"My long-term career goal is to find novel therapeutic approaches to cure malignant gliomas, through basic and translational studies in my lab and through collaboration with clinicians, patients, philanthropists, and supporting staff. My other goal is to develop my lab into a platform for training young talents and helping them launch their own scientific careers. It was my great privilege to receive the Sontag Distinguished Scientist Award, which is the most prestigious award for young faculty in the brain tumor field. I especially appreciate the foundation to foster a family-like environment, in which we can not only learn inspiring sciences from each other, but also support each other during our career development."

- Dr. Jian Hu

Dr. Hu's Biosketch

Academic Appointments

  • Assistant Professor, Department of Cancer Biology, University of Texas, MD Anderson Cancer Center, 2014-present

About DSA-Funded Research

Glioblastoma (GBM) is the most common and lethal type of brain cancer. The medium survival duration of GBM patients is only 14.6 months after standard treatments. With oncogenomic studies (for new cancer gene discovery), we identified a new tumor suppressor called Quaking (QKI), which is deleted or mutated in 25-30% of human GBM patients. Our preliminary analyses on a novel mouse model revealed that Qki deletion greatly promotes tumor growth by enhancing the ability of glioma stem cells (GSCs) to regenerate. Mechanistically, we discovered that Qki deletion led to reduction of endolysosome-dependent protein disposal machineries; therefore the ability of degrading oncoproteins on the cell membrane is impaired in the QKI-deficient glioma cells. However, on the flip side, the consequence of the downregulation of protein disposal machineries in QKI-deficient cells is that they have much higher stress caused by non-degraded proteins and organelles in comparison with QKI wild type cells. We hypothesize that this vulnerability could serve as an Achilles’ heel of QKI-deficient glioma cells, because their ability to clear up protein aggregates, unfolded proteins, and wasted organelles is greatly compromised in comparison with QKI wild type cells. To further understand the mechanism of QKI-dependent disposal machineries, we propose to identify new QKI target genes (particularly those involved in lipid metabolism). We also propose to target the vulnerability of QKI-deficient glioma cells by further inhibiting their disposal machineries. Because this therapeutic strategy is based on the vulnerabilities of certain tumors with well-defined genomic information, it can be translated to bedside and benefit patients more efficiently.

Accolades

"Jian is a remarkable young researcher who has an exceptional track record and unique expertise in the field of glioma biology. His lab is progressing extremely well and his group has already developed many innovative in vitro and in vivo systems that allow him to solve important questions bearing on glioma pathogenesis and treatment."

Amy B. Heimberger, M.D.
University of Texas, MD Anderson Cancer Center

"Jian is an extremely talented and promising young scientist. His research program is very innovative and will make tremendous impact on our understanding of malignant gliomas, which will help us discover new therapeutic approaches against this deadly disease."

Raghu Kalluri, M.D., Ph.D.
University of Texas, MD Anderson Cancer Center

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