Results 51 to 60 of about 286,663 (309)
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska +13 more
wiley +1 more source
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura +19 more
wiley +1 more source
Pair‐wise comparison of the CellSearch and FETCH enrichment technologies for circulating tumor cells (CTCs) from metastatic breast, prostate, and small cell lung cancer patients shows an increased capture of CTCs using FETCH enrichment. The clinical implementation of circulating tumor cells (CTCs) as a predictive tool for therapy efficacy in the ...
Michiel Stevens +6 more
wiley +1 more source
Hsa_circ_0003489 Drives PTX Resistance of Human NSCLC Cells Through Modulating miR-98-5p/IGF2
Shaofeng Xia,1 Chenliang Wang2 1Department of Thoracic Surgery, The First People’s Hospital of Jiujiang City, Jiujiang, Jiangxi, People’s Republic of China; 2Department of Pathology, The First People’s Hospital of Jiujiang City, Jiujiang, Jiangxi, People’
Wang C, Xia S
core
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober +16 more
wiley +1 more source
MET alterations in NSCLC-Current Perspectives and Future Challenges [PDF]
Targeted therapies have revolutionized the treatment and improved the outcome for oncogene-driven NSCLC and an increasing number of oncogenic driver therapies have become available.
Mountzios, Giannis +8 more
core +1 more source
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
Objective To explore the regulative effect of α-Hederin on the proliferation and invasion of NSCLC and investigate its related molecular mechanism. Methods After A549 and HCC-1833 cells were treated with a concentration gradient of α-Hederin for 24 and ...
CHANG Yuzhen, YANG Hao, HUANG Gang
doaj +1 more source
reservedLo studio ha lo scopo di analizzare l’outcome delle terapie per il carcinoma del polmone non a piccole cellule nella real-life negli ospedali della Regione del Veneto di Camposampiero e Cittadella (Ulss Euganea n. 6).
LAZZARO, ROSSELLA
core
The proposed mechanism of action for the CDK12/13 inhibitor and cyclin K degrader, CT7439. CDK12/13 inhibition interrupts transcription elongation, leading to increased DNA damage that results in cell death. This agent is a potentially novel treatment option for patients with colorectal cancer. Created in BioRender. Cyclin‐dependent kinase (CDK) 12 and
Wylie K. Watlington +10 more
wiley +1 more source

