Kwok Kin Wong
New York University, NY·Medicine & Clinical Research
Lung cancers often respond to treatment at first, then come back. Tumor cells can change their identity or genetic makeup and escape the drugs.
- Fields
Medicine & Clinical Research
Pharmacology
Genetics
- Topics
small cell lung cancer
lung adenocarcinoma
KRAS inhibitors
- Grants
- 3 known grants, through Jul 2029
What they work on
- Determine how co-mutations such as MYC, KMT2D, STK11 and PTEN change SCLC plasticity (cells' ability to switch identity) and transcriptional subtypes, using new mouse models built on TP53/RB1-mutant SCLC.
- Evaluate how co-mutations alter SCLC responses to CDK2 and PARP inhibitors, drugs that exploit replication stress, and test these drugs combined with immunotherapy in immune-competent models.
- Trace the origin and fate of AT1-like and squamous tumor cell states that resist KRAS inhibitors in lung adenocarcinoma, using lineage tracing in KRAS G12D/G12C genetically engineered mice.
- Test whether removing AT1-like or squamous cells by lineage ablation overcomes KRAS inhibitor resistance, and identify the molecular drivers of these states in tumors with or without LKB1.
- Measure the effect of a MUC1-C inhibitor, alone and combined with a CDK7 inhibitor, on neuroendocrine and non-neuroendocrine SCLC in cells and in orthotopic mouse models of four subtypes (ASCL1, NEUROD1, YAP1, POU2F3).
- Define how MUC1-C and CDK7 inhibition change the tumor microenvironment and anti-tumor immunity in SCLC mouse models with intact immune systems.
More about the research
These projects study how genetic mutations and shifts in cell state shape drug responses in two deadly lung cancers: small cell lung cancer (SCLC) and lung adenocarcinoma (LUAD). The goal is to design drug combinations, including some that recruit the immune system, that work longer.
Why it matters
Small cell lung cancer usually returns within a year, and treatments have changed little in decades. KRAS inhibitors for lung adenocarcinoma lose effectiveness as tumors become resistant. This work could identify biomarkers that predict resistance and relapse. It could also suggest new drug combinations, such as CDK7 with MUC1-C inhibitors or targeted drugs with immunotherapy, that may produce more lasting responses for lung cancer patients.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Impact of recurrent genetic alterations on SCLC subtypes and therapeutic response
NIH · Aug 2024 – Jul 2029
Targeting cell state transitions driving resistance to KRAS inhibitors in lung cancer
NIH · Jun 2024 – May 2029
Combining CDK7 and MUC1-C inhibition to target different subtypes of small cell lung cancer
NIH · Mar 2024 – Feb 2029
Closest labs
Pawel K. Mazur
University of Texas MD Anderson Cancer Center, TX·Genetics
Dissect how the enzyme CARM1 methylates the tumor-promoting transcription factor NFIB and signals through the effector protein TRIM29 in small cell lung cancer, using knock-in mice that carry a non-methylatable NFIB.
Ite Offringa
University of Southern California, CA·Medicine & Clinical Research
Generate a mouse monoclonal antibody that recognizes only isoaspartylated ELAVL4, a damaged protein form on small cell lung cancer cells, by immunizing with a synthetic peptide and optimizing binding speed and strength.
Wantong Yao
University of Texas MD Anderson Cancer Center, TX·Medicine & Clinical Research
Define the molecular pathways through which a newly identified stress-response regulator helps pancreatic ductal adenocarcinoma (PDAC) cells survive nutrient shortage, low oxygen and oxidative stress, and evade the immune system.
The school
New York University: 72 labs on PI Pages, $1.5B a year on research, 540 research doctorates a year.
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