Day 1 :
National Institutes of Health, United States
Time : 9:30 AM - 10:15 AM
Mukesh Verma is a Program Director and Chief in the Methods and Technologies Branch (MTB), Epidemiology and Genomics Research Program (EGRP) of the Division of Cancer Control and Population Sciences (DCCPS) at the National Cancer Institute (NCI), National Institutes of Health (NIH) with expertise in implication of epigenome, microbiome, metabolome and genomic information for risk assessment and understanding disease etiology. He has received MSc from Pantnagar University and PhD from Banaras Hindu University, India. He did his Postdoctoral research at George Washington University and was a Faculty Member at Georgetown University Medical Center. He was a Program Director in the Division of Cancer Prevention (DCP), NCI, providing direction in the areas of biomarkers, early detection, risk assessment and prevention of cancer, epigenetics, epidemiology and cancers associated with infectious agents. He has published 161 research articles and reviews and edited fi ve books in cancer biomarkers, epigenetics and epidemiology field.
Several approaches are applied to identify risk of developing cancer in diff erent ethnic and racial groups. One of the approaches is epigenetics that facilitates cancer control throughout the cancer core continuum. To understand current progress and trends in the inclusion of epigenetics in cancer epidemiology, we evaluated the published literature and the National Cancer Institute (NCI) supported research grant awards in this fi eld to identify trends in epigenetics research. We present a summary of the epidemiological studies in NCI’s grant portfolio (from January 2005 through December 2012) and in the scientifi c literature published during the same period, irrespective of support from NCI. NCI supported RPGs related to epigenetic epidemiology funded from January 01, 2005 to December 31, 2012 were included in the portfolio analysis. Th e portfolio was analyzed using NCI’s Portfolio Management Application soft ware version 13.4. Th e criteria for inclusion of a project in the analysis were as follows: (1) Th e focus of the project is cancer, (2) study involves human subjects, (3) focus of at least one of the specifi c aims in the project is cancer epigenetics, and (4) has at least 100 cases and 100 controls. Th e initial analysis identifi ed 84 RPGs. A manual analysis applying the above criteria eliminated 21 RPGs leaving 63 for further analysis. Biomarkers identifi ed in the analysis might be useful in risk prediction of diff erent cancers. Breast cancer was the most frequently studied cancer type in grants and publications. Blood cells and tumor tissue were the most commonly used biospecimens in these studies, although buccal cells, cervical cells, sputum and stool samples also were used. DNA methylation profi ling was the focus of the majority of studies, but several studies also measured microRNA profi les. We illustrate here the current status of epidemiologic studies that are evaluating epigenetic changes in large populations. Some research needs include developing improved strategies for epigenetic data analysis and interpretation; determining the stability of epigenetic marks in repeated biospecimen samples from the same people over time and studies that examine the relationship between epigenetic marks in germline DNA and tumor DNA. While there are limitations to the broad application of epigenomics to epidemiology research, there are situations where this type of research is appropriate and it should be considered.
University of New South Wales, Australia
Time : 11:15 AM - 12:00 PM
Jenny Wang is the Head of the Cancer and Stem Cell Laboratory at the University of New South Wales, Sydney, Australia. She had worked in Children’s Hospital Boston, Harvard Medical School, while doing Postdoctoral Research in Leukemia Stem Cell Biology. Her researches mainly focuses on to develop novel therapeutic strategies specifi cally targeting leukemia stem cells that are often resistant to commonly used cancer therapies and that are now believed to be the engine driving the growth of a tumor and the major cause for treatment failure and relapse in leukemia.
Acute myeloid leukemia (AML) remains a signifi cant challenge for oncologists, with a 5-year survival rate of only 27% and a standard treatment that has not changed meaningfully in the past 3 decades. Current treatments are largely ineff ective as they do not kill quiescent leukemia stem cells (LSCs) and resistant LSCs will survive to regenerate additional leukemic cells through their self-renewal capacity. Targeting self-renewal pathways that drive LSC development is essential for curative therapy. Oncogenic events including genetic, epigenetic and metabolic abnormalities enable LSCs to hijack normal stem cell of self-renewal mechanisms that allow LSCs to evade therapy and regenerate new leukemia, leading to relapse. Targeted disruption of abnormal stem cell self-renewal represents a novel therapeutic strategy that could signifi cantly reduce the capacity of a tumor to regenerate itself aft er treatment and has become a new focus for drug development in poor prognosis AML.
University of Southern California, USA
Keynote: Biomarkers of a stem cell melanoma
Time : 10:15 AM - 11:00 AM
Suraiya Rasheed is a Professor and Director of Viral Oncology and Proteomics Laboratory in the Department of Pathology at the Keck School of Medicine, University of Southern California, Los Angeles, USA. She has graduated with honors and received her fi rst PhD from Osmania University, Hyderabad, India and second PhD from London University and FRCPath from the Royal College of Pathology, London. She has also served numerous national and international Advisory Committees including Study Sections of the National Cancer Institute, National Institute of Allergy and Infectious Diseases, Antiviral Drug Development and Drug- Screening Programs for AIDS and Abstract Reviewing Committee for the International AIDS Society’s conferences.
Melanomas are a group of heterogeneous tumors that arise in the epithelial cells of the skin, eye, meninges and other parts of the body. Patients with highly malignant melanomas do not respond well to the conventional therapies because most of these tumors are detected aft er they have invaded multiple tissues. For a number of years, we have studied a highly malignant cat melanoma cell line (CT1413) and examined its genome-wide proteomes at diff erent stages of tumor growth by mass spectrometry. Subtractive proteomics analyses and comparisons of protein profi les of tumor cells with normal cat embryo fi broblasts and a human leukemia cells indicated that CT1413 had a unique profi le, which did not match any other cells. Extensive bioinformatics analysis of all proteins indicated that >95% of proteins expressed in this melanoma are similar to proteins that are normally expressed during the growth and development of mammalian embryos. Proteomics analyses of several single cell clones of the cat melanoma indicated that this is a clonal tumor which is most likely derived from a single embryonic stem cell that transformed into tumor cell due to abnormal cell signaling events during the embryonic development. Each of the clones tested in multiple experiments conducted over one year period exhibited embryonic proteins. Th is phenomenon is in contrast to many human cancer stem cells that are diff erent areas of the tumor mass and exhibit only a few stem cell markers. Our bioinformatics analyses have identifi ed proteins/enzymes and transcriptional regulators that are essential for diff erentiation of diff erent tissue types/organ systems, development of neural network in the brain and proteins that regulate self-renewal and maintain stemness in these tumor cells. Th ese proteins provide unique biomarkers for the early detection of malignant melanomas and/or as targets for the development of novel therapeutic strategies for treating stem-cellderived melanomas.