Final Program - American Society of Gene & Cell Therapy

Program Schedule, Thursday, May 16, 2013
Sensory (Ophthalmic and Auditory) Gene & Cell Therapy
(Abstracts 222-232; see page 103)
Gene Regulation
(Abstracts 233-246; see page 104)
Fetal and Adult Stem Cells
(Abstracts 247-258; Abstract 252 has been withdrawn from presentation; see pages 104-105)
Cell Processing and Vector Production
(Abstracts 259-265; see page 105)
Late Breaking Abstracts I
(Abstracts 677-700; Abstracts 687 and 698 Withdrawn from Presentation; see pages 105-107)
Thursday, May 16, 2013
Canadian Attendee Reception
6:00 pm - 7:00 pm
ROOM: 255 B
Foundation Symposium 240
6:00 pm - 8:00 pm
ROOM: BALLROOM B
Gene and Cell Therapy for Cancer
Supported by the Alliance for Cancer Gene Therapy.
CO-CHAIRS: Xandra O. Breakeield, PhD and Savio L.C. Woo, PhD
SPEAKERS
Joseph C. Glorioso, III, PhD
Targeted Cancer Therapies
Cancer cell genetic analyses have identiied driver mutations that dysregulate cell proliferation- and differentiation-related
pathways, providing focal points for targeting of cancer therapy. At least six targeting strategies have been employed: (i) the use of
drugs that block different steps in cancer causing signaling cascades leading to the arrest of tumor cell growth and the induction of
senescence, apoptosis and autophagy, (ii) application of drugs or immune mediators that attack the tumor microenvironment (iii)
the use of antibodies that inhibit tumor cell growth by blocking growth factor receptors, (iv) coupling of therapeutics to antibodies,
nanoparticles or other ligands that recognize tumor-associate antigens (v) immune based strategies to induce anti-tumor immunity,
reduce immune down regulation or exploit engineered immune acting cells to destroy tumors, and (vi) the use of designer biologics
such as viruses, bacteria or stem cells to selectively destroy tumors. Some notable successes will be highlighted for each of these
approaches, however tumor heterogeneity makes it unlikely that any one strategy will succeed. Cancer virotherapy remains a
very versatile strategy that takes advantage of advances in enhanced vector design to provide the most potent, highly selective
tumor killers. Current methods to control vector transduction and transcription, evasion of innate immunity and enhanced vector
replication and spread will be presented.
Stephen J. Russell, MD, PhD
Oncolytic Virotherapy
Oncolytic viruses (OV) selectively destroy neoplastic tissue and it is theoretically possible to engineer or adapt any naturally
occurring virus for this purpose; key engineering strategies will be reviewed. A spreading intratumoral OV infection can damage
both infected and uninfected tumor cells; the mechanisms underlying both of these activities will be discussed. Oncolytic viruses
can be combined with drugs or armed with transgenes to accelerate their spread, modulate their immunogenicity/potency or
facilitate the noninvasive monitoring of their in vivo fate; illustrative examples will be discussed. Finally, several oncolytic viruses
are currently being tested in clinical trials and the current status of this work will be summarized.
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Final Program SALT LAKE CITY, UTAH May 15–18, 2013