"My group seeks to identify the molecular determinants of malignant glioma while also translating our findings, and those of others, to the clinical setting in the form of advanced diagnostic testing. My fundamental career goal is quite simple: to significantly change the management of brain cancer for the better."

- Dr. Jason Huse

View CV

Academic Appointment

  • Associate Professor with Tenure, Departments of Pathology and Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, 9/1/2016-present
  • Assistant Member, Department of Pathology, Leon Levy Foundation Young Investigator, Memorial Hospital for Cancer and Allied Diseases, Memorial Sloan Kettering Cancer Center, 07/2009-8/2016
  • Assistant Member, Human Oncology and Pathogenesis Program; 07/2013-8/2016
  • Instructor, Department of Pathology, 10/2008-06/2009
  • Assistant Attending, Department of Pathology, 07/2009-8/2016

About DSA-Funded Research

Gliomas are a class of primary brain tumors whose shared tendency to widely infiltrate surrounding brain tissue renders them surgically incurable. High-grade gliomas (HGGs), like glioblastoma, are exceptionally aggressive and typically cause death in less than 24 months. Lower-grade gliomas (LGGs), by contrast, grow more slowly, with patients frequently surviving years to decades. Nevertheless, all LGGs inevitably evolve into HGGs, underscoring the need for more effective therapies that could be implemented prior to definitive high-grade transformation. LGGs are characterized by a fundamentally different set of molecular abnormalities than their high-grade counterparts, including, most notably, mutations in the isocitrate dehydrogenase genes, IDH1 and IDH2. While recent work has associated IDH mutations with dramatic changes in cell biology, the precise mechanisms by which they cause tumor formation remain unclear. Nevertheless, we expect that changes in the regulation of specific genes, as a direct result of IDH mutation, are at least partially responsible. MicroRNAs (miRNAs) are a family of small gene regulatory molecules whose role in both normal physiology and disease states like cancer has been repeatedly affirmed. Our preliminary work has identified a specific miRNA, miR-34a, as central to the LGG biology. Mir-34a levels decrease in response to IDH mutation, resulting in proliferation and tumor formation in glioma cell lines. In this proposal, we aim to functionally characterize miR-34a and its regulation in LGGs using disease-relevant cell lines and mouse models. Our work will shed considerable light on the mechanisms underlying LGG formation and, in this way, inform therapeutic development.


"Jason carefully processes tidbits of information (as every good pathologist must!) and synthesizes a clever model to explain the facts. He hit the ground running in the first year of his independent position and is destined for much, much more."

Charles L. Sawyers, M.D.
Memorial Sloan-Kettering Cancer Center

"Jason is one of the most collaborative and driven scientists we have here at MSKCC."

Eric C. Holland, M.D., Ph.D.
Memorial Sloan-Kettering Cancer Center


  • Omuro, A.M., Beal, K., Gutin, P., Karimi, S., Correa, D.D., Kaley, T.J., DeAngelis, L.M., Chan, T.A., Gavrilovic, I.T., Grommes, C., Reiner, A.S., Panageas, K.S., Baser, R.E., Tabar, V., Pentsova, E., Sanchez, J., Barradas-Panchal, R., Zhange, J., Brennan, C.W., Abrey, L.E., Huse, J.T. “Phase II study of bevacizumab, temozolomide, and hypofractionated stereotactic radiotherapy for newly diagnosed glioblastoma”. Clin Cancer Res 2014; 20, 5023-5031.
    Kastenhuber, E.R.*, Huse, J.T.*, Berman, S.H., Pedraza, A., Zhang, J., Suehara, Y., Viale, A., Cavatore, M., Heguy, A., Szerlip, N., Ladanyi, M., Brennan, C.W. “Quantitative assessment and genomic context of intragenic receptor tyrosine kinase deletions in glioblastoma”. Acta Neuropath 2014; 127, 747-759.
  • Huse, J.T., Diamond, E.L., Wang. L., Rosenblum, M.K. “Mixed glioma with molecular features of composite oligodendroglioma and astrocytoma: a true ‘oligoastrocytoma’?” Acta Neuropath 2015; 129, 151-153.
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