoma (GBM) is the most aggressive brain tumor in adults and remains incurable despite multimodal intensive treatment regimens. The majority of GBM tumors show a mutated or overexpressed EGFR, however, tumors treated with tyrosine kinase inhibitors (TKIs) will inevitably recur highlighting the need to identify signalling pathways involved in GBM
Hashim, Aljohani   +5 more
openaire   +3 more sources

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