Area of research
Molecular Biology · Pathology and Forensic Medicine
Research interest
Research interests include Cancer research, MEK inhibitor, Mutant, MAPK/ERK pathway, Biology, and Kinase.
PI3Kα Inhibitor and Degrader Inavolisib Can Co-opt FGFR2 to Enhance Responses in Patients with <i>PIK3CA</i> -Mutated Solid Tumors and in Preclinical Models
NRF2 supports non-small cell lung cancer growth independently of CBP/p300-enhanced glutathione synthesis
RIT1M90I Is a Driver of Lung Adenocarcinoma Tumorigenesis and Resistance to Targeted Therapy
An allosteric pan-TEAD inhibitor blocks oncogenic YAP/TAZ signaling and overcomes KRAS G12C inhibitor resistance
Targeting MCL‐1 and BCL‐2 with polatuzumab vedotin and venetoclax overcomes treatment resistance in R/R non‐Hodgkin lymphoma: Results from preclinical models and a Phase Ib study
Data from ERK Mutations and Amplification Confer Resistance to ERK-Inhibitor Therapy
Data from ERK Mutations and Amplification Confer Resistance to ERK-Inhibitor Therapy
Selective PROTAC-mediated degradation of SMARCA2 is efficacious in SMARCA4 mutant cancers
Distinct resistance mechanisms arise to allosteric vs. ATP-competitive AKT inhibitors
ARAF mutations confer resistance to the RAF inhibitor belvarafenib in melanoma
Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Adaptive Resistance to Dual BRAF/MEK Inhibition in BRAF-Driven Tumors through Autocrine FGFR Pathway Activation
Pharmacological Induction of RAS-GTP Confers RAF Inhibitor Sensitivity in KRAS Mutant Tumors
ERK Mutations and Amplification Confer Resistance to ERK-Inhibitor Therapy
USP7 small-molecule inhibitors interfere with ubiquitin binding
Combined MEK and ERK inhibition overcomes therapy-mediated pathway reactivation in RAS mutant tumors
Widespread potential for growth-factor-driven resistance to anticancer kinase inhibitors