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Friday, February 5
8:30 AM Chairperson’s Opening Remarks
Dalia Cohen, Ph.D., Chief Scientific Officer, Rosetta Genomics, Inc.
8:35 Keynote Presentation
Causes and Consequences of microRNA Dysregulation in Cancer
Carlo M. Croce, M.D., Professor, Internal Medicine, College of Medicine & Public Health, The Ohio State University
During the past several years it has become clear that alterations in the expression of microRNA genes contribute to the pathogenesis of most, perhaps all, human malignancies. These alterations can be caused by a variety of mechanisms, including deletions, amplifications or mutations involving microRNA loci, by epigenetic silencing or by dysregulation of transcription factors targeting specific microRNAs. Since malignant cells show dependence on the dysregulated expression of microRNA genes, which in turn control or are controlled by dysregulation of multiple protein coding oncogenes or tumor suppressor genes, these small RNAs provide important opportunities for development of future microRNA based therapies.
9:05 microRNA Polymorphisms and the Future of Personalized Medicine
Prasun J. Mishra, Ph.D., Laboratory of Cancer Biology & Genetics, NCI, NIH
Referred to as the micromanagers of gene expression, microRNAs are evolutionarily conserved small non-coding RNAs. Polymorphisms in the microRNA pathway can influence gene regulation and are emerging as powerful tools to study the biology of diseases. Detection of microRNA-polymorphisms can potentially improve diagnosis, treatment and prognosis in patients and has profound implications in the fields of pharmacogenomics and personalized medicine.
9:35 Living in a Sequen-omics World: Data Integration Issues and Challenges
David Sugarbaker, M.D., Chief, Thoracic Surgery, Brigham and Women’s Hospital
DNA sequencing and other “-omics” platforms (e.g., mRNA, microRNA, CGH, exon, SNP, and other arrays) have experienced a technological revolution in throughput and scale over the preceding decade that shows no sign of slowing. However, data storage and processing advances have outpaced the ability to fully integrate the resulting massive quantities of data into biologically meaningful and predictive models to apply to risk estimation, prevention, and cure of human diseases, most notably cancer. In addition, further technological innovation will continue to drive down costs which will exacerbate the problem in the near-term but over the long-term will bring more resources to bear in solving these issues and challenges. This session will provide a comprehensive view of the sequen-omics landscape and identify the key issues that will need to be addressed in the future for these platforms to positively affect human health.
10:05 Sponsored Presentation (Sponsorship Opportunity Available)
10:20 Coffee Break
11:00 The Onco-SNP and Cancer Risk: microRNA Binding Site Polymorphisms as Biomarkers
Joanne B. Weidhaas, Ph.D., Assistant Professor, Yale University
Since microRNAs are global regulators, small aberrations such as SNPs that disrupt their coding sequences or their target binding sites can alter cellular homeostasis and enhance cancer risk. MicroRNA binding site polymorphisms have turned out to be some of the strongest biomarkers of cancer risk, can act as biomarkers of outcome, and may be future targets for therapy.
11:30 Role of microRNA Based Profiling in Determining Tissue of Origin for Carcinoma of Unknown Primary
Gauri Varadhachary, M.D., Associate Professor of Medicine, Department of G.I. Medical Oncology, M.D. Anderson Cancer Center
Carcinoma of unknown primary (CUP) is a heterogeneous disease where a patient presents with metastases without an identifiable primary. As more effective cytotoxic and targeted therapies emerge for additional known cancers, accurate identification of CUP subtypes will become increasingly important to the appropriate care of these patients. MicroRNA expression profiling is an emerging tool to help with identification of tissue of origin in patients with CUP.
12:00 PM Luncheon Presentation (Sponsorship Opportunity Available) or Lunch on Your Own
1:00 Chairperson’s Remarks
1:05 Impact of Antibodies on Cancer Stem Cells: Discovering Underlying Pathways Essential to Cancer Stem Cell Biology
Tim Hoey, Ph.D., VP, Cancer Biology, OncoMed Pharmaceuticals, Inc.
Cancer stem cells are thought to mediate tumor initiation, metastasis, and recurrence. We have isolated and characterized CSCs from a variety of major tumor types and have found that these cells are preferentially resistant to many current therapies. As part of our effort to develop novel agents targeting CSCs, we have developed an anti-DLL4 antibody that blocks Notch signaling. Anti-DLL4 inhibits tumor growth through multiple mechanisms including a reduction in CSC frequency.
1:35 Understanding Tumor Cell Heterogeneity in NSCLC: Contributions to Resistance and Relapse
Erica L. Jackson, Ph.D., Scientist, Genentech, Inc.
Tumors are made up of a heterogeneous mixture of cell types and it is possible that distinct cell populations play unique roles in tumorigenesis. We are studying functionally defined cell populations to determine what distinguishes chemo-resistant cells from bulk tumor cells.
2:05 ABC Transporters’ Role in Cancer Stem Cell Drug Resistance
Muhammad Al-Hajj, Ph.D., Director, Stem Cell Discovery Unit, GlaxoSmithKline
One of the mechanisms by which residual disease become chemo-resistant is via the decreased efficiency of chemo-therapeutics through the action of ATP-binding cassette (ABC) proteins that are variably expressed by the tumor cells and tend to be up-regulated in some cancer stem cells. The clinical relevance of the ABC transporters in the context of cancer stem cells is paramount and their application requires better understanding of the role individual transporters play in the mechanism and the development of more specific inhibitors with minimal off target effects. Here we'll discuss the role of two specific transporters in pancreatic and colon cancer stem cells and their value as therapeutic targets.
2:35 New Visions of Cancer Therapy through the Prism of the Cancer Stem Cell Hypothesis
Justin D. Lathia, Ph.D., Research Associate, Department of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic Foundation
The failure of conventional therapies to fundamentally alter the survival of advanced and metastatic cancers has many causes but one appears to be the striking cellular heterogeneity in most cancers. The cancer stem cell hypothesis posits that tumors contain a cellular hierarchy of differentiation and tumor propagation potential. As studies have demonstrated that cancer stem cells display therapeutic resistance, angiogenic potential, and a propensity towards invasion/metastasis, the identification of signaling pathways and molecular targets in cancer stem cells may yield improved cancer therapies.
3:05 Close of Conference
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