2016 Archived Content

Translating Cancer Genomics Header

Cancer Genomics is set to greatly impact oncology, both from a drug discovery and therapeutic standpoint. With improvements in sequencing, transcriptomics and data analysis accelerating the growth of knowledge and scientific discovery, cancer genomics can now be used more widely and effectively. Cancer genomic data coupled with the right functional screening tools, can be exploited to reveal new disease biology and new drug targets for intervention. In translational research it can be used to identify and classify tumors from healthy tissue and differentiate between various cancer types, which can then impact treatment options and outcomes. Clinical cancer genomics can be used to better diagnose and track disease progression, identify patient responders and evaluate therapeutic efficacy. Cambridge Healthtech Institute’s inaugural conference on Translating Cancer Genomics brings together experts from academia and industry to share ideas and strategies on how to further explore the promise of cancer genomics.

Final Agenda


• September 19 Symposium: NK Cell-Based Cancer Immunotherapy

• September 20-21 Conference: Advances in Gene Editing and Gene Silencing - Part 1

• September 21-22 Conference: Translating Cancer Genomics

• September 21 Short Course: Functional Screening Strategies Using CRISPR and RNAi

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Wednesday, September 21

11:20 am Conference Registration Open

11:25 Enjoy Lunch on Your Own

2:40 Refreshment Break in the Exhibit Hall with Poster Viewing


3:20 Chairperson’s Opening Remarks

Arthur L. Shaffer, III, Ph.D., Staff Scientist, Laboratory of Dr. Louis Staudt, Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health

3:35 Revealing Cancer Landscape by Sequencing Single Cells and Cell-free DNA

J. Christopher Love, Ph.D., Associate Member, Broad Institute; Associate Professor, Chemical Engineering, Koch Institute for Integrative Cancer Research at MIT; and Associate Member, Ragon Institute of MGH, MIT, and Harvard

Metastatic cancer remains a significant cause of mortality. Limited access to lesions and sparse samples have hindered genomic analyses of this stage of disease.  This talk will describe advances in whole-exome sequencing from single cells and circulating tumor DNA and computational analysis for detecting somatic mutations, indels, and copy number alterations. These methods may complement tumor biopsies for both translational studies and precision medicine.   

4:20 Single-Cell Analysis Reveals Enriched EMT Pathway in Castration Resistant Prostate Cancer and CTCs Affected by Enzalutamide and Abiraterone

Chun-Liang Chen, Ph.D., Assistant Professor, Molecular Medicine, University of Texas Health Science Center at San Antonio

Single cell qRT-PCR and RNA sequencing show that epithelial-to-mesenchymal transition (EMT) gene expression is unregulated in castration resistant prostate cancer cells and circulating tumor cells. We explored the effects of emalutaminde and arbiraterone on EMT molecular profiling and aggressive behaviors of castration resistant cancer cells. The data are consistent with our previous study of EMT expression in circulating tumor cells indicating that high EMT gene expression is a biomarker for castration resistance and a potential therapeutic target. 

5:05 Refreshment Break in the Exhibit Hall with Poster Viewing

5:40 Cancer Mutations of the SMARCA4 ATPase Domain Lead to Altered Polycomb Activity

Benjamin Stanton, Ph.D., Research Associate, Laboratory of Dr. Gerald Crabtree, Stanford University School of Medicine and Howard Hughes Medical Institute; Laboratory of Dr. Keji Zhao, Laboratory of Epigenome Biology, NHLBI, National Institutes of Health

Genetic alterations of the subunits of the mammalian SWI/SNF (mSWI/SNF or BAF) complex contribute to a wide range of human cancers. We sought to examine defects of Brg (SMARCA4), where mutations observed in cancer cluster at highly conserved regions. We characterized many interesting downstream effects of mSWI/SNF ATPase mutations, including alterations in Polycomb activity.

6:10 Untangling Bad Wiring: Using CRISPR/Cas9 to Understand Lymphoma

Arthur L. Shaffer, III, Ph.D., Staff Scientist, Laboratory of Dr. Louis Staudt, Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health

CRISPR/Cas9 technology is a powerful tool that permits the easy exploration of human genetics using cell line models. Our lab focuses on understanding the wiring of lymphoma cells in an effort to discover essential signaling pathways, leading to new therapeutic options. I will relate some of our recent successes with CRISPR/Cas9 in the study of lymphoma.

6:40 End of Day

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Thursday, September 22

7:30 am Registration Open and Morning Coffee


8:30 Chairperson’s Remarks

Jeff MacKeigan, Ph.D., Associate Professor, Innovation and Integration Program, Center for Cancer and Cell Biology, Van Andel Research Institute

8:45 Therapeutic Targets and the Genomic Landscape in a Rare Pediatric Tumor Syndrome

Jeff MacKeigan, Ph.D., Associate Professor, Innovation and Integration Program, Center for Cancer and Cell Biology, Van Andel Research Institute

Tuberous sclerosis complex (TSC) is a rare disease, characterized by mutations in TSC1 or TSC2, two tumor suppressor genes located in the mTOR pathway. Often diagnosed during childhood, the disease causes benign tumors in major organs including the brain, kidneys, skin, and heart. We will present our latest data on new and existing therapeutic targets along with the genomic landscape of this disease.

9:15 Optimized Synthetic Lethal Screening Approaches for Drug Target Discovery

Benjamin Housden, Ph.D., Post-Doctoral Fellow, Laboratory of Dr. Norbert Perrimon, Department of Genetics, Harvard Medical School

Synthetic lethal screens represent a promising approach to identify candidate drug targets for tumorigenic diseases. However, detection of robust synthetic lethal interactions has proved challenging with existing screening methods. We have developed an optimized approach combining CRISPR and RNAi in cross-species screens. I will describe these new methods and their application to identify candidate drug targets for TSC deficient tumors.

9:45 Super Enhancing Precision Medicine by Integrating Genomic, Epigenetic and Functional Screen Data

Berkley E. Gryder, Ph.D., Research Scientist, Laboratory of Dr. Javed Khan, Genetics Branch, National Cancer Institute, National Institutes of Health

Precision medicine hopes to succeed in treating diseases individually by leveraging patient-specific genomics and targeted therapy, but most cancers lack highly recurrent and therapeutically actionable protein-coding alterations. Studying childhood cancers, we show that despite genomic heterogeneity, epigenetic landscapes are highly consistent among patients. Translating epigenetic knowledge into biological vulnerabilities, by overlaying high-throughput drug and functional genomics datasets, is promising new avenues of therapy which are being pursued.

10:15 Coffee Break in the Exhibit Hall with Poster Viewing and Poster Competition Winner Announced

11:10 Using Data Visualization for Discovery and Subtype Characterization

Nils Gehlenborg, Ph.D., Assistant Professor, Department of Biomedical Informatics, Harvard Medical School

Studies like The Cancer Genome Atlas are providing the biomedical community with multidimensional datasets that offer a comprehensive view on cancer. I will present visualization approaches that enable researchers to gain deeper insights into populations of cancer patients by integrating multiple such datasets and multiple visualizations within a single user interface. I will also show how algorithmic analysis can efficiently be linked with visual analysis.

11:55 Associating Tumor Phenotype with Genomics across Biological Scale

Arvind Rao, Ph.D., Assistant Professor, Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center

With the availability of large public repositories of cancer genomics and phenotype (pathology, radiology) data, there is an unprecedented opportunity to link cancer-induced phenotype with cancer genomic data. This permits the inference of the phenotypic basis of cancer, in terms of the molecular characteristics of the disease. In this talk, we’ll focus on methods and results intended to understand the genomic-phenomic confluence, using Gliomas as a case study.

12:40 Lunch on Your Own

1:30 Refreshment Break in the Exhibit Hall with Poster Viewing


2:15 Chairperson’s Remarks

Roderick Beijersbergen, Ph.D., Group Leader, Netherlands Cancer Institute and Head, NKI Robotics and Screening Center

2:20 Large-Scale CRISPR Screens for Discovery of Genotype Specific Combination Therapies

Roderick Beijersbergen, Ph.D., Group Leader, Netherlands Cancer Institute and Head, NKI Robotics and Screening Center

The complexity and heterogeneity of cancer, the extensive crosstalk between pathways and unanticipated feedback control are underlying the limited long-term success of targeted therapeutics in the clinic. We use large-scale functional genomic screening technologies including shRNA/CRISPR-based gene editing in combination with (clinically) relevant screening models for the identification of dependencies in the context of specific genetic alterations. Using this platform we have identified novel effective drug combinations that are currently in the clinic.

2:50 GPCR-Mediated cAMP as an Immune Checkpoint in Cancer Identified by RNAi Screening

Tillmann Michels, Head of Research Group, Immune Checkpoint Inhibitors, Department of Interventional Immunology, Regensburg Center for Interventional Immunology; Member, Department of Translational Immunology, German Cancer Research Center

Immune checkpoint blockade has revolutionized cancer therapy. Our group screened several tumor entities in conjunction with tumor-infiltrating lymphocytes (TILs) for novel immune modulators. We found that many immune checkpoints are tumor-restricted but the underlying mechanisms are shared between tumor entities. These mechanisms range from inhibition of TIL-mediated apoptosis to cAMP-mediated inhibition of TILs.

3:20 Session Break

3:30 CRISPR-Based Mutagenesis Approach for Cancer Drug Target Identification

Junwei Shi, Ph.D., Assistant Professor, Department of Cancer Biology, University of Pennsylvania School of Medicine

CRISPR-Cas9 genome editing technology provides high-throughput genetic knockout screening strategies for cancer therapeutic target identification. We recently reported a domain-focused CRISPR screening approach to nominate protein domains that would sustain cancer cell growth and are suitable for drug targeting. Here, I will present an optimized CRISPR system, which could achieve robust genome editing efficiency in a broad variety of human cancer cell lines.

4:00 Applying Functional Genomics in Mouse Models of Human Cancer

Yejing Ge, Ph.D., Postdoctoral Fellow, Laboratory of Dr. Elaine Fuchs, Department of Mammalian Cell Biology and Development, Rockefeller University

Using skin as paradigm, we describe the first panoramic view of microRNAs during the development, homeostasis and malignant transformation of skin epithelium. We devised lentiviral microRNAs expression platform and conducted pooled in vivo functional screens for oncomiRs in mice. Empowered by mouse genetics and high throughput approaches, we unveiled a rich set of putative microRNAs that drive skin malignancy, and their oncogenic targets.

4:30 A CRISPR/Cas9 System to Increase Homologous Recombination Repair

Ciro Bonetti, Ph.D., Postdoctoral Scientist, Laboratory of Dr. Andrea Ventura, Memorial Sloan-Kettering Cancer Center

CRISPR/Cas9 genome editing technology has been shown to be very effective to perform inactivation or activation of specific genes. However, engineering precise genomic modifications remains a challenge due to the low efficiency of repair of the double strand breaks through the homologous recombination pathway. Here, I will discuss a novel method to skew the repair away from non-homologous end-joining towards homologous repair pathway.

5:00 Close of Conference

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