Jonathan Kurie
University of Texas MD Anderson Cancer Center, TX·Medicine & Clinical Research
Lung cancer becomes lethal mainly when it spreads, and patients whose tumors lack drug-targetable receptor mutations have few options. Tumor cells do not spread unaided: they secrete proteins that build a protective, nourishing niche around themselves, and they chemically remodel collagen, the main structural protein of tissue, into stiffer scaffolding that drives invasion.
- Fields
Medicine & Clinical Research
Biochemistry
Pharmacology
- Topics
lung cancer
metastasis
p53
- Grants
- 2 known grants, through Dec 2026
What they work on
- Determine how the GRASP55-containing Golgi protein complex, assembled when the tumor suppressor p53 is lost, enhances protein secretion and drives lung cancer growth and progression.
- Determine why that Golgi protein complex increases sensitivity to the drug the lab identified, which blocks complex formation and reduces secretion in lung cancer cells.
- Test whether electrostatic contacts between lysyl hydroxylase 2 and collagen telopeptides cause formation of stable hydroxylysine aldehyde-derived cross-links and metastasis, using defined collagen matrices and an orthotopic KRAS-mutant lung cancer model.
- Test whether inclusion of LH2's alternatively spliced exon 13a, which confers glucosylgalactosyltransferase activity, causes collagen glucosylation and metastasis.
- Test whether LH2's combined collagen-modifying activities suppress anti-tumor immunity through LAIR-1, an immune-cell receptor for collagen, in the orthotopic lung cancer model.
More about the research
Both projects in this lab ask how lung cancer cells reshape their surroundings to grow and metastasize, and whether those processes can be blocked with drugs.
Why it matters
Lung cancers without actionable receptor tyrosine kinase mutations, including KRAS-mutant disease, remain hard to treat. Identifying a secretion pathway switched on by TP53 mutation and acting through GRASP55, and showing that two collagen-modifying activities of lysyl hydroxylase 2 drive spread and dampen anti-tumor immunity, could justify testing drugs that block secretion and selective LH2 antagonists in lung cancer patients.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
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.
Jason Weber
Washington University in St Louis, MO·Biochemistry
Test whether the ARF tumor suppressor traps the RNA-editing enzyme ADAR1 in the nucleolus, a compartment inside the nucleus. This trapping would stop ADAR1 from holding back type I interferon alarm signaling in TNBC cells that lack working p53.
Kwok Kin Wong
New York University, NY·Medicine & Clinical Research
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.
The school
University of Texas MD Anderson Cancer Center: 23 labs on PI Pages, $1.4B a year on research.
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