Other
23 Authors
- Davidoff AM,
- Liu L,
- Wang R,
- Lu M,
- Chen X,
- Confer T,
- Turner G,
- Sheppard H,
- Fang J,
- Natarajan S,
- Easton J,
- Murphy A,
- Wang T,
- Ha L,
- Johnson M,
- Ma X,
- Glazer ES,
- Yang J,
- Jain R,
- Yadak N,
- Steinberg J,
- Jin H,
- Picketts DJ
| First Author | Wang T | Year | 2025 |
| Journal | Cancer Res | Volume | 85 |
| Issue | 3 | Pages | 424-441 |
| PubMed ID | 39531507 | Mgi Jnum | J:361615 |
| Mgi Id | MGI:7861358 | Doi | 10.1158/0008-5472.CAN-24-1142 |
| Citation | Wang T, et al. (2025) Conditional Activation of c-MYC in Distinct Catecholaminergic Cells Drives Development of Neuroblastoma or Somatostatinoma. Cancer Res 85(3):424-441 |
| abstractText | c-MYC is an important driver of high-risk neuroblastoma. A lack of c-MYC-driven genetically engineered mouse models (GEMM) has hampered the ability to better understand mechanisms of neuroblastoma oncogenesis and to develop effective therapies. In this study, we showed that conditional c-MYC induction via Cre recombinase driven by a tyrosine hydroxylase promoter led to a preponderance of PDX1+ somatostatinoma, a type of pancreatic neuroendocrine tumor. However, c-MYC activation via an improved Cre recombinase driven by a dopamine beta-hydroxylase promoter resulted in neuroblastoma development. The c-MYC murine neuroblastoma tumors recapitulated the pathologic and genetic features of human neuroblastoma and responded to anti-GD2 immunotherapy and difluoromethylornithine, an FDA-approved inhibitor targeting the MYC transcriptional target ODC1. Thus, c-MYC overexpression results in different but related tumor types depending on the targeted cell. The GEMMs represent valuable tools for testing immunotherapies and targeted therapies for these diseases. Significance: The development of c-MYC-driven genetically engineered neuroblastoma and somatostatinoma mouse models provides useful tools for understanding the tumor cell origin and investigating treatment strategies. |
