Michael Graner,
Professor, Dept of Neurosurgery,
University of Colorado Anschutz School of Medicine
Michael Graner received his PhD in Biochemistry from the University of Illinois followed by post-doctoral and research faculty work at the University of Arizona, shifting gears from the Drosophila extracellular matrix to cancer immunotherapy. He then took at faculty position at Duke University’s Tisch Brain Tumor Center, followed by his current position as Professor in Neurosurgery at the University of Colorado Denver (Anschutz Medical Campus). He is also a member of the University of Colorado Cancer Center, the Colorado Clinical and Translational Sciences Institute, the MAVRC Program, and holds a Visiting Professorship Appointment at the Shenzhen Third People’s Hospital (China) and an adjunct faculty appointment at Colorado State University. Graner has a long-standing interest in cell stress responses, which led to cancer vaccine development (including one in clinical trials), which somehow led to the world of extracellular vesicles (EVs). His lab currently concentrates on signaling mechanisms involving EVs, in particular the transfer of stressed phenotypes from stressed tumor cells to unstressed ones via EVs.
Glioma Exosomes and Astrocytes: Conversion to the Dark Side
Thursday, 29 March 2018 at 11:00
Add to Calendar ▼2018-03-29 11:00:002018-03-29 12:00:00Europe/LondonGlioma Exosomes and Astrocytes: Conversion to the Dark SideSELECTBIOenquiries@selectbiosciences.com
Glioblastomas (GBMs, WHO grade IV astrocytomas) are the worst of the
central nervous system tumors; despite maximum (and damaging)
therapeutic intervention, median survival time for patients is <15
months, and overall quality of life is poor. These abysmal outcomes have
changed little in 20 years. Clearly, our current therapies are
inadequate; we need innovative strides in understanding GBM biology to
rectify this situation. One “hot” research area is that of the impact of
tumor extracellular vesicles (EVs) on normal recipient cells. Tumor EVs
have extraordinary abilities to manipulate tumor microenvironments and
recipient cells both proximally and distally. Tumor EVs prepare the
“metastatic niche” for circulating tumor cells prior to colonization of a
target organ, deflect immune responses, and alter normal cells. Thus,
tumor EVs impact recipient cells to support tumor growth and
progression, which undoubtedly holds true for GBMs as well. However,
little is known about effects of GBM EVs on normal astrocytes—do GBM EVs
drive astrocyte phenotypic changes, potentially making the astrocytes
into tumor promotors? The answers could re-shape our paradigms on
gliomagenesis, particularly for recurrent tumors. Here we show that GBM
EVs activate cancer-type signaling pathways in recipient astrocytes,
promoting astrocyte migration towards the EVs, as well as astrocyte
anchorage-independent growth in soft agar. Astrocytes release of various
factors to generate a tumor-promoting milieu with increased tumor cell
growth, particularly in the areas of inflammatory responses to entities
that seem like viruses. We discuss the consequences of these phenomena
in the context of our current therapies with a view towards therapeutic
improvement.
Add to Calendar ▼2018-03-28 00:00:002018-03-29 00:00:00Europe/LondonCirculating Nucleic Acids and Circulating Rare Cells: Liquid Biopsy for Early Cancer Detection SELECTBIOenquiries@selectbiosciences.com
Add to Calendar ▼2018-03-29 11:00:002018-03-29 12:00:00Europe/LondonGlioma Exosomes and Astrocytes: Conversion to the Dark SideSELECTBIOenquiries@selectbiosciences.com
