Heather M. Ames, MD, PhD

2013: M.D., University of Michigan, Ann Arbor, MI
2013: Ph.D., Cell and Molecular Biology, University of Michigan, Ann Arbor, MI
2015: Residency, Anatomic Pathology, Johns Hopkins Hospital, Baltimore, MD
2017: Fellowship, Neuropathology, Johns Hopkins Hospital, Baltimore, MD

I am an early stage investigator and assistant professor who joined the department of Pathology at the University of Maryland School of Medicine in May 2018.  I completed a master’s degree in Neuroscience at Brandeis University and worked in a neurobiology laboratory at the Massachusetts Institute of Technology for one year prior to enrollment in the Medical Scientist Training Program at the University of Michigan Medical School. At the University of Michigan, I rotated in neuroscience laboratories, but ultimately chose to study protein trafficking in cancer cells due to a personal interest in cancer biology. My interest in neuroscience remained, and I became particularly intrigued by the molecular diversity demonstrated by brain tumors. I then pursued residency training in anatomic pathology and neuropathology at the Johns Hopkins School of Medicine and pursued both basic and clinical postdoctoral research projects investigating the diagnosis and pathogenesis of gliomas.

My main research focus is brain-specific invasion programs in glioblastoma. Glioblastoma is the highest grade diffuse glioma and the most common primary malignant brain tumor in adults. Diffuse gliomas have a unique ability among both primary and metastatic brain tumors to travel along white matter tracts, namely the corpus callosum, to establish bilateral, unresectable disease. Because of the ability of glioblastoma tumor cells to sparsely infiltrate normal brain, it is particularly difficult to identify the furthest extent of glioblastoma spread at both the gross and microscopic level. These tumors are therefore often recurrent, with only one-third of patients surviving for more than 5 years. The over-arching goals of my research are to identify and clinically target those biological pathways that allow high grade gliomas to traverse and colonize the unique microenvironments present in the brain.

Glioblastoma; brain tumor neuroinvasion; neurodevelopment; microRNA; cell-cell interactions; brain tumor heterogeneity

Spina R, Voss DM, Yang X, Sohn JW, Vinkler R, Schraner J, Sloan A, Welford SM, Avril N, Ames HM, Woodworth GF, Bar EE. MCT4 regulates de novo pyrimidine biosynthesis in GBM in a lactate independent manner. Neuro-Oncology Advances. 2020 Jan 01; 2(1): vdz062.

Schreck KC, Ranjan S, Skorupan N, Bettegowda C, Eberhart CG, Ames HM**, Holdhoff, M**. Incidence and clinicopathologic features of H3 K27M mutations in adults with radiographically-determined midline gliomas. J Neurooncol. 2019 May;143(1):87-93. (**equal contribution)

Ames HM, Rooper LM, Laterra JJ, Eberhart CG, Rodriguez FJ. INSM1 expression is frequent in primary central nervous system neoplasms but not in the adult brain parenchyma. J Neuropathol Exp Neurol. 77: 374-382.

Ho, CY, Ames HM, Tipton A., Vezina G, Liu JS, Scafidi J, Torii M, Rodriguez,FJ, du Plessis A, DeBiasi RL. 2017. Differential neuronal susceptibility and bystander apoptosis in congenital ZIKV infection. Ann Neurol. 82: 121-127.

Ames HM*, Yuan M*, Vizcaino MA, Yu W, Rodriguez FJ. 2017. MicroRNA profiling of low-grade glial and glioneuronal tumors shows an independent role for cluster 14q32.31 member miR-487b. Mod Pathol. 30: 204-216. (*equal contribution)