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Jnm Abstract 3..35 AACR/SNMMI State-of-the-Art Molecular Imaging in Cancer Biology and Therapy: Abstracts Exciting developments in the fi eld of cancer imaging have led to important insights into the origins and biology of cancer, as well as novel techniques for early diagnosis, accurate staging, and monitoring of response to therapy for cancer patients. These new discoveries have great potential as tools for basic and translational research in cancer biology and for clinical use to improve patient outcomes. The Society of Nuclear Medicine and Molecular Imaging (SNMMI) and the American Association for Cancer Research (AACR) have come together to cosponsor State-of-the-Art Molecular Imaging in Cancer Biology and Therapy, a conference to be held February 27 to March 2, 2013, at the Manchester Grand Hyatt in San Diego, California. The focus of the conference will be to educate, promote, and support the application and use of molecular imaging in cancer biology. The conference will cover molecular imaging and therapy in cancer-related basic, translational, and clinical research and the integration and application of molecular imaging to the understanding of cancer biology. The goal of this joint AACR– SNMMI conference is to bring imaging scientists together with basic, translational, and clinical cancer researchers in a focused, smaller meeting setting to discuss the latest developments in imaging genetic and molecular processes of cancer as they occur in cells, animal models, and patients. The conference will feature several concurrent educational sessions on Wednesday, including “Imaging Therapeutic Response with PET,” “Emerging Technologies,” and “In Vivo Studies of Cancer Biology at Cellular Resolution.” Wednesday evening will include the welcome reception and a special keynote address from Douglas Hanahan, PhD, Professor of Molecular Oncology and Merck Serono Oncology Chair at the École Polytechnique Fédérale de Lausanne and Director of the Swiss Institute for Experimental Cancer Research. Thursday and Friday will feature 8 plenary sessions focused on cancer stem cells; imaging of the tumor microenvironment, stroma, and metastatic niche; imaging and genomics; innovative therapies guided by imaging; and more. This conference will also offer opportunities for participation from junior scientists, with presentations selected from the most highly rated abstracts. In addition to the didactic lectures, the meeting will also include over 90 poster presentations. The abstracts presented in this supplement issue to The Journal of Nuclear Medicine represent some of the most interesting ideas in molecular imaging research as applied to cancer biology and therapy. The abstracts are listed alphabetically by the last name of the presenting author, with the main abstracts followed by the invited speaker abstracts. Please note that the presenting author at the conference is not always the fi rst author of the abstract. In addition, abstracts selected to receive Young Investigator Travel Awards (AACR-Afl ac, Incorporated, Scholar-in-Training Awards and SNMMI/AACR Young Investigator Awards) are indicated by a footnote. We hope that many of our members will be able to attend this exciting conference. Carolyn J. Anderson, PhD Cochair, State-of-the-Art Molecular Imaging in Cancer Biology and Therapy; and Professor of Radiology and Director of the Molecular Imaging Laboratory, University of Pittsburgh David Piwnica-Worms, MD, PhD Cochair, State-of-the-Art Molecular Imaging in Cancer Biology and Therapy; and Professor of Radiology, Professor of Cell Biology and Physiology, Director of the Molecular Imaging Center, and Director of the BRIGHT Institute, Washington University in St. Louis Abstract Reviewers David Piwnica-Worms, MD, PhD Steve Larson, MD, FACNM Washington University School of Medicine, St. Louis, MO Memorial Sloan-Kettering Cancer Center, New York, NY Carolyn J. Anderson, PhD Jason Lewis, PhD University of Pittsburgh Medical Center, Pittsburgh, PA Memorial Sloan-Kettering Cancer Center, New York, NY Christopher Contag, PhD Martin Pomper, MD, PhD Stanford University, Stanford, CA Johns Hopkins Kimmel Comprehensive Cancer Center, Baltimore, MD Kim Kelly, PhD University of Virginia, Charlottesville, VA Zena Werb, PhD University of California, San Francisco, CA Hisataka Kobayashi, MD, PhD National Cancer Institute, Bethesda, MD COPYRIGHT © 2013 by the Society of Nuclear Medicine and Molecular Imaging, Inc. DOI: 10.2967/jnm542abs Molecular Imaging in Cancer 3A MAIN ABSTRACTS bifunctionalized isothiocyanate spacer and the construct was chemically characterized using size exclusion chromatography and electrophoresis. The immunoconjugate was biologically tested using ELISA test to verify the 1 immuno affinity with NY-ESO-1. Furthermore, E978-CpG conjugate was in Image-guided treatment of pancreatic cancer using cathepsin vitro and in vivo evaluated. After CpG modification, E978-CpG conjugate E-activatable prodrug. W.R. Abd-Elgaliel1, Z. Cruz-Monserrate2, H. was allowed to be formed overnight incubated at room temperature. The Wang2, C.D. Logsdon2, C. Tung1; 1The Methodist Hospital Research construct was separated from unreacted DNA using size exclusion Institute–Weill Cornell Medical College, Houston, TX, 2The University of chromatography. The electrophoresis confirmed the conjugation efficiency, Texas MD Anderson Cancer Center, Houston, TX showing an additional heavier band (higher molecular weight) for the new construct as compared to E978. ELISA test demonstrated a minimum Purpose: Upregulated cathepsin E (Cath E) protease has been found immunological action change of modified E978 as compared to E978. This associated with pancreatic cancer. Here we assessed the competence of construct responded to NY-ESO-1 test with a comparable affinity to that pancreatic cancer-associated Cath E as a drug activator for non-invasive of E978. Furthermore, the in vitro evaluation on DC indicated a dramatical imaging and treatment of pancreatic cancer in mice. Specific activation of enhancement of cell maturation with CpG-E978, 70% of DCs were the prodrug is expected to kill pancreatic cancer cells without harming observed maturated as compared to only 10% for E978. Furthermore, CpG- normal pancreatic cells. Procedures: A Cath E-activatable prodrug and E978 was comparatively evaluated on DC maturation with CpG alone in imaging probe was synthesized and evaluated for its enzyme susceptibility order to define the number of DNA strand per antibody. It was found that and selectivity. Fluorescence imaging of pancreatic cancer was validated one antibody was conjugated to one CpG. Finally, the modified antibody using cells and animals with different expression of Cath E activity. E978 was evaluated in vivo using tumor bearing mice (BALB/c mice Potential of laser treatment was assessed by detecting the intracellularly xenografted with CT26, NY-ESO-1 expressing cells). A comparative study activated prodrug in Cath E-positive cancer cells (Mpanc96-CTSE). The with 6 animal groups was conducted looking at the tumor growth over 25 conversion of the drugs was monitored by newly formed fluorescent signal days with: no treatment; 5-FU treatment; 5-FU + E978; 5-FU + E978-CpG; and their phototoxicity was demonstrated by applying specific laser. 5-FU + A33 as a control antibody, 5-FU + A33-CpG. As expected our Negative controls were assessed in parallel with low Cath E expressing positive control group, 5-FU + E978, showed significant inhibition of tumor cells. Data: Non-invasive imaging of pancreatic cancer was achieved using growth as compared to 5-FU and the A33 control groups. However, no a Cath E-sensitive prodrug. Images illustrate the capability of detecting the augmented tumor growth inhibition was seen when treating the mice fluorescence within Cath E-positive tumors but not within the normal with 5-FU + E978-CpG as compared to 5-FU + E978. E978-CpG was pancreas. Treatment results indicate that prodrug was activated specifically successfully synthesized and characterized, validating the conjugation within Cath E-positive tumors. No signs of prodrug activation in the normal strategy. The novel antibody construct showed high immune response to DC pancreatic tissues were detected. When used in combination with light maturation. DC maturation was 7 times higher when treated with our construct illumination, it shows selective therapeutic effect to the cancerous tissues, as compared to control. The results were seen to be very promising in vitro, with minimal harm to the adjacent normal tissues. Conclusions: The novel demonstrating the possible synergistic therapeutic and targeting effect of Cath E-mediated prodrug activation approach allows the detection of CpG associated with E978, however, the inhibition of tumor growth was pancreatic cancer cells accurately and specifically impairs their viability. limited in vivo. A possible difficulty may have risen regarding the amount Most importantly, it does not harm the adjacent normal pancreatic cells. The of antibody construct delivered on the tumor site, due to possible different treatment experiments substantiate the usefulness of site-specific pharmacokinetics between E978 and E978-CpG. References: 1. Noguchi T endogenous activation of Cath E-sensitive prodrug for pancreatic cancer et al., Cancer Research. 2012 Apr 1;72(7):1672–82. 2. Karbach J et al., treatments. The study demonstrates the potential of applying Cath Cancer Research. 2012 Sep 1;72(17):4304–10. E-activatable prodrug with laser in treating Cath E-rich pancreatic cancer. This
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