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Detailed Program Schedule

Saturday, May 31

ASGT Business Meeting

7:30 am – 8:00 am
Room 304 - 306
A light continental breakfast will be available at 7:15 am.

Scientific Symposium 400

8:00 am - 10:00 am
Room 302
Cardiovascular Gene Therapy: Cardiac Regeneration: Disease and Repair Mechanisms and Non-Invasive Imaging

Matthew L. Springer, PhD


Seppo Yla-Herttuala, MD, PhD, FESC
Cardiovascular Gene Therapy
Cardiovascular gene therapy may provide potential new treatments for ischemic heart disease, peripheral vascular disease, in-stent and vascular graft stenosis, cardiomyopathies and various types of lipid disorders. In this presentation, general outlines of cardiovascular gene therapy will be presented with examples of treatments for cardiac ischemia, in-stent restenosis and hypercholesterolemia.

Marc Penn, MD, PhD
Cell Penetrating Peptide Based Gene Therapy for Modulating Cardiac Remodeling

Roger J. Hajjar, MD
Gene Therapy for Heart Failure
While progress in conventional treatment modalities has improved survival in patients with congestive heart failure, the disease progresses relentlessly in these patients. Recent advances in understanding of the molecular basis of myocardial dysfunction, together with the evolution of increasingly efficient gene transfer technology, has placed heart failure within reach of gene-based therapy. We have developed new techniques for gene therapy in large animal models of heart failure that will be readily applicable to humans. Based on these promising results, we have initiated a number of clinical gene therapy trials including 1) a Phase 1/2 clinical trial of dose escalation of AAV1.SERCA2a administered percutaneously that will determine the optimal safe dose of this vector and will be powered to detect biological activity, and 2) a Phase 1/2 clinical trial of dose of AAV6.SERCA2a administered surgically either at the time of or >30 days following left ventricular assist device placement in patients with advanced heart failure. These human studies are the first trials of gene therapy in heart failure using adeno-associated vectors and will test the hypotheses that restoring a key calcium cycling protein, SERCA2a, by gene therapy will improve ventricular function in patients with advanced heart failure.

Kari Alitalo, MD, PhD
VEGFs for More Vessels and Muscle
Kari Alitalo and collaborators

Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Haartman Institute and Biomedicum Helsinki, P.O.B. 63 (Haartmaninkatu 8), 00014 University of Helsinki, Finland

Members of the VEGF family, currently comprising five mammalian proteins, are major regulators of blood and lymphatic vessel development and growth. VEGF-A is essential for vasculogenesis and angiogenesis, whereas VEGF-C is required for the development of the lymphatic vasculature. Although not required for embryonic development, VEGF-B, PlGF and VEGF-D likely play more subtle modifying roles in the control of angiogenesis and lymphangiogenesis, respectively, or function under pathological conditions. Some recent studies suggest that PlGF mediates at least part of its effects via recruiting growth factor-secreting monocytes and macrophages. - This talk will deal with the activities of the VEGF family members in the skeletal and cardiac muscle.

Scientific Symposium 401

8:00 am - 10:00 am
Room 304 - 306
Cancer: Cancer Clinical Trials

Daniel H. Sterman, MD


Min Liang, MD
The Development and Commercialization of an Oncolytic Adenovirus Product H101
The H101 is a oncolytic adenovirus product which has received the NDA approval for nasopharyngeal carcinoma by Chinese SFDA in Nov. 2005, and passed the GMP certification in Aug. 2006. This talk will briefly summarise the development process of H101 from preclinical study to phase III clinical trial, and introduce the industrialization works for this product including manufacture, quality control and quality assurance. The current development of H101 project, such as clinical trial for new indication and lyophilization formulation of this adenovirus product, will also be included in this talk.

Evanthia Galanis, MD, DSc
Clinical Trials with Engineered Oncolytic Measles Virus Strains
Engineered vaccine strains of measles virus have significant antitumor activity against a variety of tumor types including lymphoma (Grote et al, 2001), multiple myeloma (Peng et al, 2001), ovarian cancer (Peng et al, 2002), brain tumors (Phuong et al, 2003), breast cancer (McDonald et al, 2006), and hepatocellular carcinoma (Blechacz et al, 2006). Three phase I/II clinical trials of engineered oncolytic measles virus strains in the treatment of cancer have been activated at the Mayo Clinic Cancer Center. Two of the trials investigate locoregional delivery of a measles virus derivative expressing the human carcinoembryonic antigen CEA (MV-CEA): intraperitoneal delivery in patients with recurrent ovarian cancer and CNS intratumoral/resection cavity administration in patients with recurrent glioblastoma multiforme. In the third trial, a measles virus derivative expressing the human sodium iodine symporter (MV-NIS) is administered intravenously in multiple myeloma patients as a single agent and in combination with cyclophosphamide, with subsequent I123 imaging. Trial design and clinical results to date will be discussed.

Steven A. Rosenberg, MD, PhD
The Treatment of Patients with Metastatic Cancer using Gene-Modified Lymphocytes
The adoptive cell transfer of lymphocytes with anti-tumor activity can media the regression of cancer in approximately 50 to 70% of patients with metastatic melanoma. Based on these results we have isolated the genes encoding high affinity anti-tumor T cell receptors from these lymphocytes and constructed retroviral vectors capable of inserting these T cell receptors into normal lymphocytes. These gene modified lymphocytes then acquire the ability to recognize cancer cells in vitro. We have recently published a clinical trial demonstrating that the adoptive transfer of these cells can mediate tumor regression in some patients (Morgan et al, Science 314:126-129, 2006). We are now conducting clinical trials utilizing genes encoding high avidity T cell receptors capable of recognizing the MART-1 and gp100 melanoma antigens and are administering these cells to patients with metastatic melanoma. The updated results of these trials will be presented.

Daniel H. Sterman, MD
Gene Therapy Clinical Trials for Mesothelioma and other Pleural Malignancies

Scientific Symposium 402

8:00 am - 10:00 am
Room 309
Ethics: Building Your Strategic Tool Kit for Safe Patient Accrual

Bernard Lo, MD


Robyn S. Shapiro, JD
Ethical Issues Surrounding Recruitment and Enrollment in Clinical Trials
Challenging ethical issues surround subject recruitment and enrollment in Phase I gene transfer trials – including the potential for therapeutic misconception, the danger that prospective participants will fail to differentiate the goals of the current phase of the study from the overall research goals, the challenges of determining disease severity inclusion/exclusion criteria as they pertain to the risk/benefit ratio of the research, and potential conflicts of interest that can be intertwined in the relationships among funding sources, investigators and affected individuals or their families. This talk will explore these issues and suggest approaches for facing these challenges.

Round Table Participants
Gail E. Henderson, PhD
Elizabeth L. Hohmann, MD
Diane Wara, MD
Theodore Friedmann, MD

Scientific Symposium 403

8:00 am - 10:00 am
Room 112
Infectious Disease: Novel Gene Therapy Strategies against Infection

William F. Goins, PhD
Stefan Worgall, MD, PhD


John A. Zaia, MD
Gene Therapy Approaches for Treatment of HIV/AIDS: Current Status
The question of how best to target HIV/AIDS using genetic strategies has recently been given some impetus with the application of lentivirus vectors in clinical trials. At present in the U.S., more that 50 persons with HIV/AIDS have been treated with lentivirus vectors. Early data from VirXsys-supported T cell-based clinical trials indicate that genetically modified T cells appear to affect HIV-1 infection, including HIV plasma load, HIV quasispecies number, and even the fitness of the virus to replicate. At City of Hope, a hematopoietic stem cell-based trial has begun using a lentivirus encoding shRNA and other anti-HIV RNAs. These studies will be described. Evidence will be presented showing the in vitro effects of gene transfer on protection from antiviral drug resistance induction and in vivo results suggesting that gene-modified T cells appear to force mutational changes that effect the virus biology. If this can be confirmed, then treatment with gene therapy early after HIV infection could be justified, and, if such treatment delayed the need for antiviral chemotherapy, gene transfer would likely become an important strategy for treatment of HIV infection.

Carl H. June, MD
Anti-sense HIV Lentiviral Vector Confers Antiviral Effects In Vivo
The current status of an ongoing trial testing repeated infusions of T cells modified to express anti-sense envelope sequences will be reviewed. Interim analysis indicates that multiple infusions of lentiviral engineered autologous T cells are well tolerated, and traffic to rectal lymphoid mucosal tissues. The pre-clinical studies supporting a second proof of concept trial using lentiviral modified T cells that are redirected to target gag will be presented. In this study, high affinity MHC class I restricted T cell receptors will be tested for safety and antiviral effects.

Mark A. Kay, MD, PhD
Defining the Rate-Limiting Steps for RNAi Based Therapeutics Directed against Viral Hepatitis

Stefan Worgall, MD, PhD
Capsid-Modified Adenovirus Vector Vaccine against Pseudomonas Aeruginosa
A vaccine against pulmonary infections with P. aeruginosa, would be beneficial for individuals with cystic fibrosis. Our vaccine strategy uses an Ad gene transfer vector to express the gene for OprF, an outer membrane protein of P. aeruginosa, based on the knowledge that Ad vectors infect DC in vivo and thus function as adjuvants, while expressing the antigen in a manner that evokes both humoral and cellular immunity. Preclinical studies enhanced this approach with two innovations: (1) genetic modification of the Ad fiber to incorporate an RGD sequence to enhance binding and gene delivery to DC; and (2) genetic modification of the outer loops of the hexon to incorporate Epi8, a conserved, highly immunogenic epitope from OprF. This has led to a candidate in vivo vaccine (Ad5CUOprF.RGD.Epi8) that not only delivers the OprF P. aeruginosa antigen effectively to DC, but also “boosts” anti-P. aeruginosa humoral immunity upon vector re-administration, by virtue of the anti-capsid immune response to Epi8. In addition a similar vector, based on the non-human primate AdC7 serotype, is being developed that can be used in the context of pre-existing anti-Ad immunity.

Scientific Symposium 404

8:00 am - 10:00 am
Room 100
Musculo-Skeletal: Stem Cells in Musculo-Skeletal Gene Therapy

George Karpati, MD


Alan J. Nixon, BVSc, MS
Stem Cells and Gene Transduced Stem Cells for Cartilage Repair
Bone marrow derived pluripotent MSCs improve short-term cartilage repair in large animal models. However, despite a robust early chondrogenic response, longer term studies reveal that MSC induced repairs fail to mature to hyaline cartilage. Gene induced chondrogenesis using TGF superfamily members and Sox transcription factors can drive this process by extending the differentiated MSC function in culture models. This may hold the key to improved cartilage regeneration. In vitro models of mesenchymal condensation verify adenovirus and integrating transposable elements such as transposon/transposase based Sleeping Beauty TGF-B systems bolster the chondrogenic profile of MSCs. In vivo, the stable chondrogenic phenotype of MSC-derived cartilage repair cells may be further enhanced by implanting cells over-expressing growth factors after repair site integration. Combination of a dedicated autograft MSC line, transformed by TGF-superfamily members, and transduced with chromosomally stable growth factor genes provides real promise for durable cartilage repair. Additionally, pro-inflammatory cytokine suppression through stable short hair-pin RNA gene silencing of IL-1 and TNF in the defect site may further improve the articular environment, leading to more robust cartilage formation.

Jacques P. Tremblay, PhD
Transplantation of Normal Allogeneic or Genetically Corrected Autologous Myoblasts: Possible Treatments of Muscular Dystrophies
Muscle bers can be repaired by several kinds of muscle precursor cells present in muscles (satellite cells, muscle derived stem cells, myobroblasts) or in blood vessels (mesoangioblasts and pericytes). When they proliferate, satellite cells give raise to myoblasts which are committed stem cells. Each of these types of cells has been shown to fuse with existing muscle bers to repair them. These cells can be delivered to the muscle either by intramuscular injection or in the case of mesoangioblasts and pericytes by systemic delivery using intra-arterial injection. When these cells fuse with the existing patient muscle fibers, they introduce their own nucleus into the muscle syncytium.

To correct a recessive muscular dystrophy, many normal nuclei have to be introduced throughout each muscle ber because the nuclear domain is rarely above 1000 microns. Using this strategy, we have been able to obtain expression of dystrophin in MD
x mice and also in patients with muscular dystrophy. This approach may prevent the development of any recessive muscular dystrophy if done early while at a later stage expression of the normal gene may stop progression but not reverse existing myofiber destruction and scarring. An alternate source of allogeneic cells for muscle repair may be cells derived from embryonic stem cells. We have achieved success with this approach in animal models. However, transplantation of normal allogeneic cells requires sustained immunosuppression because muscle bers express major histocompatibility complex antigens in the context of inflammation or excessive activity. Alternative approaches to immunosuppression may be the development of immunological tolerance. We already have achieved some success with this approach. A second alternative is to transplant dystrophic patients with their own muscle precursor cells which have been genetically modified in culture. We have used lentiviral vectors and a new integrative hybrid vector system, the adenoAAV vector, to integrate either the micro-dystrophin or full length dystrophin gene in myoblasts, respectively. Ex vivo genetic correction has the advantage of eliminating exposure of patients to viral vectors. In principle, ex vivo corrected cells may be tested for tumorigenicity in animal models before they are retransplanted into patients adding a measure of safety to this approach.

Maurilio Sampaolesi, PhD
Cell-Mediated Gene Therapy for Muscular Dystrophy: Challenges and Prospects

Elizabeth A. Olmsted-Davis, PhD
Stem Cell Recruitment for Bone Tissue Engineering
Using a cell based gene therapy model which induces rapid targeted ossification, our laboratory has been able to identify the earliest cellular stages of endochondral bone formation. In this model, BMP2 is used to induce rapid bone formation which undergoes all stages of chondro-osseous differentiation within a 7 day period. Within 24 hours of induction, cells within the nerve sheath start to proliferate and express key factors involved in cytoskeletal organization and migration. Within 48 hours, cells migrating from the nerve appear to be assembling into new blood vessels. These cells carry markers of pluripotency including Nanog, Klf4, Sox 2, Oct4 and the embryonic antigen SSEA-1. A portion of these cells also appear to be undergoing adipogenesis to form brown adipocytes, or cells that have high levels of mitochondria, and are undergoing aerobic respiration. The data suggests that these nerve sheath cells may be involved in establishing the appropriate oxygen micro-environment for chondro-osseous development. At approximately 3-4 days after induction, we observe the expression of key factors known to function in mesenchymal stem cell extravasation at the site of new bone formation. This period is also the peak of new vessel formation within the tissues. Interestingly, the mesenchymal stem cells for bone and cartilage are actually myeloid origin cells expressing CD68. By 4-5 days after induction, these myelo-mesenchymal progenitors replicate, and establish a tentative perichondrium. This is followed on day 6-7 with establishment of a growth plate, and transition to bone formation. The data collectively suggests that several stem and progenitor populations are required for this process, both to establish a conducive microenvironment and to provide precursors for chondrocytes and osteoblasts.

Scientific Symposium 405

8:00 am - 10:00 am
Room 311
Neural Disorders: Glial Cells in Neural Disease and Repair

Maria G. Castro, PhD


Erin D. Milligan, PhD
Spinal Interleukin-10 Gene Therapy to Control Pathological Pain
Controlling chronic pain in humans is a major unresolved problem. Recent data strongly support that spinal cord glia (astrocytes & microglia) are critically involved in the creation & maintenance of diverse enhanced pain states. Spinal cord glia create enhanced pain via the release of a variety of factors that include proinflammatory cytokines tumor necrosis factor, interleukin-1 & interleukin-6. Recognition of the key importance of spinal cord glia, and glial proinflammatory cytokines in pathological pain opens new avenues for pain control. One potential means is via anti-inflammatory factors. Interleukin-10 (IL-10) is most widely known as an anti-inflammatory cytokine that acts as an endogenous suppressor of proinflammatory cytokine production & activity. As such, IL-10 is an excellent candidate for preventing & reversing PIC-driven pathological pain states. Control of pain requires chronic delivery of IL-10. However, IL-10 cannot cross the blood-brain barrier, thus negating systemic administration. To resolve these issues, we are exploring the feasibility of prolonged spinal release of IL-10 induced by gene therapy. Here, vectors encoding IL-10 are injected into the cerebrospinal fluid surrounding the spinal cord (intrathecal; IT), to mimic a clinically relevant route of delivery. These data provide strong support that spinal IL-10 gene therapy with IL-10 prevents & reverses pathological in various rodent models of pathological pain. Advantages of this approach as well as several experimental hurdles encountered during these studies will be discussed. The global concept of this talk will address whether IL-10 is worthy of clinical development for controlling diverse pathological pain states. This approach to pain control represents a departure from all other available pain therapies.

Steven A. Goldman, MD, PhD
Progenitor Cell-Based Treatment of Congenital Myelin Disease

Harald Neumann, MD
Microglial Clearance Function in Neuronal Homeostasis, Injury and Death
Microglia are the resident immune cell type of the central nervous system (CNS). They populate the CNS early during development. In the adult, bone marrow-derived myeloid precursor cells are recruited to sites of acute injury. Microglia become activated in acute or chronic CNS diseases and could act neurotoxic by release of pro-inflammatory cytokines and reactive oxygen species. However, microglia have also beneficial function. Microglia remove apoptotic cells and cellular debris. Microglial triggering receptor expressed on myeloid cells-2 (TREM2) is involved in this phagocytosis of CNS tissue debris.

We investigated whether bone marrow-derived myeloid precursor cells genetically modified to express TREM2 affect the disease course of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. EAE was induced in mice by immunization with the myelin oligodendrocyte glycoprotein (MOG). Intravenous transplantation of TREM2-transduced bone marrow–derived myeloid precursor cells after onset of clinical disease ameliorated the symptoms, reduced axonal damage, and prevented further demyelination. The TREM2-transduced myeloid precursors migrated into the inflammatory spinal cord lesions of EAE-diseased mice, showed increased lysosomal and phagocytic activity, cleared degenerated myelin and created an anti- inflammatory cytokine milieu.

Thus, TREM2-transduced myeloid precursor cells limit tissue destruction and facilitate repair within the murine CNS by clearance of cellular debris during EAE.

Scott R. Whittemore, PhD
Stem Cell Repair of Spinal Cord Injury
Stem cell therapy holds great promise for the neural repair. However, the microenvironment of the injured central nervous system (CNS) is a hostile environment for the survival and differentiation of grafted cells. Pluripotent embryonic neural stem/precursor cells (NSPCs) that in vitro can differentiate into neurons, astrocytes, and oligodendrocytes have a restricted lineage potential when grafted into spinal cord. In uninjured spinal cord, these cells differentiate predominantly into astrocytes with few oligodendrocytes, but not neurons and only astrocytes and undifferentiated NSPCs are seen following engraftment into the contused spinal cord. Thus obtaining large numbers of neurons and oligodendrocytes will require partial lineage restriction prior to grafting and/or blockade of intrinsic factors expressed in the injured spinal cord that direct differentiation to an astrocytic fate. If embryonic neuronal-restricted precursors (NRPs) are grafted into the uninjured spinal cord, they show an identical lineage restriction as they do in vitro – expression of neuronal antigens in all cells with differentiation into subsets of GABAeric, glutamatergic, and cholinergic neurons. In contrast, when NRPs are grafted into a contused spinal cord, most of the cells no longer express neuronal markers, indicating active restriction of a neuronal fate. Glial-restricted precursors (GRPs), which in vitro differentiate into astrocytes and oligodendrocytes differentiate predominantly into astrocytes when grafted into the contused spinal cord, an effect mediated by bone morphogenetic proteins (BMPs). Inhibition of BMP signaling by grafting noggin-expressing GRPs was insufficient to potentiate oligodendrocyte differentiation and actually exacerbated lesion severity by unmasking a previously unknown role of BMP to suppress chronic inflammation. Grafting neurotrophin (BDNF, NT3) or ciliary neurotrophic factor (CNTF) expressing GRPs into the contused spinal cord enhanced remyelination and only partial functional recovery. Optimal remyelination strategies will require partial lineage restriction, providing neurotrophic factors necessary for survival and maturation, and inhibition of intracellular signaling pathways that drive unwanted cell fate. Successful NSPC grafting strategies must incorporate an understanding of the basic biology of both the engrafted cells and the host microenvironment.


10:00 am – 10:15 am

Oral Abstract Session 410

10:15 am – 12:15 pm
Development of AAV Vectors
(Abstracts 673-680)
Room 304

Hiroyuki Nakai, MD, PhD
David V. Schaffer, PhD

Oral Abstract Session 411

10:15 am – 12:15 pm
Adenovirus: Cancer Therapy
(Abstracts 681-688)
Room 311

Michael A Barry, PhD
William S.M. Wold, PhD

Oral Abstract Session 412

10:15 am – 12:15 pm
Mechanistic Studies and Carrier Design
(Abstracts 689-696)
Room 210

David A. Dean, PhD
Uta Griesenbach, PhD

Oral Abstract Session 413

10:15 am – 12:15 pm
Inborn Errors of Lysosomal Metabolism
(Abstracts 697-704)
Room 309

Kathrine M. Ponder, MD
Alessandra Biffi, MD

Oral Abstract Session 414

10:15 am – 12:15 pm
Neurologic – Alzheimer’s and Parkinson’s Diseases
(Abstracts 705-712)
Room 112

Martha C. Bohn, PhD
Michael Kaplitt, MD, PhD

Oral Abstract Session 415

10:15 am – 12:15 pm
Vaccine Delivery and Immune Responses for Infectious Diseases
(Abstracts 713-720)
Room 208

John A. Zaia, MD
Bruce E. Torbett, PhD, MSPH

Oral Abstract Session 416

10:15 am – 12:15 pm
Cancer – Immunotherapy: Viral-based Immune Modulation
(Abstracts 721-728)
Room 100

Alex W. Tong, MD
J. Victor Garcia-Martinez, PhD

Oral Abstract Session 417

10:15 am – 12:15 pm
Cancer – Targeted Gene Therapy: Virotherapy
(Abstracts 729-736)
Room 207

Adele Fielding, MRCP, MRCPath, PhD
Xiaoliu Zhang, MD, PhD

Oral Abstract Session 418

10:15 am – 12:15 pm
Hematologic – Immunodeficiencies and Hemoglobinopathies
(Abstracts 737-744)
Room 312

John F. Tisdale, MD
Isabelle Riviere, PhD

Oral Abstract Session 419

10:15 am – 12:15 pm
Small Nucleic Acids in Blood Diseases and Cancer
(Abstracts 745-752)
Room 302

Faye A. Rogers, PhD
Toni Cathomen, PhD

Lunch Break

12:15 pm – 2:00 pm

Meet the Investigator 420

12:30 pm - 1:45 pm
Room 108
Meet the Investigator Lunch


Cynthia Dunbar, MD
Art Krieg, MD
Career Development: Academic vs. Industry

Meet the Investigator 421

12:30 pm - 1:45 pm
Room 107
Meet the Investigator Lunch

Christopher Baum, MD
Assays to Evaluate Potential Genotoxicity of Integrating Retroviruses

Presidential Symposium 430
2:00 pm - 5:00 pm
Room Ballroom A - C
Advances in Gene Therapy Research

Arthur W. Nienhuis

Arthur W. Nienhuis, MD

Outstanding Achievement Award Winner

R. Jude Samulski

R. Jude Samulski, PhD
AAVolution of a Smart Virus


Luigi M. Naldini

Luigi M. Naldini, MD, PhD
Targeting Gene Transfer to Enhance the Efficacy and Safety of Gene Therapy

Frederic D. Bushman

Frederic D. Bushman, PhD
Retroviral DNA Integration: Mechanism and Consequences

Xandra O. Breakefield

Xandra O. Breakefield, PhD
MicroRNA and Microvesicle Mediated Transfer of Genetic Information in Brain Tumor Pathogenesis

Poster Session III

5:15 pm – 7:00 pm
Room Exhibit Hall B, Plaza Level

RNA Virus Vectors II
(Abstracts 753 through 766; Abstract 765 Withdrawn)

Development of AAV Vectors
(Abstracts 767 through 779)

Preclinical Applications of AAV Vectors
(Abstracts 780 through 792)

Adenovirus Vectors: Biology and Pharmacology
(Abstracts 793 through 809)

Adenovirus Vectors: Chemical and Genetic Engineering
(Abstracts 810 through 826)

DNA Vectorology: In Vivo Non-Viral Delivery
(Abstracts 827 through 837)

Physical Method for Gene Delivery
(Abstracts 838 through 8514)

Nonviral Gene Transfer
(Abstracts 852 through 866; Abstract 858 Withdrawn)

Inborn Errors of Metabolism II
(Abstracts 867 through 885)

Neurologic – Genetic and Peripheral Nerve
(Abstracts 886 through 900; Abstracts 512 & 526 have been moved here from Poster Session II)

Lung and Respiratory Disease
(Abstracts 901 through 918)

Musculoskeletal Gene and Cell Therapy: Bone, Joint, Tendon and Muscle Therapy
(Abstracts 919 through 933)

Oligonucleotide Therapies II
(Abstracts 935 through 948; Abstract 934 Withdrawn)

Hematopoietic, Lung, Liver, Skin and Cancer Stem Cells
(Abstracts 949 through 964)

Saturday Night Party

7:00 pm – 9:30 pm
Back Bay Ballroom, Sheraton Boston
Join us for a Saturday Night Party at the Sheraton Boston Hotel in the Back Bay Ballroom A&B from 7:00 pm - 9:30 pm. Featuring live music by Soul City, a cash bar and light snacks.