Welcome to the Translational Research in Mitochondria, Aging, and Disease (TRiMAD) Symposium 2016 hosted by the Center for Mitochondrial and Epigenomic Medicine (CMEM) at the Children’s Hospital of Philadelphia (CHOP) and the University of Pennsylvania (Penn). The TRiMAD Symposia are dedicated to the elucidation of the biology and biophysics of the mitochondrion and the role of the human mitochondrion in health and disease.
We have an extraordinary array of speakers for this year’s symposium with interests encompassing Mitochondrial and Quantitative Biology; Mitochondrial Quality Control; Mitochondria and Metabolism; Mitochondrial-Nuclear Interactions; Mitochondrial Pathology and Critical Care; and Mitochondrial Physiological Regulation. Keynote speakers will include Shoukhrat Mitalipov, PhD, Director of the Center for Embryonic Cell and Gene Therapy at the Oregon Health & Science University, speaking on nuclear transplantation under the title, “Germline and Somatic mtDNA Mutations” and Chi Van Dang, MD, PhD, Director of the Penn Cancer Center, speaking on “MYC, Mitochondria, and Cancer Therapy.”
The human eukaryotic cell arose through a symbiotic collaboration of two co-equal microorganisms in the order of two billion years ago. These two organisms progressively became specialized, one specializing in structure and giving rise to the nucleus-cytosol and the other specializing in energy and giving rise to the numerous cellular mitochondria. While enormous resources have been invested in studying the structure and function of the nucleus and nuclear DNA in hopes of understanding the causes and developing cures for the common “complex” diseases (degenerative, metabolic, autoimmune and inflammatory diseases, cancer and aging), the results have been disappointing. Something important has been missed. This symposium will indicate that a major missed factor is the other human cell, the mitochondrion.
The mitochondria are the metabolic environmental sensors utilizing the energy of our food and the oxygen that we breathe to meet the myriad of energy demands including for activity, thermal regulation, reproduction, and to counteract infection and trauma. Moreover, the nucleus-cytosol cannot function without energy, so the nucleus-cytosol is linked to mitochondrial energy production through the cytosolic signal transduction and epigenomic systems.
It is little wonder then, that investigators from a broad range of biomedical disciplines are now “discovering” the mitochondrion. Indeed, the number of medically related publications involving the mitochondrion continues to rise while those related to the nucleus decline. As a result, the annual output of mitochondrial publications now outnumbers nuclear publications (Figure 1).
Figure 1: Normalized proportions of published Medline-indexed medical articles from 1980 to January 1, 2016, related to mitochondria, nucleus, endoplasmic reticulum (ER) and Golgi apparatus. From Picard, Wallace, and Burelle (2016) The Rise of Mitochondria in Medicine. Mitochondrion Jul 13. pii: S1567-7249(16)30098-8.
Because of the enormous medical implications of the mitochondrion, our symposium will have two concurrent sessions. One will pertain to the exciting new discoveries and insights in medicine that are being obtained by focusing on the mitochondrion. The other will focus on the direct clinical issues associated with mitochondrial diseases. This session is co-sponsored by the CHOP Mitochondrial Medicine Program and United Mitochondrial Disease Foundation (UMDF). Physicians and families are welcome.
We hope to see you in Philadelphia to join us in the rediscovery of the mitochondrion. We promise intellectual discourse and fellowship, and anticipate fostering new ideas, friendships, and collaborations.
Douglas C. Wallace, PhD
The symposium is being hosted by The Children’s Hospital of Philadelphia Research Institute and is a collaboration between the University of Pittsburgh Cancer Institute, Penn State University and the University of Pennsylvania Perelman School of Medicine.
Program Director: Douglas C. Wallace, PhD
Organizing Committee: Douglas C. Wallace, PhD; Ameena Al-Amin; Deborah Murdock, PhD; Xilma Ortiz-Gonzalez, MD, PhD; Liming Pei, PhD; Cheri Seifert; Larry Singh, PhD; and Marc Vermulst, PhD
Shoukhrat Mitalipov, PhD, Director of the Oregon Health & Science University Center for Embryonic Cell and Gene Therapy
Shoukhrat Mitalipov is Director of the newly formed Center for Embryonic Cell and Gene Therapy of Oregon Health & Science University (OHSU). He is also a Senior Scientist in the Division of Reproductive & Developmental Sciences at Oregon National Primate Research Center, OHSU. Dr. Mitalipov earned his PhD degree in Developmental & Stem Cell Biology from Research Center for Medical Genetics in Moscow, Russia. He came to Utah State University in 1995 to conduct his postdoctoral research in stem cell and developmental biology and moved to OHSU in 1998.
Dr. Mitalipov’s research interest is to understand the mechanisms of cytoplasmic control of nuclear genome identity and reprogramming of somatic cells to the totipotent and pluripotent states. Another objective is to develop novel germline gene therapy approaches for the treatment of inherited human diseases. Dr. Mitalipov is known for his leading discoveries in producing human patient-matched embryonic stem cells using somatic cell nuclear transfer. His team has also pioneered a gene therapy approach that prevents transmission of genetic defects in mitochondrial genes from mothers to their children.
Chi Van Dang, MD, PhD, Professor & Director, Abramson Cancer Center, the Perelman School of Medicine at the University of Pennsylvania Health System
Chi Van Dang is Professor and Director of the Abramson Cancer Center of the University of Pennsylvania. He is a member of the National Academy of Medicine, American Academy of Arts & Sciences, American Society for Clinical Investigation and The Association of American Physicians. He is chair of the NCI Board of Scientific Advisors and serves on the editorial boards of Cancer & Metabolism, Cancer Research, eLIFE, Genes & Cancer, MCB, Neoplasia, and Oncotarget. He identified the function of the MYC oncogene, which is expressed highly in many human cancers, by defining the functional domains of the MYC transcription factor and its target genes. His lab documented that MYC binds broadly to the genome, and induces genes involved in glycolysis, glutaminolysis, mitochondrial and ribosome biogenesis, and cell cycle progression. He established the first mechanistic link between an oncogene, MYC, and cellular metabolism and linked MYC to the circadian clock, contributing to the concept that genetic alterations in cancers re-program fuel utilization by tumors. His laboratory is now exploiting these concepts for therapeutic targeting of cancer metabolism in cancers.