K.-K. Wong

Adeno-to-squamous transition drives resistance to KRAS inhibition in LKB1 mutant lung cancer

The paper identifies adeno-to-squamous transition (AST) as a mechanism of resistance to KRAS inhibitors in LKB1 mutant lung cancer and links KRT6A expression to poor patient outcomes.

Tumor-intrinsic LKB1-LIF signaling axis establishes a myeloid niche to promote immune evasion and tumor growth

This study identifies a LKB1-LIF signaling axis in tumors that promotes immune evasion by reprogramming myeloid cells, and shows that inhibiting LIF signaling reduces tumor growth.

Glutamine antagonist DRP-104 suppresses tumor growth and enhances response to checkpoint blockade in KEAP1 mutant lung cancer

This study shows that DRP-104, a glutamine antagonist, suppresses KEAP1 mutant lung tumor growth and enhances response to checkpoint blockade by inhibiting glutamine metabolism and improving T cell function.

Acquired Cross-resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of MYC paralogs

This paper identifies extrachromosomal DNA amplification of MYC paralogs as a recurrent driver of acquired cross-resistance in small cell lung cancer using patient-derived xenograft models.

EZH2 inhibition promotes tumor immunogenicity in lung squamous cell carcinomas

EZH2 inhibition increases immune checkpoint inhibitor response in lung squamous cell carcinomas by enhancing antigen presentation and immune cell infiltration.

In vivo metabolomics identifies CD38 as an emergent vulnerability in LKB1-mutant lung cancer

The paper identifies CD38 as a therapeutic target in LKB1-mutant lung cancer through in vivo metabolomics and shows that targeting CD38 inhibits tumor growth.

KEAP1 mutation in lung adenocarcinoma promotes immune evasion and immunotherapy resistance

This study shows KEAP1 mutations in lung adenocarcinoma lead to immune evasion by reducing dendritic cell and T cell responses, contributing to immunotherapy resistance.

Identification of TAZ as the essential molecular switch in orchestrating SCLC phenotypic transition and metastasis

The paper identifies TAZ as a molecular switch driving phenotypic transition and metastasis in SCLC by analyzing mouse models and human data.

Loss of Smad4 promotes aggressive lung cancer metastasis by de-repression ofPAK3 via miRNA regulation

This study shows that Smad4 loss promotes lung cancer metastasis by upregulating PAK3 through miRNA regulation, suggesting Smad4 LOF as a prognostic marker and therapeutic target.

Combined Inhibition of SHP2 and CXCR1/2 Promotes Anti-Tumor T Cell Response in NSCLC

This study shows that combining SHP2 and CXCR1/2 inhibitors enhances anti-tumor T cell responses in NSCLC by reducing immunosuppressive gMDSCs and promoting effector T cells.

SHP2 Inhibition Abrogates Adaptive Resistance to KRASG12C-Inhibition and Remodels the Tumor Microenvironment of KRAS-Mutant Tumors

This study shows that combining SHP2 inhibitors with KRASG12C inhibitors enhances efficacy in PDAC and NSCLC by overcoming resistance and remodeling the tumor microenvironment.

Ontogeny and Vulnerabilities of Drug-Tolerant Persisters in HER2+ Breast Cancer

This study identifies drug-tolerant persisters (DTPs) in HER2+ breast cancer and reveals their origins and vulnerabilities to TKI resistance.

Branched-Chain Amino Acid Metabolic Reprogramming Orchestrates Drug Resistance to EGFR Tyrosine Kinase Inhibitors

This study identifies BCAT1-mediated metabolic reprogramming as a mechanism of EGFR TKI resistance in lung cancer and shows that combining TKI with ROS-inducing agents can overcome resistance.