Eveline Barbieri
Baylor College of Medicine, TX·Medicine & Clinical Research
Neuroblastoma is an aggressive childhood cancer that causes about 15% of pediatric cancer deaths. It begins in neural crest cells, embryonic cells that normally mature into parts of the nervous system.
- Fields
Medicine & Clinical Research
Microbiology & Immunology
Genetics
- Topics
neuroblastoma
pediatric cancer
MYCN amplification
- Grants
- 3 known grants, through Jul 2029
What they work on
- Develop a genetically engineered mouse model in which the epigenetic regulator CHAF1A can be switched on in neural crest, and test whether it increases neuroblastoma incidence, metastasis and shortens survival.
- Determine how CHAF1A shapes tumor initiation, the immune environment, and MYCN-driven cancer using ATAC-seq, lipidomics and single-cell RNA sequencing in the new mouse model.
- Test whether MYCN-driven tumor metabolism and cysteine-consuming PMN-MDSC immune cells deplete cysteine, an amino acid T cells cannot make, blocking anti-tumor T cells in TH-MYCN and syngeneic mice.
- Modulate the metabolic environment of MYCN-amplified neuroblastoma, such as by restoring cysteine to T cells, to enhance immune-based therapies.
- Determine how MYCN rewires T cell metabolism and whether MYCN-driven de novo lipogenesis, the making of new fats, creates a lipid-rich environment that impairs T cell function.
More about the research
In high-risk cases, survival is below 45%, more than half of patients relapse, and survival after relapse is only 10%. The research asks two connected questions. What genes stop neural crest cells from maturing and so start tumors? And how do cancer-driving genes change tumor metabolism so that immune cells cannot fight back? It centers on CHAF1A and on MYCN, an oncogene (cancer-driving gene) that is often amplified in high-risk disease.
Why it matters
Children with high-risk, MYCN-amplified neuroblastoma face high relapse and death rates, and current immunotherapies work poorly against these immune-quiet tumors. Understanding how CHAF1A and MYCN block cell maturation and starve T cells of nutrients could guide treatments that push tumor cells to mature, along with metabolic strategies that make immunotherapy more effective.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Hamilton Hodges
Baylor College of Medicine, TX·Biochemistry
Determine how cellular signals influence which binding partners SWI/SNF chromatin remodelers (cBAF, PBAF, GBAF) select, using rapid perturbations in living cells with epigenomic and proteomic readouts.
April M. Weissmiller
Middle Tennessee State University, TN·Biochemistry
Map which genes are bound and regulated by N-MYC and its partner proteins WDR5 and G9a in MYCN-amplified neuroblastoma cells, using genetic, genomic, and chemical-biology approaches to see how combined inhibition reshapes N-MYC-driven transcription.
Bernice E Morrow
Albert Einstein College of Medicine, NY·Genetics
Trace the origins and fates of three cardiac neural crest populations (Tbx2/3, Isl1 and Acta2) in mouse embryos using dual lineage tracing, which labels cells and their descendants, and build gene regulatory networks that control their development.
The school
Baylor College of Medicine: 38 labs on PI Pages, $881M a year on research, 115 research doctorates a year.
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