It’s inspiring to see what happens when a hospital dedicated to providing the best treatments for children partners with a world-class technology and engineering institution. Children’s Hospital Boston and MIT have embarked upon an exciting program of collaboration and cross-fertilization in research, teaching and mentoring. The goal is to connect outstanding disease-oriented research with cutting-edge innovation and technologies, taking our ability to care for children to a new level while training the next generation of clinicians and scientists.
The historical ties between Children’s and MIT run deep. Individual scientists and clinicians have teamed up to design new medical devices; to identify gene mutations that underlie cancer and disorders of development; to create new approaches to drug delivery using slow-release polymers to extend medication efficacy; to monitor the activity of nerve cells in the brain with sophisticated new devices; and to implement new ways to analyze MRI and other advanced imaging methods. Building on this legacy, bringing the two institutions together in a formal collaboration will speed advances in the diagnosis and treatment of diseases in children.
To kick off the collaboration, Children’s and MIT took turns hosting half-day, standing-room-only minisymposia celebrating research in the developing brain, one of the last great frontiers in science. Nine scientists from Children’s spoke at MIT on June 13, and last week, nine from MIT spoke here at Children’s, exposing each community to the diversity of research at the other.
As each new MIT speaker took the podium, my excitement about the collaboration increased. John Gabrieli demonstrated how brain development is altered in children with dyslexia, complementing some of our own work. Hazel Sive presented a tour-de-force series of experiments in zebrafish, building on the discovery that deletions or duplications on chromosome 16 (16p11.2) account for 1 percent of autism. While Sive’s zebrafish can’t be said to have autism, she did show that the 16p11.2 region contains highly neurally important genes. Nancy Kanwisher shared research complementing that of Charles Nelson of our Laboratories of Cognitive Neuroscience, confirming that the proposed deficit in face processing in autism is real.
Mriganka Sur made a powerful case for giving IGF-1 to Children with Rett syndrome, work that spurred a clinical trial in progress in Children’s Rett program, directed by Omar Khwaja. Mark Bear demonstrated that a drug treatment can strengthen synapses and alleviate neurological symptoms in mice with Fragile X syndrome, another condition we see at Children’s, spurring a number of clinical trials. Rosalind Picard showed the power of skin-conductance monitors in tracking emotions in nonverbal children, such as those with autism. M. Fatih Yanik dazzled the audience with high-throughput tools for imaging zebrafish and worms and doing drug screens.
This summer, a new competition will be opened for several one-year, $50,000 awards to graduate students or postdoctoral fellows from both Children’s and MIT, who will pair up on joint projects and make use of complementary facilities and experts at both institutions. In a new mentoring program, clinical faculty at Children’s will interact with the MIT premedical students and faculty, providing premedical advisees and offering clinical shadowing opportunities.
Great discoveries and true progress can be made by combining the best resources of institutions with complementary expertise to work toward a common goal. By combining unparalleled access to world-class clinical and research programs at Children’s with the innovative and creative faculty of MIT, the CHB-MIT Research Enterprise is poised to take pediatrics to new heights.
Scott Pomeroy, MD, PhD, is Neurologist-in-Chief at Children’s Hospital Boston and the Bronson Crothers Professor of Neurology at Harvard Medical School. His laboratory is seeking the genetic causes of medulloblastomas, the most common malignant brain tumors of childhood, focusing on how genes that regulate cerebellar development become disrupted to promote medulloblastoma growth.