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UnknownDisclosure of erlotinib as a multikinase inhibitor in pancreatic ductal adenocarcinoma.
Not available
S-EPMC3223607 | biostudies-literature
UnknownExploiting features of adenovirus replication to support mammalian kinase production.
Not available
S-EPMC275485 | biostudies-literature
UnknownData concerning the chromatographic isolation of bovine IgG from milk- and colostral whey.
Not available
S-EPMC6199771 | biostudies-literature
UnknownAn efficient proteomics method to identify the cellular targets of protein kinase inhibitors.
Not available
S-EPMC307585 | biostudies-literature
UnknownPhosphosignature predicts dasatinib response in non-small cell lung cancer.
Not available
S-EPMC3434785 | biostudies-literature
UnknownPhosphoproteome Analysis Reveals Differential Mode of Action of Sorafenib in Wildtype and Mutated FLT3 Acute Myeloid Leukemia (AML) Cells.
Not available
S-EPMC5500767 | biostudies-literature
UnknownGlobal phosphoproteome analysis of human bone marrow reveals predictive phosphorylation markers for the treatment of acute myeloid leukemia with quizartinib.
Not available
S-EPMC3948157 | biostudies-literature
UnknownCDK/CK1 inhibitors roscovitine and CR8 downregulate amplified MYCN in neuroblastoma cells.
Not available
S-EPMC4087096 | biostudies-literature
ProteomicsPhosphoproteome Analysis Reveals Differential Mode of Action of Sorafenib in Wildtype and Mutated FLT3 AML Cells
Constitutively activating internal tandem duplication (ITD) alterations of the receptor tyrosine kinase FLT3 (Fms-like tyrosine kinase 3) are common in acute myeloid leukemia (AML) and classifies FLT3 as an attractive therapeutic target. So far, application of FLT3 small molecule inhibitors such as ...
ORGANISM(S): Homo sapiens (Human) 
2017-05-02 | PXD004442 | Pride
Phosphoproteomics Sorafenib Flt3 Acute myeloid leukemia 
ProteomicsGlobal phosphoproteome analysis of human bone marrow reveals predictive phosphorylation markers for the treatment of acute myeloid leukemia with quizartinib
Treatment with inhibitors of the receptor tyrosine kinase FLT3 are currently studied as promising therapies in acute myeloid leukemia (AML). However, only a subset of patients benefit from these treatments and the presence of activating mutations within FLT3 can predict response to a certain extent ...
ORGANISM(S): Homo sapiens (Human) 
2017-05-10 | PXD006475 | Pride
Biomarker  classification  aml  ac220  quizartinib  phosphoproteomics  response prediction 
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