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MetabolomicsHypoxia Dependent Inhibition of Glioblastoma Cell Proliferation, Invasion, and Metabolism by the Choline-Kinase Inhibitor JAS239
Background: Elevated choline kinase alpha (ChoK) levels are observed in most solid tumors, including glioblastomas (GBM), and ChoK inhibitors have demonstrated limited efficacy in GBM models. Given that hypoxia is associated with resistance to GBM therapy, we hypothesized that tumor hypoxia c...
2024-06-18 | MTBLS6212 | MetaboLights
MetabolomicsTargeting PI3K inhibitor resistance in breast cancer with metabolic drugs

Activating PIK3CA mutations, present in up to 40% of hormone receptor-positive (HR+), human epidermal growth factor receptor 2-negative (Her2-) breast cancer (BC) patients, can be effectively targeted with the alpha isoform-specific PI3K inhibitor Alpelisib. This treatment significantly improves ...

2026-08-21 | MTBLS11671 | MetaboLights
TranscriptomicsAberrant ERK signaling causes resistance to EGFR kinase inhibitors
The clinical efficacy of EGFR kinase inhibitors is limited by the development of drug resistance. The irreversible EGFR kinase inhibitor WZ4002 is effective against the most common mechanism of drug resistance mediated by the EGFR T790M mutation. Here we show that in multiple complementary models ha...
ORGANISM(S): Homo sapiens 
2012-10-01 | E-GEOD-37699 | biostudies-arrayexpress
MetabolomicsThe phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 inhibitor 3PO is a modulator of neutrophil metabolism, ROS production and NET release
Neutrophils are key effector leukocytes of the innate immune system and play a pivotal role in defending the host against microbial infections. Recent studies have identified a crucial link between glycolysis and neutrophil cellular functions. We have investigated in human neutrophils, the intricate...
2025-08-14 | MTBLS6215 | MetaboLights
OtherChemical proteomics uncovers EPHA2 as a mechanism of acquired resistance to small molecule EGFR kinase inhibition.
Data from ProteomeXchange, PXD ID: PXD001333. File: 000249_D01_P001442_B00_A00_R1.mzml. Published as part of J Proteome Res. 2015 May 12 . From the Abstract: {{i}} ... Here, we describe a chemical proteomic approach comprising kinase affinity purification (kinobeads) and quantitative mass spectrome...
ORGANISM(S): Homo_sapiens_viruses, Human_female 
GPM32310019962 | GPMDB
Resource Reanalysis 
ProteomicsProteomic profiling by array of tyrosine kinase activity in metastatic malignant melanoma from human tissue specimens
Tyrosine kinase activity profiling of metatstatic malignant melanoma and normal skin tissue samples was performed using peptide kinase arrays. All samples were run in triplicates with and withouth inhbitor PLX4032 and Sutent Malate in order to identify how tyrosine kinases responds to kinase inhibit...
ORGANISM(S): Homo sapiens 
2013-01-17 | E-MTAB-1245 | biostudies-arrayexpress
TranscriptomicsAT13148 is a novel, oral multi-AGC kinase inhibitor with potent pharmacodynamic and antitumor activity
Purpose: Deregulated phosphatidylinositol 3-kinase pathway signaling through AGC kinases including AKT, p70S6 kinase, PKA, SGK and Rho kinase, is a key driver of multiple cancers. The simultaneous inhibition of multiple AGC kinases may increase antitumor activity and minimize clinical resistance com...
ORGANISM(S): Homo sapiens 
2012-07-19 | E-GEOD-38008 | biostudies-arrayexpress
TranscriptomicsCharacterising the cellular activity of new Fibroblast Growth Factor Receptor tyrosine kinase inhibitors and identification of a gatekeeper mutation in FGFR3 as a mechanism of acquired resistance.
Fibroblast growth factor receptors (FGFRs) can act as driving oncoproteins in certain cancers due to mutation, over-expression or activating gene fusions and are therefore attractive drug targets. Here we have characterized tumour cell responses to three new inhibitors of FGFR1-3, AZ12576089, AZ129...
ORGANISM(S): Homo sapiens 
2012-10-02 | E-TABM-1222 | biostudies-arrayexpress
ProteomicsProteomics-based insights into mitogen-activated protein kinase inhibitor resistance of cerebral melanoma metastases
Background MAP kinase inhibitor (MAPKi) therapy for BRAF mutated melanoma is characterized by high response rates but also development of drug resistance within a median progression-free survival (PFS) of 9 to 12 months. Understanding mechanisms of resistance and identifying effective therapeutic al...
ORGANISM(S): Homo Sapiens (ncbitaxon:9606) 
MSV000082948 | MassIVE
TranscriptomicsSpectrum, clinical correlates and clinical implications of BRAF-inhibitor resistance mechanisms in melanoma
Multiple BRAF inhibitor resistance mechanisms have been described, however their relative frequency, clinical correlates, and effect on subsequent therapy have not been assessed in patients with metastatic melanoma. Excised progressing BRAFV600 mutant melanoma metastases (Prog) from patients treated...
ORGANISM(S): Homo sapiens 
2014-02-19 | E-GEOD-50509 | biostudies-arrayexpress
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