about
Synthetic lethal interaction of combined BCL-XL and MEK inhibition promotes tumor regressions in KRAS mutant cancer modelsA murine lung cancer co-clinical trial identifies genetic modifiers of therapeutic response.Counterbalance between RB inactivation and miR-17-92 overexpression in reactive oxygen species and DNA damage induction in lung cancersApoptosis induction by antisense oligonucleotides against miR-17-5p and miR-20a in lung cancers overexpressing miR-17-92Triple inhibition of EGFR, Met, and VEGF suppresses regrowth of HGF-triggered, erlotinib-resistant lung cancer harboring an EGFR mutationmTOR inhibitors control the growth of EGFR mutant lung cancer even after acquiring resistance by HGF.Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK.Not just gRASping at flaws: finding vulnerabilities to develop novel therapies for treating KRAS mutant cancersAbility of the Met kinase inhibitor crizotinib and new generation EGFR inhibitors to overcome resistance to EGFR inhibitors.Assessment of ABT-263 activity across a cancer cell line collection leads to a potent combination therapy for small-cell lung cancer.Japanese Society of Medical Oncology Clinical Guidelines: RAS (KRAS/NRAS) mutation testing in colorectal cancer patientsBIM expression in treatment-naive cancers predicts responsiveness to kinase inhibitors.Measurement of PIP3 levels reveals an unexpected role for p110β in early adaptive responses to p110α-specific inhibitors in luminal breast cancer.Recurrence of renal cell carcinoma diagnosed using contralateral adrenal biopsy with endoscopic ultrasound-guided fine-needle aspiration.High efficacy of third generation EGFR inhibitor AZD9291 in a leptomeningeal carcinomatosis model with EGFR-mutant lung cancer cellsEpithelial-to-Mesenchymal Transition Defines Feedback Activation of Receptor Tyrosine Kinase Signaling Induced by MEK Inhibition in KRAS-Mutant Lung Cancer.mTOR inhibition specifically sensitizes colorectal cancers with KRAS or BRAF mutations to BCL-2/BCL-XL inhibition by suppressing MCL-1.Apoptosis in targeted therapy responses: the role of BIM.A systematic review and meta-analysis of individual patient data on the impact of the BIM deletion polymorphism on treatment outcomes in epidermal growth factor receptor mutant lung cancer.Lack of association between the BIM deletion polymorphism and the risk of lung cancer with and without EGFR mutations.Receptor ligand-triggered resistance to alectinib and its circumvention by Hsp90 inhibition in EML4-ALK lung cancer cells.EGFR-TKI resistance due to BIM polymorphism can be circumvented in combination with HDAC inhibition.Phase I and pharmacokinetic study of sorafenib, an oral multikinase inhibitor, in Japanese patients with advanced refractory solid tumors.Novel NBS1 heterozygous germ line mutation causing MRE11-binding domain loss predisposes to common types of cancer.Co-active receptor tyrosine kinases mitigate the effect of FGFR inhibitors in FGFR1-amplified lung cancers with low FGFR1 protein expression.Identification of decatenation G2 checkpoint impairment independently of DNA damage G2 checkpoint in human lung cancer cell lines.Key roles of EMT for adaptive resistance to MEK inhibitor in KRAS mutant lung cancer.Combined EGFR/MET or EGFR/HSP90 inhibition is effective in the treatment of lung cancers codriven by mutant EGFR containing T790M and MET.Epithelial-to-mesenchymal transition antagonizes response to targeted therapies in lung cancer by suppressing BIM.Relationship of deregulated signaling converging onto mTOR with prognosis and classification of lung adenocarcinoma shown by two independent in silico analyses.Pharmacokinetic and pharmacodynamic comparison of fluoropyrimidine derivatives, capecitabine and 5'-deoxy-5-fluorouridine (5'-DFUR).[Pharmacokinetic comparison of capecitabine and 5'-deoxy-5-fluorouridine (doxifluridine; 5'-DFUR)].Extragonadal germ cell tumors in Japan.Resistance mediated by alternative receptor tyrosine kinases in FGFR1-amplified lung cancer.Distinct dependencies on receptor tyrosine kinases in the regulation of MAPK signaling between BRAF V600E and non-V600E mutant lung cancers.Pan-Asian adapted ESMO consensus guidelines for the management of patients with metastatic colorectal cancer: a JSMO-ESMO initiative endorsed by CSCO, KACO, MOS, SSO and TOS.Prospective study of positron emission tomography for evaluation of the activity of lapatinib, a dual inhibitor of the ErbB1 and ErbB2 tyrosine kinases, in patients with advanced tumors.Japanese Society of Medical Oncology Clinical Guidelines: Molecular Testing for Colorectal Cancer Treatment, Third Edition.ADAM17 selectively activates the IL-6 trans-signaling/ERK MAPK axis in KRAS-addicted lung cancerGenetic polymorphisms of CYP2B6 affect the pharmacokinetics/pharmacodynamics of cyclophosphamide in Japanese cancer patients
P50
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P50
description
hulumtues
@sq
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Hiromichi Ebi
@ast
Hiromichi Ebi
@en
Hiromichi Ebi
@es
Hiromichi Ebi
@sl
type
label
Hiromichi Ebi
@ast
Hiromichi Ebi
@en
Hiromichi Ebi
@es
Hiromichi Ebi
@sl
prefLabel
Hiromichi Ebi
@ast
Hiromichi Ebi
@en
Hiromichi Ebi
@es
Hiromichi Ebi
@sl
P106
P1153
6603124271
P21
P31
P496
0000-0003-3155-7576
P569
2000-01-01T00:00:00Z