“Our research is focused on the molecular biology and treatment of brain tumors, and on understanding the pathophysiology of Normal Pressure Hydrocephalus, a brain disorder that can develop spontaneously or as a result of brain tumor therapy. Our hope is that scientific advances in these areas will improve diagnosis, treatment and quality of life for brain tumor patients.”
- Dr. Mark Johnson
- Chair, Department of Neurosurgery, UMass Medical School and UMass Memorial Medical Center, 2016-present
- Associate Neurosurgeon, Neurosurgery, Brigham and Women's Hospital, 2003-2016
- Associate Professor of Neurosurgery, Harvard Medical School, 2013-2016
- Assistant Professor of Neurosurgery, Harvard Medical School, 2003-2012
About DSA-Funded Research
Dr. Johnson's laboratory has focused on understanding mechanisms of programmed cell death occurring in the nervous system after injury, in oncogenesis and in neurodegenerative disorders.
The p53 protein is a site specific transactivator or repressor of transcription that promotes injury-induced programmed cell death by modulating the expression of select target genes. Defects in the p53 signaling pathway have been identified in nearly half of all human cancers, including many central nervous system malignancies. Studies have also implicated p53 in the pathogenesis of neuronal cell death occurring after DNA damage or ischemia, or in neurodegenerative diseases such as Huntington’s Disease and Alzheimer’s Disease. Moreover, the effects of many of the current clinical therapies for brain tumors (including radiation and some forms of chemotherapy) require activation of p53-dependent pathways.
The cellular consequences of p53 activation in the nervous system are poorly understood, and a comprehensive study of p53-dependent changes in gene and protein expression in neurons, glia and brain tumor cells is needed.
Dr. Johnson's research combines mRNA microarray and mass spectrometry proteomics with other cell and molecular biology techniques to examine cell death pathways activated by various forms of injury in mouse neurons or glia, or in primary human glioma cells. Once identified, proteins essential to injury-mediated programmed cell death are investigated further to elucidate their function. A better understanding of these cell death mechanisms may lead to the development of more effective therapies for the treatment of brain tumors or nervous system injury.
"Mark possesses a unique set of intellectual and personal skills, which will greatly benefit the research he pursues in the field of Neuro-oncology. He is clearly among the elite of postdoctoral fellows and medical scientists I have encountered over the course of eighteen years of running my own laboratory. I would rank Mark as the single best resident I have ever trained."
Richard S. Morrison, Ph.D.
University of Washington School of Medicine, Seattle
"Dr. Johnson's training to date has been obtained at some of the finest and most competitive institutions in the country, and his performance has been exceptional? He is an outstanding young investigator who is at a critical stage of his career, and the Sontag Distinguished Scientist Award will have a pivotal influence on his academic development."
Peter McL. Black, M.D., Ph.D.
Harvard Medical School, Boston
- Jiang X, Yu Y, Yang HW, Agar NY, Frado L, Johnson MD. The imprinted gene PEG3 inhibits Wnt signaling and regulates glioma growth. J Biol Chem. 2010 Mar 12;285(11):8472-80. PMID: 20064927