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Fate Therapeutics

Life and Brain


Cell Therapy News

Stem Cells in Drug Discovery and Development - Day 2

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Tuesday, November 9

7:30-8:00 am Conference Registration

8:00-9:00 Breakfast Roundtable Discussions

Table 1: Stem Cells for Toxicity Assessment

Moderator: Joshua E. Babiarz, Ph.D., Principal Scientist, Non-Clinical Safety, F. Hoffmann-LaRoche, Ltd.


Table 2: Cancer Stem Cells

Moderator: Stephen Wong, Ph.D., Chair, Professor and Director, Center for Bioengineering and Informatics, The Methodist Hospital Research Institute, Weill Cornell Medical College


Table 3: Stem Cells for Drug Screening

Moderator: Davide Danovi, M.D., Ph.D., Neural Stem Cells Group, UCL Cancer Institute, University College London


Table 4: Stem Cells as Drug Targets

Moderator: Jan M. Van Tornout, M.D., M.Sc., Group Director & Lead EDT #2, Discovery Medicine Oncology/Immunology, Bristol-Myers Squibb Co.



Cancer Stem Cells

Chairperson's Opening Remarks

Stephen Wong, Ph.D., Chair, Professor and Director, Center for Bioengineering and Informatics, The Methodist Hospital Research Institute, Weill Cornell Medical College

9:00-9:30 Systems Biology Strategy for Drug Repositioning and Combination for Breast Cancer Stem Cells

Stephen Wong, Ph.D., Chair, Professor and Director, Center for Bioengineering and Informatics, The Methodist Hospital Research Institute, Weill Cornell Medical College

Current failure with cancer treatment is not usually due to a lack of primary response or initial induction of remission, but to relapse or tumor recurrence after therapy, in which tumor-initiating cells (TICs) or Cancer Stem Cells (CSCs) are thought to have crucial roles. Our recent clinical data and experimental evidence in both mouse and human xenograft models supports the existence of a subpopulation of cancer cells present in the original tumor that are greatly enriched in residual cancers after conventional systemic therapies. These residual cancer cells are characterized by their intrinsic resistance to chemotherapy and relative growth quiescence. However, a discreet subset of these residual cells possesses enhanced self-renewal capacity, as well as the ability to form tumors upon transplantation. This lecture will present how to discover agents and strategies that target cancer and tumor relapse at their apparent source – CSCs. To achieve translational impact, our strategy is to reposition existing drugs to inhibit the self-renew of CSCs. Specifically, our workflow is to generate a signaling network signature for CSCs; then map all FDA drugs to the protein targets in the network; model the pathway cross-talks to identify combination drugs to inhibit the self-renewal of CSCs; test the efficacy of the repositioned single and combination drugs on pre-clinical models; and refine the systems biology modeling by the data generated from the validation.

9:30-10:00 Cancer Stem Cells: Biology and Clinical Translation

William Matsui, M.D., Associate Professor, Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine

In multiple myeloma, malignant plasma cells make up the vast majority of tumor cells, phenotypically characterize the disease, and are responsible for clinical symptoms, but we have found that the clonogenic growth capacity of the disease is restricted to small populations of cells phenotypically resembling memory B cells. Furthermore, the drug resistance and self-renewal potential of these myeloma stem cells suggest they play a central role in disease relapse and progression. We will discuss our efforts to identify therapeutic targets in myeloma stem cells and translate these findings to the clinic.

10:00-10:30 Targeting the Jak-STAT Pathway in Glioblastoma Stem Cells

Brent Cochran, Ph.D., Principle Investigator, Department of Physiology, Tufts University School of Medicine

Glioblastoma multiforme (GBM) is the most common brain cancer and has an average survival from time of diagnosis of only 14 months. Stem like cells isolated from this tumor are highly efficient in generating tumors in mouse xenografts and retain the ability to differentiate into neurons, astrocytes and oligodendrocytes. We have shown that inhibitors of the Jak-STAT pathway and the transcription factor STAT3 in particular abrogate the multipotency of GBM stem cells. Moreover, we have found that STAT3 maintains multipotency in these cells by regulation of key enzymes that modulate the epigenome by histone methylation.

10:30-11:15 Networking Coffee Break with Poster and Exhibit Viewing

11:15-11:45 Selection of Cancer Stem-Like Cells from Solid Tumors: Characterization and Use in Drug Discovery

Jennie Mather, Ph.D., Senior Vice President, Stem Cell Research, MacroGenics

We use defined in vitro culture conditions that select for minority cancer stem like cells (CSLC) from different solid tumor types. These provide a controlled, unlimited source of CSLC from different patients.  These CSLC are valuable tools for our industrial drug target/antibody discovery and screening platform for the development of anti-cancer drugs that have the potential of eliminating this critical component of the tumor. We describe a series of such lines derived from colorectal tumors that have the properties of CSC, and their use in drug discovery.

11:45-12:15 Speaker to be Announced

12:15-12:45 Speaker to be Announced

12:45 Close of Conference

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