Results 61 to 70 of about 2,223,573 (201)

Characterisation and modulation of drug resistance in lung cancer cell lines [PDF]

open access: yes, 2010
Chemotherapy drug resistance is a major obstacle in the treatment of cancer. It can result from an increase in levels of cellular drug efflux pumps such as P-glycoprotein (P-gp).
Dunne, Gráinne
core   +2 more sources

STE029 Overcomes EGFR-TKI Resistance in Human Lung Adenocarcinoma

open access: yesChinese Journal of Lung Cancer, 2022
Background and objective Acquired and primary resistance to epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) is still the bottleneck of clinical treatment of advanced non-small cell lung cancer (NSCLC).
Lin HUANG   +5 more
doaj   +1 more source

A novel quinazolinone insulin receptor inhibitor and its synergy with an EGFR inhibitor in glucose‐driven glioblastoma

open access: yesMolecular Oncology, EarlyView.
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka   +9 more
wiley   +1 more source

Supramolecular Degraders: An Emerging Paradigm in Targeted Protein Degradation

open access: yesAdvanced Science, EarlyView.
Dynamic supramolecular assembly reshapes targeted protein degradation by coordinating modular degrader construction, delivery, functional integration, and intracellular assembly or activation across proteasomal, endosomal–lysosomal, and autophagy–lysosomal pathways.
Kongjun Liu   +8 more
wiley   +1 more source

TROP2‐Targeting Chimeras (TRTACs) for Tumor Cell‐Selective Membrane Protein Degradation and Enhanced Drug Delivery

open access: yesAdvanced Science, EarlyView.
TROP2 is identified as a novel tumor‐selective lysosomal‐targeting receptor with established clinical relevance. TROP2‐targeting chimeras (TRTACs) are developed by genetically fusing a TROP2‐binding nanobody to nanobodies against specific target proteins.
Luping Chen   +10 more
wiley   +1 more source

BST2 promotes growth and induces gefitinib resistance in oral squamous cell carcinoma via regulating the EGFR pathway

open access: yesArchives of Medical Science, 2019
Introduction Gefitinib, well known as a new antitumor agent, has been applied in various cancers such as oral squamous cell carcinoma (OSCC). However, most patients eventually acquire resistance to gefitinib, and the molecular mechanism of gefitinib ...
Huang Jin   +3 more
doaj   +1 more source

The potential impact of H1 antihistamines on clinical outcomes in NSCLC patients undergoing EGFR‐TKIs treatment

open access: yesBritish Journal of Clinical Pharmacology, EarlyView.
Background Epidermal growth factor receptor–tyrosine kinase inhibitors (EGFR‐TKIs) have substantially improved outcomes in non‐small cell lung cancer (NSCLC); however, the development of treatment resistance remains a major clinical challenge. This study examines the association between concomitant prescriptions of H1‐antihistamines (H1AHs) and ...
Van Thuan Nguyen   +10 more
wiley   +1 more source

Imaging Patterns and Prognosis of Patients with Gefitinib-Related Interstitial Lung Disease

open access: yes, 2012
Purpose: We aimed to summarize the imaging findings of 25 patients with gefitinib-related interstitial lung disease ( ILD), and identify the factors related to prognosis of gefitinib-related ILD in patients with non -small-cell-lung cancer. Materials and
YUAN, MEI-KANG;CHANG, CHENG-YU;CHANG, SHIH-CHIEH;CHANG, SHU-JU;TANG, KAO-CHUN;WEI, YU-FENG;CHEN, CHENG-YU;YU, CHONG-JEN   +1 more
core   +1 more source

Challenges of drug resistance in the management of pancreatic cancer [PDF]

open access: yes, 2010
The current treatment of choice for metastatic pancreatic cancer involves single agent gemcitabine or combination of gemcitabine with capecitabine and erlotinib (tyrosine kinase inhibitor).
Naomi Walsh   +10 more
core   +1 more source

N6-methyladenosine (m6A) methyltransferase KIAA1429 accelerates the gefitinib resistance of non-small-cell lung cancer

open access: yesCell Death Discovery, 2021
N6-methyladenosine (m6A) modification has been convincingly identified to be a critical regulator in human cancer. However, the contribution of m6A to NSCLC gefitinib resistance is still largely unknown.
Jun Tang   +4 more
doaj   +1 more source

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