DYRK1A inhibition suppresses STAT3/EGFR/Met signalling and sensitizes EGFR wild‐type NSCLC cells to AZD9291

The anti-tumor effect of regorafenib in lung squamous cell carcinoma in vitro

(2018) Xiu Hu et al.   BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS

Osimertinib resistance in non-small cell lung cancer: Mechanisms and therapeutic strategies

(2018) Zheng-Hai Tang et al.   CANCER LETTERS

STAT3 Interactors as Potential Therapeutic Targets for Cancer Treatment

(2018) Federica Laudisi et al.   INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES

Dual-Specificity Tyrosine Phosphorylation-Regulated Kinase 1A (DYRK1A) Inhibitors as Potential Therapeutics

(2018) Dnyandev B. Jarhad et al.   JOURNAL OF MEDICINAL CHEMISTRY

Randomized phase II study of fulvestrant and erlotinib compared with erlotinib alone in patients with advanced or metastatic non-small cell lung cancer

(2018) Edward B. Garon et al.   LUNG CANCER

Osimertinib in Untreated EGFR-Mutated Advanced Non–Small-Cell Lung Cancer

(2018) Jean-Charles Soria et al.   NEW ENGLAND JOURNAL OF MEDICINE

DYRK1A inhibition and cognitive rescue in a Down syndrome mouse model are induced by new fluoro-DANDY derivatives

(2018) Fernanda Neumann et al.   Scientific Reports

Targeting S1PR1/STAT3 loop abrogates desmoplasia and chemosensitizes pancreatic cancer to gemcitabine

(2018) Manendra Babu Lankadasari et al.   Theranostics

STAT3 regulatedmiR-216apromotes ovarian cancer proliferation and cisplatin resistance

(2018) Pengfei Jin et al.   BIOSCIENCE REPORTS

STAT3 activation confers trastuzumab-emtansine (T-DM1) resistance in HER2-positive breast cancer

(2018) Lei Wang et al.   CANCER SCIENCE

Acquired Resistance of MET-Amplified Non-small Cell Lung Cancer Cells to the MET Inhibitor Capmatinib

(2018) Seulki Kim et al.   Cancer Research and Treatment

Dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) inhibitors: a survey of recent patent literature

(2017) Thu Lan Nguyen et al.   EXPERT OPINION ON THERAPEUTIC PATENTS

Novel EGFR (T790M)-cMET dual inhibitors: putative therapeutic agents for non-small-cell lung cancer

(2017) Pankaj Kumar Singh et al.   Future Medicinal Chemistry

Lung cancer: current therapies and new targeted treatments

(2017) Fred R Hirsch et al.   LANCET

STAT3 signaling mediates tumour resistance to EGFR targeted therapeutics

(2017) Ahmad A. Zulkifli et al.   MOLECULAR AND CELLULAR ENDOCRINOLOGY

Sensitization of EGFR Wild-Type Non–Small Cell Lung Cancer Cells to EGFR-Tyrosine Kinase Inhibitor Erlotinib

(2017) Judith Raimbourg et al.   MOLECULAR CANCER THERAPEUTICS

Osimertinib or Platinum–Pemetrexed in EGFR T790M–Positive Lung Cancer

(2017) Tony S. Mok et al.   NEW ENGLAND JOURNAL OF MEDICINE

Clinical staging of NSCLC: current evidence and implications for adjuvant chemotherapy

(2017) David J. Heineman et al.   Therapeutic Advances in Medical Oncology

Immunotherapy for Non-small-cell Lung Cancer: Current Status and Future Obstacles

(2017) Ju Hwan Cho   Immune Network

Met gene amplification and protein hyperactivation is a mechanism of resistance to both first and third generation EGFR inhibitors in lung cancer treatment

(2016) Puyu Shi et al.   CANCER LETTERS

Heterogeneous Mechanisms of Primary and Acquired Resistance to Third-Generation EGFR Inhibitors

(2016) S. Ortiz-Cuaran et al.   CLINICAL CANCER RESEARCH

EGFR tyrosine kinase inhibitor (TKI) in patients with advanced non-small cell lung cancer (NSCLC) harboring uncommon EGFR mutations: A real-world study in China

(2016) Jianlin Xu et al.   LUNG CANCER

Evodiamine induces apoptosis and enhances apoptotic effects of erlotinib in wild-type EGFR NSCLC cells via S6K1-mediated Mcl-1 inhibition

(2016) Yang-ling Li et al.   MEDICAL ONCOLOGY

Acquired Resistance Mechanisms to Combination Met-TKI/EGFR-TKI Exposure in Met-Amplified EGFR-TKI–Resistant Lung Adenocarcinoma Harboring an Activating EGFR Mutation

(2016) Toshimitsu Yamaoka et al.   MOLECULAR CANCER THERAPEUTICS

TC-N19, a novel dual inhibitor of EGFR and cMET, efficiently overcomes EGFR-TKI resistance in non-small-cell lung cancer cells

(2016) D-W Wu et al.   Cell Death & Disease

Second and third-generation epidermal growth factor receptor tyrosine kinase inhibitors in advanced nonsmall cell lung cancer

(2015) Bin-Chi Liao et al.   CURRENT OPINION IN ONCOLOGY

DYRK1A overexpression enhances STAT activity and astrogliogenesis in a Down syndrome mouse model

(2015) N. Kurabayashi et al.   EMBO REPORTS

A novel DYRK1A (Dual specificity tyrosine phosphorylation-regulated kinase 1A) inhibitor for the treatment of Alzheimer's disease: effect on Tau and amyloid pathologiesin vitro

(2015) Séverine Coutadeur et al.   JOURNAL OF NEUROCHEMISTRY

Acquired EGFR C797S mutation mediates resistance to AZD9291 in non–small cell lung cancer harboring EGFR T790M

(2015) Kenneth S Thress et al.   NATURE MEDICINE

Tumor-suppressive microRNA-206 as a dual inhibitor of MET and EGFR oncogenic signaling in lung squamous cell carcinoma

(2014) HIROKO MATAKI et al.   INTERNATIONAL JOURNAL OF ONCOLOGY

Role of p38 MAPK in enhanced human cancer cells killing by the combination of aspirin and ABT-737

(2014) Chong Zhang et al.   JOURNAL OF CELLULAR AND MOLECULAR MEDICINE

Butein, a novel dual inhibitor of MET and EGFR, overcomes gefitinib-resistant lung cancer growth

(2014) Sung Keun Jung et al.   MOLECULAR CARCINOGENESIS

AZD9291, an Irreversible EGFR TKI, Overcomes T790M-Mediated Resistance to EGFR Inhibitors in Lung Cancer

(2014) D. A. E. Cross et al.   Cancer Discovery

Inhibition of DYRK1A destabilizes EGFR and reduces EGFR-dependent glioblastoma growth

(2013) Natividad Pozo et al.   JOURNAL OF CLINICAL INVESTIGATION

Online Survival Analysis Software to Assess the Prognostic Value of Biomarkers Using Transcriptomic Data in Non-Small-Cell Lung Cancer

(2013) Balázs Győrffy et al.   PLoS One

DYRK1A and DYRK3 Promote Cell Survival through Phosphorylation and Activation of SIRT1

(2010) Xiumei Guo et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Development of a novel selective inhibitor of the Down syndrome-related kinase Dyrk1A

(2010) Yasushi Ogawa et al.   Nature Communications