“The support from the Sontag Foundation will be vital to accomplishing my project, and I am humbled to be sharing this honor with prior awardees, who have shaped the neuro-oncology field over the past 20 years. ”
About DSA-Funded Research
GBM evades toxicity from therapies by activating genetic programs, which induce damage repair, escape from the immune system, and regress to a more undifferentiated state. This response is mediated at the epigenetic level by the activation of a multitude of oncogenes which are often redundant, making their targeting extremely challenging, and current therapies largely ineffective. MicroRNAs, short non-coding genes which regulate protein expression, are a promising solution to this problem, as we recently found that in normal cells a specific group of them is the natural gatekeeper of a large component of this epigenetic survival response. We have also observed that microRNA genes produce previously unrecognized accessory RNA sequences, which are leftovers from a process of sequence “pruning”, and which persist within the cell, providing a tool for expanded gene therapy applications.
Associate Surgeon, Harvard Medical School, Boston, MA
Assistant Professor in Neurosurgery, Brigham and Women’s Hospital, Boston, MA
Universita’ La Sapienza, M.D., Medicine
The Ohio State University, Ph.D., Molecular Biology
The Ohio State University, Postdoc, Neuro-oncology and Neuroscience