Antony MichealRaj, PhD, joined the faculty of the University of Pittsburgh Department of Neurological Surgery in September of 2021.
Dr. MichealRaj graduated from the Madurai Kamaraj University with a bachelor of science degree in zoology. He then earned his master of science degree in biotechnology in 2007 from the University of Madras and PhD in genetics from the University of Delhi where he functionally characterized the rare and common variants of dopaminergic pathway genes associated with schizophrenia and other neurological disorders. He subsequently completed his postdoctoral training in neuro-oncology and tumor metabolism at the Arthur and Sonia Labatt Brain Tumor Research Centre at the Hospital for Sick Children (SickKids) in Toronto. While at SickKids, Dr. MichealRaj studied molecular disease mechanisms of pediatric brain tumors ependymoma and medulloblastoma using clinically relevant disease models of patients and mouse models. Dr. MichealRaj’s independent research lab at University of Pittsburgh of School of Medicine is focused on unravelling molecular and metabolic dependency of pediatric brain tumors and their mechanistic role in tumor initiation, maintenance and recurrence/resistance
Dr. Michealraj’s publications can be reviewed through the National Library of Medicine's publication database.
Specialized Areas of Interest
Professional Organization Membership
Education & Training
- BSc, Zoology, Madurai Kamaraj University, 2004
- MSc, Biotechnology, Loyola College, University of Madras, 2007
- PhD, Genetics, University of Delhi, 2014
- Postdoctoral Fellowship, Hospital for Sick Children, Toronto, 2021
Research Activities
Medulloblastoma
Dr. MichealRaj’s functional genomics and tumor metabolism laboratory made significant progress in unravelling MYC dependent metabolic reprogramming that drives aggressive pediatric group 3 medulloblastoma. His comprehensive multiomics analysis on 450 medulloblastoma reveal, a proteomic subset of Group 3 (G3) tumors driven by high MYC expression is characterized by dramatically up-regulated rates of de novo lipid synthesis. The observed increase in lipid synthesis is facilitated by high protein abundance and activity of fatty acid synthesis pathway enzymes including FASN and SCD1. Furthermore, an increase in DGAT1 activity effectively protects against lipid oxidative stress through ROS-sensitive fatty acid storage into lipid droplets. Genetic or pharmacologic abrogation of DGAT1 activity confers susceptibility to oxidative stress and increased rates of cell death in vitro and in murine tumor models of medulloblastoma. This unpublished study has been submitted and is undergoing peer review process in reputed journal.
Ependymoma
Pediatric ependymomas are lethal malignancies which are more common in males. Dr. MichealRaj’s functional genomics and tumor metabolism laboratory highlight transcriptional sex differences between male and female hindbrain cells, driven by cell-extrinsic sex hormonal differences and their role in PFA pathogenesis, primarily in the poor prognosis of male patients. He has identified that androgens contribute to the PFA tumor niche by inhibiting differentiation, increasing cell proliferation in vitro and supporting the progenitor pool, a fraction that is higher in male PFA tumors. These cell-extrinsic factors support PFA tumor maintenance, and consequently the worse prognosis in males with PFA. This unpublished study has been submitted and is undergoing peer review process in reputed journal.