Our Projects
The primary objective of our research program is to identify and therapeutically exploit genetic determinants of immune vulnerability in brain tumors.
CHEK2 as
an Immune Checkpoint in Gliomas
We identified CHEK2 as a tumor-intrinsic kinase that enables gliomas to evade CD8⁺ T-cell–mediated killing. Genetic deletion or pharmacological inhibition of CHEK2 sensitizes tumors to PD‑1/PD‑L1 blockade in preclinical models. Our ongoing work is focused on dissecting the CHEK2–YBX1/YBX3 axis and exploring YBX1 as a therapeutic target to enhance antitumor immunity.
Immune-Stimulatory Effects of CHEK2 Mutations in
Brain Tumors
CHEK2 mutations and deletions are prevalent in gliomas and meningiomas and may predict responsiveness to immunotherapy. We are investigating how germline pathogenic CHEK2 variants influence CD8⁺ T-cell function and immune gene signatures in tumors. This work aims to identify biomarker-driven strategies for selecting patients with CHEK2-mutant tumors for immune-based therapies.
Targeting EphA3
to Improve Checkpoint Blockade
Response
in Glioma
EphA3 emerged from an in vivo CRISPR screen as a key mediator of glioma resistance to PD‑1 blockade. We are testing the combination of EphA3-targeting strategies with PD‑1 inhibitors in glioma models and profiling immune responses. This approach may uncover new combinatorial strategies to overcome immune resistance in GBM.