about
Synthetic lethal interaction of combined BCL-XL and MEK inhibition promotes tumor regressions in KRAS mutant cancer modelsThe BCL2 Family: Key Mediators of the Apoptotic Response to Targeted Anticancer TherapeuticsExploitation of the Apoptosis-Primed State of MYCN-Amplified Neuroblastoma to Develop a Potent and Specific Targeted Therapy CombinationIdentification of determinants of ligand binding affinity and selectivity in the prostaglandin D2 receptor CRTH2Characterization of a rabbit kidney prostaglandin F(2{alpha}) receptor exhibiting G(i)-restricted signaling that inhibits water absorption in the collecting duct.Assessment of ABT-263 activity across a cancer cell line collection leads to a potent combination therapy for small-cell lung cancer.Extracellular loop II modulates GTP sensitivity of the prostaglandin EP3 receptormTOR inhibition specifically sensitizes colorectal cancers with KRAS or BRAF mutations to BCL-2/BCL-XL inhibition by suppressing MCL-1.Heterogeneity Underlies the Emergence of EGFRT790 Wild-Type Clones Following Treatment of T790M-Positive Cancers with a Third-Generation EGFR Inhibitor.Failure to induce apoptosis via BCL-2 family proteins underlies lack of efficacy of combined MEK and PI3K inhibitors for KRAS-mutant lung cancersColon carcinoma cell growth is associated with prostaglandin E2/EP4 receptor-evoked ERK activation.EGFR Mutations and ALK Rearrangements Are Associated with Low Response Rates to PD-1 Pathway Blockade in Non-Small Cell Lung Cancer: A Retrospective Analysis.Programmed Cell Death Ligand (PD-L1) Expression in Stage II and III Lung Adenocarcinomas and Nodal Metastases.Distinct evolutionary paths to TKI resistance in NSCLC.IR and Raman spectra of beta''-(BEDT-TTF)(2)RCH(2)SO(3) (R = SF(5), CF(3)): dimerization related to hydrogen bonding
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description
investigador
@es
researcher
@en
wetenschapper
@nl
name
Aaron N Hata
@en
Aaron N Hata
@nl
type
label
Aaron N Hata
@en
Aaron N Hata
@nl
prefLabel
Aaron N Hata
@en
Aaron N Hata
@nl
P31
P496
0000-0002-6127-318X