Frank Furnari
· Ph.D.University of California, San Diego · Medical Genetics
Active 2005–2024
About
Frank Furnari is a Professor in the Department of Medicine, Division of Regenerative Medicine at UC San Diego. His lab’s research program focuses on decoding the molecular mysteries that drive adult and pediatric brain cancers, particularly glioblastoma. The research aims to understand how specific mutations and gene amplifications enhance tumor aggressiveness and enable tumors to outsmart therapeutic interventions, with the overarching goal of identifying vulnerabilities within these cancers. Using a variety of approaches including tumor biology, bioinformatics, and orthotopic models, Furnari’s lab is engineering next-generation brain tumor models that capture the full spectrum of these aggressive cancers. His mission is to molecularly understand and ultimately outwit glioblastoma and other brain cancers through precision oncology approaches.
Research topics
- Cancer research
- Biology
- Cell biology
- Chemistry
- Medicine
Selected publications
EBioMedicine · 2020 · 60 citations
- Cancer research
- Biology
- Medicine
BACKGROUND: Recurrence after radiation therapy is nearly universal for glioblastomas, the most common form of adult brain cancer. The study aims to define clinically pertinent mechanisms underlying this recurrence. METHODS: -methylguanine-DNA methyltransferase promoters (umMGMT) and wild-type isocitrate dehydrogenase (wtIDH). The most altered miRNA, miR-603, was characterized. FINDINGS: While nearly all miRNAs remained unchanged after treatment, decreased levels of few, select miRNAs in the post-treatment specimens were observed, the most notable of which involved miR-603. Unbiased profiling of miR-603 targets revealed insulin-like growth factor 1 (IGF1) and IGF1 receptor (IGF1R). Ionizing radiation (IR) induced cellular export of miR-603 through extracellular vesicle (EV) release, thereby de-repressing IGF1 and IGF1R. This de-repression, in turn, promoted cancer stem-cell (CSC) state and acquired radiation resistance in glioblastomas. Export of miR-603 additionally de-repressed MGMT, a DNA repair protein responsible for detoxifying DNA alkylating agents, to promote cross-resistance to these agents. Ectopic miR-603 expression overwhelmed cellular capacity for miR-603 export and synergized with the tumoricidal effects of IR and DNA alkylating agents. INTERPRETATION: Profiling of matched pre- and post-treatment glioblastoma specimens revealed altered homeostasis of select miRNAs in response to radiation. Radiation-induced EV export of miR-603 simultaneously promoted the CSC state and up-regulated DNA repair to promote acquired resistance. These effects were abolished by exogenous miR-603 expression, suggesting potential for clinical translation. FUNDING: NIH 1R01NS097649-01, 9R44GM128223-02, 1R01CA240953-01, the Doris Duke Charitable Foundation Clinical Scientist Development Award, The Sontag Foundation Distinguished Scientist Award, the Kimmel Scholar Award, and BWF 1006774.01 (C.C.C).
Frequent coauthors
- 19 shared
Webster K. Cavenee
University of California, San Diego
- 11 shared
Shunichiro Miki
University of California, San Diego
- 8 shared
Alison D. Parisian
- 8 shared
C. Ryan Miller
University of Alabama at Birmingham
- 8 shared
Tomoyuki Koga
University of Minnesota
- 7 shared
Kasey Skinner
University of Alabama at Birmingham
- 5 shared
Akitake Mukasa
Kumamoto University
- 5 shared
Harshil Dhruv
Awards & honors
- 10+ Awards
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