Jason Yustein
Emory University, GA·Medicine & Clinical Research
Childhood bone and muscle cancers, called sarcomas, are often curable when caught early. Once they spread or come back, however, long-term survival falls sharply, often to 20–30%.
- Fields
Medicine & Clinical Research
Pharmacology
Genetics
- Topics
pediatric sarcoma
osteosarcoma
Ewing sarcoma
- Grants
- 3 known grants, through Feb 2030
What they work on
- Map single-cell protein and RNA signatures and cell-cell communication in MYC-amplified human and mouse osteosarcoma, using patient-derived xenografts and engineered mice, and disrupt candidate metastasis-linked signals genetically.
- Determine how MYC reprograms the osteosarcoma immune environment using a dTAG-MYC rapid-degradation system, focusing on the immune signal CCL9 and its effects on T cells and myeloid cells, then test combination therapies.
- Identify direct substrates and signaling networks of the kinase PAK4 in primary and metastatic Ewing sarcoma, and test whether PAK4 regulates alternative RNA splicing and the activity of the EWS::FLI1 fusion oncogene.
- Evaluate PAK4 inhibitors combined with chemotherapy or other targeted agents in orthotopic and metastatic Ewing sarcoma models.
- Test whether PAK4 acts as a splicing-regulating kinase in rhabdomyosarcoma and how it shapes the tumor microenvironment, using syngeneic mouse models developed in the lab.
- Test synergistic PAK4 inhibitor combinations found by high-throughput drug screens in ex vivo 3D lung metastasis models and in orthotopic and metastatic rhabdomyosarcoma mice.
More about the research
Many of these tumors are driven by proteins that drugs cannot block directly. Three projects therefore look for weaker points in the signaling networks around those drivers: in osteosarcoma driven by the MYC gene, and through a signaling enzyme called PAK4 in Ewing sarcoma and rhabdomyosarcoma. Each combines mechanism with testing of drug combinations in mouse and patient-derived models.
Why it matters
Children and adolescents with relapsed or metastatic osteosarcoma, Ewing sarcoma or rhabdomyosarcoma currently have survival rates as low as 20–30%. By identifying weak points in MYC-driven and PAK4-dependent tumors, this work could provide new drug targets and combination treatments. It could also help identify high-risk patients early for upfront targeted therapy, and these treatments may eventually move to clinical trials with fewer toxic effects than current chemotherapy.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Luis Parada
Indiana University-Purdue University-Indianapolis, IN·Medicine & Clinical Research
Test whether NF1-mutant glioblastomas have distinct tumor cell properties and immune microenvironments, using engineered mice lacking NF1, Tp53 and Pten compared with NF1-normal QKi/Tp53/Pten mice.
Steffi Oesterreich
University of Pittsburgh, PA·Medicine & Clinical Research
Compare ILC cell lines, patient-derived organoids, xenografts, homografts and genetically engineered mice with human ILC tumors using histopathology plus genomic, epigenomic and transcriptomic profiling.
David Benner Lombard
University of Miami, FL·Medicine & Clinical Research
Determine how SIRT5, an enzyme that strips succinyl tags from proteins, controls histone succinylation and gene expression in Ewing sarcoma cells, using mass spectrometry with transcriptomic and epigenomic profiling.
The school
Emory University: 70 labs on PI Pages, $1.2B a year on research, 286 research doctorates a year.
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