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Casey Finnerty

Research - A Neuro-Oncology Laboratory at Northwestern University in Chicago - 1 views

  • Most adenoviruses that have been historically used for gene therapy have been based on serotype 5 (AdWT). Unfortunately, expression of the primary receptor for Ad5 (the coxsackie-adenovirus receptor, CAR) is highly variable on cancer cells. In fact, several studies have demonstrated a resistance of malignant glioma to adenoviral vectors, a finding that was subsequently attributed to the quantitative deficiency of CAR on brain tumor cells.
  • First, we tested a variety of tumor specific promoters and identified survivin (S) as an excellent tumor specific promoter for transcriptional control of E1a, a gene essential for CRAd replication (J Neurosurg 104:583, 2006; Cancer Biol Ther 6:679, 2007).
  • Based on the above date data, we then created a novel oncolytic adenoviral vector which utilizes the survivin promoter and binds to heparan sulfate proteoglycans expressed on malignant brain tumors and named this new vector CRAd-S-pk7 (Hum Gene Ther 18:589, 2007).
    • Casey Finnerty
       
      How specific is the binding/tropism? HS is fairly widespread throughout the body.
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  • Second, we have identified several receptors that are over-expressed on brain tumor cells and created a series of pseudotyped Ad5 vectors that recognize these receptors
  • Our studies with CRAd-S-pk7 indicate that the virus provides the highest level of viral replication and tumor oncolysis in glioma cell lines. At the same time, we observed minimal viral replication and toxicity in normal human brain. Injection of CRAd-S-pk7 inhibited xenograft brain tumor growth by more than 300%.
  • We were the first group in the country to show that human mesenchymal stem cells can be effectively loaded with a replication competent virus and effectively deliver it to an experimental glioma model
  • When oncolytic vectors are loaded onto stem cells, the virus effectively "hides" from the immune system for an extended period of time. The ability of stem cells to suppress the anti-viral immune response in a permissive and tumor-bearing animal model is the subject of one of our latest manuscript
  • Finally, to further enhance the therapeutic efficacy of stem cells, we have optimized them to specifically traffic to intracranial tumors via genetic modification with single-chain antibodies against antigens expressed on gliomas
  • Our latest work in this area supports the development of neural stem cell based cell carriers for oncolytic virotherapy
Matthew Marshall

Dengue - 0 views

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    Follow up research subsequent to viewing Dr. Eva Harris's Lecture, Dengue Fever: Breaking Epidemic Cycles. Research focused on mechanisms behind severe dengue forms DHF and DSS.
Casey Finnerty

We Now Have the Cure for Hepatitis C, but Can We Afford It? - Scientific American - 13 views

  • Later this year the U.S. Food and Drug Administration is expected to approve a new pill that can cure hepatitis C
  • It will contain two drugs, one of which is already available at $1,000 per dose, or $84,000 for a complete 12-week course. The dual-drug combination will likely cost even more
  • They also determined that the virus's genes mutate very fast—a process that has generated several equally successful varieties, called genotypes, and rendered an effective vaccine impossible to create so far.
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  • its genetic material, which is made up of RNA
  • After several false starts, researchers at Vertex Pharmaceuticals, in collaboration with others, developed a protease inhibitor known as telaprevir, while scientists at Schering-Plough (which merged with Merck in 2009), created one called boceprevir.
  • The medications had harsh side effects and worked only for those patients with a particular genetic variant of the virus known as genotype 1
  • What scientists had learned from their earlier research, however, was that inactivating an enzyme or protein was not enough. To stop hepatitis C, any effective drug also had to incorporate itself into the virus's genetic code, where it would need to halt the virus's ability to make new copies of its genes and thus to make new virus.
  • Michael Sofia, then at Pharmasset, solved the problems by adding two compounds known as esters to the analogue.
  • During sofosbuvir's development, they had studied other drugs that inhibited different viral proteins and that might eliminate the need for continued use of interferon and ribavirin.
  • It is this combination, mixed in a single daily pill, that industry watchers expect the FDA to approve by October 2014. It heralds a new era of curative treatment for patients with hepatitis C. Similar drugs that work equally well for all genotypes are now in the final stages of clinical development.
Casey Finnerty

Fish-Killing Virus Spreading in the Great Lakes - New York Times - 0 views

  • “We anticipate that this will continue and get worse over the next few years,” said Dr. Jim Casey, associate professor of virology at Cornell University. “We fear there may be more widespread presence of the virus.”One of Dr. Casey’s colleagues researching the virus, Dr. Paul Bowser, a professor of aquatic animal medicine, added, “This is a new pathogen and for the first number of years — 4, 5 or 10 years — things are going to be pretty rough, then the animals will become more immune and resistant and the mortalities will decline.”
Casey Finnerty

Correlation Between Infectivity and Physical Virus Particles in Human Cytomegalovirus - 0 views

  • Unlike the high particle-infectivity ratio of 106 to 108 previously reported for these viruses, the number of total particles per PFU ranged from 160 to 490 with strain AD-169 and from 176 to 1,050 for strain C-87.
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