Cancer Modeling Using Patient Derived iPSCs and 3-Dimensional Organoids
Several landmark discoveries in cancer genetics have come from studies on a childhood cancer of the developing retina called retinoblastoma. In parallel, advances in preclinical testing and clinical research has led to improvements in outcome for children with this devastating disease. Despite these advances, there are still fundamental questions in the retinoblastoma field that remain unanswered. Are retinal cells fully transformed once they sustain biallelic inactivation of the RB1 gene or is retinoblastoma tumorigenesis a multistage process? Why do some family members with the same germline RB1 mutation have bilateral multifocal retinoblastoma at a young age while others have no evidence of disease? Can treatment induce a process of tumor cell clonal evolution and selection that leads to tumor progression and enucleation? These questions have been impossible to answer because retinoblastomas are not biopsied and enucleation is only performed for advanced stage disease. In order to overcome this barrier in the field, we have developed the first spontaneous human retinoblastoma tumor model using 3D retinal organoids produced from patients with germline RB1 mutations. I am seeking a highly motivated postdoctoral fellow to work as part of a multidisciplinary team made up of computational and stem cell biologists, pediatric oncologists, pathologists and biostatisticians to use this innovative new model of retinoblastoma to answer fundamental questions in the field. Training in cancer biology, cancer clonal evolution and/or human stem cell research is preferred.
Michael A. Dyer, Ph.D.
Chair and Member, Developmental Neurobiology Department
Co-leader Developmental Biology and Solid Tumor Program
St. Jude Children’s Research Hospital
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