Photo of Mark D. Johnson,  MD, PhD

Mark D. Johnson, MD, PhD

Brigham And Women's Hospital

Brigham And Women's Hospital
Phone: (617) 525-8135
Fax: (617) 713-3050


mjohnson27@partners.org

Mark D. Johnson, MD, PhD

Brigham And Women's Hospital

EDUCATIONAL TITLES

  • Associate Professor, Neurosurgery, Harvard Medical School
  • Associate Neurosurgeon, Neurosurgery, Brigham And Women's Hospital

DF/HCC PROGRAM AFFILIATION

Research Abstract

This 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. Our 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.

Publications

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  • Rahman R, Catalano PJ, Reardon DA, Norden AD, Wen PY, Lee EQ, Nayak L, Beroukhim R, Dunn IF, Golby AJ, Johnson MD, Chiocca EA, Claus EB, Alexander BM, Arvold ND. Incidence, risk factors, and reasons for hospitalization among glioblastoma patients receiving chemoradiation. J. Neurooncol. 2015; 124:137-46. PubMed
  • Liu Y, Alexander BM, Chen YH, Horvath MC, Aizer AA, Claus EB, Dunn IF, Golby AJ, Johnson MD, Friesen S, Mannarino EG, Wagar M, Hacker FL, Arvold ND. Salvage whole brain radiotherapy or stereotactic radiosurgery after initial stereotactic radiosurgery for 1-4 brain metastases. J. Neurooncol. 2015. PubMed
  • Ansari KI, Ogawa D, Rooj AK, Lawler SE, Krichevsky AM, Johnson MD, Chiocca EA, Bronisz A, Godlewski J. Glucose-based regulation of miR-451/AMPK signaling depends on the OCT1 transcription factor. Cell Rep 2015; 11:902-9. PubMed
  • Arvold ND, Tanguturi SK, Aizer AA, Wen PY, Reardon DA, Lee EQ, Nayak L, Christianson LW, Horvath MC, Dunn IF, Golby AJ, Johnson MD, Claus EB, Chiocca EA, Ligon KL, Alexander BM. Hypofractionated Versus Standard Radiation Therapy With or Without Temozolomide for Older Glioblastoma Patients. Int J Radiat Oncol Biol Phys 2015. PubMed
  • Ramkissoon SH, Bi WL, Schumacher SE, Ramkissoon LA, Haidar S, Knoff D, Dubuc A, Brown L, Burns M, Cryan JB, Abedalthagafi M, Kang YJ, Schultz N, Reardon DA, Lee EQ, Rinne ML, Norden AD, Nayak L, Ruland S, Doherty LM, LaFrankie DC, Horvath M, Aizer AA, Russo A, Arvold ND, Claus EB, Al-Mefty O, Johnson MD, Golby AJ, Dunn IF, Chiocca EA, Trippa L, Santagata S, Folkerth RD, Kantoff P, Rollins BJ, Lindeman NI, Wen PY, Ligon AH, Beroukhim R, Alexander BM, Ligon KL. Clinical implementation of integrated whole-genome copy number and mutation profiling for glioblastoma. 2015. PubMed
  • Yang HW, Xing H, Johnson MD. A major role for microRNAs in glioblastoma cancer stem-like cells. Arch Pharm Res 2015; 38:423-34. PubMed
  • Rajakesari S, Arvold ND, Jimenez RB, Christianson LW, Horvath MC, Claus EB, Golby AJ, Johnson MD, Dunn IF, Lee EQ, Lin NU, Friesen S, Mannarino EG, Wagar M, Hacker FL, Weiss SE, Alexander BM. Local control after fractionated stereotactic radiation therapy for brain metastases. J. Neurooncol. 2014; 120:339-46. PubMed
  • Godlewski J, Krichevsky AM, Johnson MD, Chiocca EA, Bronisz A. Belonging to a network-microRNAs, extracellular vesicles, and the glioblastoma microenvironment. 2014. PubMed
  • Aizer AA, Arvold ND, Catalano P, Claus EB, Golby AJ, Johnson MD, Al-Mefty O, Wen PY, Reardon DA, Lee EQ, Nayak L, Rinne ML, Beroukhim R, Weiss SE, Ramkissoon SH, Abedalthagafi M, Santagata S, Dunn IF, Alexander BM. Adjuvant radiation therapy, local recurrence, and the need for salvage therapy in atypical meningioma. 2014. PubMed
  • Kim TM, Xi R, Luquette LJ, Park RW, Johnson MD, Park PJ. Functional genomic analysis of chromosomal aberrations in a compendium of 8000 cancer genomes. Genome Res 2012. PubMed
  • Jiang X, Xing H, Kim TM, Jung Y, Huang W, Yang HW, Song S, Park PJ, Carroll RS, Johnson MD. Numb regulates glioma stem cell fate and growth by altering epidermal growth factor receptor and Skp1-Cullin-F-box ubiquitin ligase activity. Stem Cells 2012; 30:1313-26. PubMed
  • Kim TM, Huang W, Park R, Park PJ, Johnson MD. A developmental taxonomy of glioblastoma defined and maintained by microRNAs. Cancer Res 2011. PubMed
  • Agar NY, Malcolm JG, Mohan V, Yang HW, Johnson MD, Tannenbaum A, Agar JN, Black PM. Imaging of Meningioma Progression by Matrix-Assisted Laser Desorption Ionization Time-of-Flight Mass Spectrometry. Anal Chem 2010; 82:2621-5. PubMed
  • 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; 285:8472-80. PubMed
  • Kim H, Huang W, Jiang X, Pennicooke B, Park PJ, Johnson MD. Integrative genome analysis reveals an oncomir/oncogene cluster regulating glioblastoma survivorship. Proc Natl Acad Sci U S A 2010; 107:2183-8. PubMed
  • Yang HW, Menon LG, Black PM, Carroll RS, Johnson MD. SNAI2/Slug promotes growth and invasion in human gliomas. BMC Cancer 2010; 10:301. PubMed
  • Dreyfuss JM, Johnson MD, Park PJ. Meta-analysis of glioblastoma multiforme versus anaplastic astrocytoma identifies robust gene markers. Mol Cancer 2009; 8:71. PubMed
  • Kim Y, Johnson M, Trombetta MG, Parda DS, Miften M. Investigation of Interfraction Variations of MammoSite Balloon Applicator in High-Dose-Rate Brachytherapy of Partial Breast Irradiation. Int J Radiat Oncol Biol Phys 2008; 71:305-13. PubMed
  • Yu Y, Jiang X, Schoch BS, Carroll RS, Black PM, Johnson MD. Aberrant splicing of cyclin-dependent kinase-associated protein phosphatase KAP increases proliferation and migration in glioblastoma. Cancer Res 2007; 67:130-8. PubMed
  • Liu F, Park PJ, Lai W, Maher E, Chakravarti A, Durso L, Jiang X, Yu Y, Brosius A, Thomas M, Chin L, Brennan C, DePinho RA, Kohane I, Carroll RS, Black PM, Johnson MD. A genome-wide screen reveals functional gene clusters in the cancer genome and identifies EphA2 as a mitogen in glioblastoma. Cancer Res 2006; 66:10815-23. PubMed
  • Feltmate CM, Lee KR, Johnson M, Schorge JO, Wong KK, Hao K, Welch WR, Bell DA, Berkowitz RS, Mok SC. Whole-genome allelotyping identified distinct loss-of-heterozygosity patterns in mucinous ovarian and appendiceal carcinomas. Clin Cancer Res 2005; 11:7651-7. PubMed
  • Johnson MD, Wu X, Aithmitti N, Morrison RS. Peg3/Pw1 is a mediator between p53 and Bax in DNA damage-induced neuronal death. J Biol Chem 2002; 277:23000-7. PubMed
  • Yu LR, Johnson MD, Conrads TP, Smith RD, Morrison RS, Veenstra TD. Proteome analysis of camptothecin-treated cortical neurons using isotope-coded affinity tags. Electrophoresis 2002; 23:1591-8. PubMed
  • Johnson MD, Kinoshita Y, Xiang H, Ghatan S, Morrison RS. Contribution of p53-dependent caspase activation to neuronal cell death declines with neuronal maturation. J Neurosci 1999; 19:2996-3006. PubMed
  • Johnson MD, Xiang H, London S, Kinoshita Y, Knudson M, Mayberg M, Korsmeyer SJ, Morrison RS. Evidence for involvement of Bax and p53, but not caspases, in radiation-induced cell death of cultured postnatal hippocampal neurons. J Neurosci Res 1998; 54:721-33. PubMed
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