Scientific Program

Conference Series LLC Ltd invites all the participants across the globe to attend 11th International Conference on Genomics and Pharmacogenomics Philadelphia, Pennsylvania, USA.

Day 1 :

Keynote Forum

Dr.Henry M. Sobell

University of Rochester, USA

Keynote: The centers of premeltons signal the beginning and ends of genes
Genome 2018 International Conference Keynote Speaker Dr.Henry M. Sobell photo
Biography:

Henry M. Sobell completed his studies at Brooklyn Technical High School (1948-1952), Columbia College (1952-1956), and the University of Virginia School of Medicine (1956-1960).  Instead of practicing clinical medicine, he then went to the Massachusetts Institute of Technology (MIT) to join Professor Alexander Rich in the Department of Biology (1960-1965), where, as a Helen Hay Whitney Postdoctoral Fellow, he learned the technique of single crystal X-ray analysis.  He then joined the Chemistry Department at the University of Rochester, having been subsequently jointly appointed to both the Chemistry and Molecular Biophysics departments (the latter at the University of Rochester School of Medicine and Dentistry), becoming a full tenured Professor in both departments (1965-1993). He is now retired and living in the Adirondacks in New York, USA

Abstract:

Premeltons are examples of emergent structures (i.e., structural solitons) that  arise  spontaneously in  DNA  due  to  the  presence  of  nonlinear excitations  in  its  structure.   They  are   of  two  kinds:  B-B  (or   A-A) premeltons form at specific DNA-regions to nucleate site-specific DNA melting.   These are stationary and, being globally nontopological, undergo breather motions that allow drugs and dyes to intercalate into DNA.    B-A (or  A-B) premeltons, on the other hand, are  mobile, and being  globally  topological,  act as  phase-boundaries  transforming B- into  A-  DNA  during  the  structural  phase-transition.    They  are   not expected to undergo breather-motions.  A key feature of both types of premeltons is  the presence of an intermediate structural-form   in their central regions (proposed as being a  transition-state intermediate in DNA-melting and in the B- to A- transition), which differs from either A- or B- DNA. Called beta-DNA, this is both metastable and hyperflexible– and contains an alternating sugar-puckering pattern  along the polymer-backbone combined with the partial-unstacking (in  its  lower energy-forms) of every  other base-pair.   Beta-DNA is  connected to either  B-  or  to A-  DNA  on either  side  by  boundaries  possessing  a gradation  of nonlinear  structural-change,  these being  called  the kink and the antikink regions.   The presence of premeltons in DNA leads to a  unifying theory to understand much of DNA physical-chemistry  and molecular-biology.   In  particular,  premeltons  are  predicted  to define the  5’  and  3’  ends  of  genes  in  naked-DNA   and  DNA  in  active- chromatin,  this having important implications for understanding physical aspects of the initiation, elongation and  termination of RNA-synthesis during transcription.   For these and other reasons, the model will be of broader  interest to the general audience  working in these areas.   The model explains a wide variety of data,  and carries within it a number of  experimental  predictions  –  all  readily  testable  –  as  will   be described in my talk.

Keynote Forum

Dr. David I Smith

Department of Laboratory Medicine and Pathology,Mayo Clinic,USA

Keynote: Whole Genome Sequencing As A Valuable Clinical Tool For the Management of Cancer Patients
Genome 2018 International Conference Keynote Speaker Dr. David I Smith photo
Biography:

David I Smith is the Chairman of the Technology Assessment Group for the Mayo Clinic Center for Individualized Medicine. He is an expert of advanced DNA sequencing methodologies and how to use these to study the molecular alterations that occur during cancer development. His research focuses on the different roles that human papillomavirus plays in the development of different cancers. His group also studies genome instability during cancer development and the role that the common fragile sites plays in this.

Abstract:

Advances in DNA sequencing, based upon massively parallel sequencing, has resulted in dramatic advances in DNA sequence output in the past few years. It is now possible to generate terrabases of accurate DNA sequence with a single run on several DNA sequencing platforms. This has then made it possible to characterize alterations that occur during cancer development. Genomic alterations can be characterized by targeted sequencing of genes that are frequently altered during cancer development, by sequencing of the entire exome, transcriptome sequencing, and even by whole genome sequencing. Each of these has their own inherent strengths and weaknesses. I will describe why I believe that the best strategy moving forward for the management of cancer patients is whole genome sequencing (WGS). This can currently be done reliably and inexpensively on two completing platforms. The first is the Illumina sequencing platform and the second is from BGI. WGS is a comprehensive technology that can detect all the alterations in a cancer genome and I will describe how and why this may prove to be the best approach for the management of cancer patients.

Keynote Forum

Prof.Xiaoliang Sunney Xie

Director, Beijing Advanced Innovation Center for Genomics, China and Professor of Chemistry and Chemical Biology Harvard University , USA

Keynote: Single Cell Genomics: When Stochasticity Meets Precision
Genome 2018 International Conference Keynote Speaker Prof.Xiaoliang Sunney Xie photo
Biography:

Xie received his B.S. from Peking University (1984), Ph.D. from UCSD (1990) and became a tenured Professor of Chemistry at Harvard University in 1999. Currently he is the Mallinckrodt Professor of Chemistry and Chemical Biology at Harvard, the Director of Beijing Advanced Innovation Center for Genomics (ICG), and the Director of Biodynamics Optical Imaging Center (BIOPIC), both at Peking University.

Xie is a founder of single-molecule biophysical chemistry and its applications to biology and medicine. He also pioneered coherent Raman scattering microscopy and single cell genomics.  Among his many honors is the Albany Prize in Medicine and Biomedical Research. He is a fellow of American Academy of Arts and Sciences, a member of the National Academy of Sciences, and a member of National Academy of Medicine. 

 

Abstract:

 

DNA exists as single molecules in individual cells. Consequently, genomic variations such as copy-number    variations    (CNVs)    and   single nucleotide variations (SNVs) in a single-cell occur in a stochastic way, necessitating single-cell and single-molecule measurements to be identified. However, existing single-cell   whole   genome amplification (WGA) methods are limited by low accuracy  of  CNV  and  SNV  detection.  We  have developed     transposase based     methods    for singlecell     WGA,     which     have     superseded previous  methods. With  the  improved  genome coverage of our new WGA method, we have also developed       a       high-resolution       single-cell chromatin conformation capture method, which allows for the first 3D genome map of a human diploid cell.

Gene  expression  is  also  stochastic  due  to the fact that the DNA exists as single-molecules in   individual   cells.   The   correlations  among different   mRNAs   in   a   single-cell   are   masked within the stochastic gene expression noise. We have    developed    a    method for singlecell transcriptome       with       improved       detection efficiency    and    accuracy,    revealing    intrinsic correlations  among  all  detected  mRNAs  in  a single-cell. For a particular human cell type, we uncovered    ~120    transcriptionally    correlated modules (TCMs) from the gene expression data of  ~700  individual  cells  under  a  steady  state condition. We found that the TCMs are cell type dependent.

 

Genome 2018 International Conference Keynote Speaker M. Eileen Dolan photo
Biography:

M. Eileen Dolan’s lab is focused on improving the quality of life of cancer patients through the identification of genetic variants associated with risk for severe and persistent toxicities following chemotherapy (i.e. peripheral neuropathy, ototoxicity, tinnitus), particularly in children and young adults whose adverse sequelae could persist throughout their lifetimes. To this end, they perform clinical genome wide association studies (GWAS) to identify genetic variants associated with toxicity in patients following chemotherapy. In addition, they develop preclinical models to elucidate the biochemical and cellular impact of genes identified in clinical GWAS studies of chemotherapeutic toxicity. More recently, her laboratory has developed an induced pluripotent stem cell derived neuronal cell model to evaluate genes contributing to chemotherapeutic-induced neuropathy, a common adverse event of multiple chemotherapeutic agents. Using patient derived induced pluripotent stem cells, they are developing models that will have broad applicability for gaining insight on druggable targets to treat or prevent this devastating side effect of chemotherapy.

Abstract:

Statement of the Problem: There are now over 28 million cancer survivors worldwide, and as a result, there is a heightened awareness of the long-term toxicities resulting from treatment and their impact on quality of life. Understanding the role of germline genetic factors in the development of cancer treatment-related toxicities is critical for the identification of patients at risk as well as for the development of drugs to treat or prevent these toxicities. The purpose of this presentation is to review current understanding of genetic susceptibility to adverse outcomes among cancer survivors following chemotherapy with a particular focus on genome wide association studies (GWAS). Few of the findings from earlier narrowly focused candidate gene studies have been replicated in independent populations. A major strength of genome-wide approaches is that they do not require a priori assumptions about the genes or pathways involved in the pharmacologic trait. The challenges include the need for large cohorts of patients with homogeneous treatment exposures and systematic evaluation of well-defined outcomes as well as replication in independent study populations. Persistent calls to incorporate ancestrally diverse populations into genomic efforts resulted in a recent rise in the number of studies utilizing cohorts of East Asian descent; however, few pharmacogenomic studies to date include cohorts of African, Native American and admixed populations. These disparities could contribute to the widening gaps in health outcomes. In addition to discussing an overview of this approach, the presentation will pay particular attention to recent studies identifying genetic variants associated with chemotherapy-induced peripheral neuropathy and ototoxicity (hearing loss and tinnitus). Conclusion & Significance: Genetic associations hold tremendous promise for more precisely identifying patients at highest risk for developing adverse treatment effects and potential identification of targets for prevention or treatment of the long term toxicities associated with chemotherapy.