FAST Congress


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7:00 am Registration Open

8:00-8:30 Morning Coffee 

Targeted Cancer Therapy

8:25-8:30 Chairperson’s Opening Remarks

8:30-9:00 Rare Cancers: A Paradigm for Precision Medicine

Glen Weiss, M.D., Co-Head, Lung Cancer Unit, Translational Genomics Research Institute (TGen); Director, Thoracic Oncology, TGen Clinical Research Services at Scottsdale Healthcare

In this presentation, I will show why the application of Precision (Personalized) Medicine to treat patients with rare cancers is important. The presentation will highlight the identification of the Hedgehog Pathway, how discovery of this pathway led to development of novel agents that target it, and published clinical results of at least one of these Hedgehog pathway inhibitors that demonstrated promising clinical benefit and published in the New England Journal of Medicine (Sept 2009). The talk will also cover what was learned from this real life example could be applied to other rare and common cancers, and current barriers that need to be dealt with to realize this potential.

9:00-9:30 Molecular Insight into Metastatic Potential and Response to Tamoxifen in Breast Cancer

Andrew Grupe, Ph.D., Senior Director, Pharmacogenomics Research & Development, Celera Diagnostics

Prognostic expression signatures can aid in selecting the most appropriate treatment regimen relative to the expected course of disease. Expression signatures with different gene sets have been shown to have similar performance. Correlating breast cancer
signatures with drug response in widely used cell lines that model human tumors provides a test system to assess the predictive power of these signatures for novel therapeutics during the early stages of drug development. Here we will describe a signature that is prognostic of distant metastasis formation and predictive of tamoxifen treatment in breast cancer patients. Furthermore we will describe correlation with other reported signatures, thereby suggesting similar clinical utility.

9:30-10:00 Comprehensive Profiling of EGFR/HER Receptors

Nita Maihle, Ph.D., Professor, Ob/Gyn & Reproductive Sciences and Pathology, Yale University School of Medicine

While EGF/HER receptors are clinically validated targets in cancer therapy, the success of this new biologically-targeted therapeutics has been limited by our inability to accurately predict which patients will respond to therapy. New evidence suggests that this problem is caused at least in part, by our failure to incorporate the complexities of regulation of this receptor family in the development of these assays, and specific examples of improvements based on comprehensive profiling of EGF/HER receptor expression will be presented.

10:00-10:30 Networking Coffee Break


Translation of the Cancer Genome

Chairperson's Opening Remarks
Thomas Ried, M.D., Chief, Section of Cancer Genomics, National Institutes of Health, National Cancer Institute

10:30-11:00 A Systems Genomic Approach to Identify and Validate Colorectal Cancer Genes

Thomas Ried, M.D., Chief, Section of Cancer Genomics, National Institutes of Health, National Cancer Institute

Despite major improvements in elucidating the genetic changes underlying the initiation and progression of colorectal cancer (CRC), there remains a clinical need to implement novel targeted therapeutic strategies. Proteins that are highly overexpressed in tumor cells have the potential to be selective therapeutic targets. We focused in our analyses on genes on chromosome 13 that were consistently overexpressed. Using cell based model systems that recapitulate the genomic and gene expression changes we have previously observed in primary CRC we applied a functional genomics strategy to identify such anti-CRC targets. We identified 69 genes within the amplified regions that were over-expressed in the tumors compared to matching normal mucosa samples. Next, we validated the expression levels of these 69 genes in 25 colorectal cancer cell lines using real-time PCR, and confirmed over-expression of 44 genes out of these 69 genes. Subsequently, we conducted an RNAi screen in the colorectal cancer cell lines SW480 and HT29. For 15 out of these 44 genes, we observed a decreased cellular viability as a consequence of mRNA silencing. Our experimental strategy led to the identification of genes that were amplified and/or over-expressed in primary colorectal cancers. We surmise that some of these genes represent potential oncogenes residing on chromosome 13q. In order to identify the underlying signaling pathways involved in reduction of viability, we subsequently analyzed the global transcriptomic changes following RNAi using whole-genome microarrays, and could identify the disruption of a variety of pathways relevant for colorectal tumorigenesis.

11:00-11:30 Genome-Wide Association Studies in Cancer

Meredith Yeager, Ph.D., Scientific Director, Core Genotyping Facility, NCI/NIH

Recent advances in human genomics have provided the oppor-tunity to rapidly scan the genomes of large numbers of individuals in genome-wide association studies (GWAS). These scans measure large numbers of single-nucleotide polymorphisms (SNPs) in search of common, low-penetrance markers associated with human traits or diseases. Currently, over eighty regions have been identified in GWAS of different cancer types, with very few regions overlapping between cancers. A number of GWAS and follow-up studies in cancer and related phenotypes are ongoing at the Core Genotyping Facility (CGF) of the Division of Cancer Epidemiology and Genetics (DCEG) of the National Cancer Institute (NCI). Studies of prostate, breast, pancreatic, lung, renal, bladder, brain, gastric and testicular cancers have been conducted in more than 60,000 individuals and have yielded association findings that warrant further investigation to determine the underlying genetic variants contributing to disease. Discussed here is our GWAS approach, progress to date, initial findings, and future directions.

11:30-12:00 pm Lethal Mutagenesis of HIV and Cancer

Lawrence A. Loeb, Ph.D., Professor & Director, Gottstein Memorial Lab & Pathology, University of Washington

We have asked whether increasing mutation rates using nucleoside analogs that incorrectly base-pair can be therapeutically advantageous in HIV and cancer. Serial passage of the HIV infected cells in nM 5-aza-5,6,-dihydro-2’-dihydro-deoxycytidine (KP1212) ablates HIV infection causing A->G and G->A substitutions, as predicted by nuclear magnetic resonance. In a phase II clinical trial, A->G and G->A mutations, also progressively increased. The observed increase in mutations in patients treated by KP1212 support a new approach to antiretroviral therapy in humans. Can the same concept can be applied to human cancer particularly those that have failed chemotherapy. A further increase in the mutation frequency in the cancer genome may lead to an error catastrophe similar to that obtained in viruses.

12:00-12:30 Translating Cancer Genome Sequencing into Oncology Diagnostics

Hanlee P. Ji, M.D., Assistant Professor, Oncology, Stanford University School of Medicine; Senior Associate Director, Stanford Genome Technology Center

12:30 Close of Conference