Rudolf Jaenisch
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Beatrice Mintz Date of Birth 24 January 1921 Place New York, NY (USA) Nomination 9 June 1986 Field Genetics Title Jack Schultz Chair in Basic Science
Beatrice Mintz Date of Birth 24 January 1921 Place New York, NY (USA) Nomination 9 June 1986 Field Genetics Title Jack Schultz Chair in Basic Science Professional address The Institute for Cancer Research Fox Chase Cancer Center 7701 Burholme Avenue, Room 215 Philadelphia, PA 19111 (USA) Most important awards, prizes and academies Awards: Bertner Foundation Award in Fundamental Cancer Research (1977); New York Academy of Sciences Award in Biological and Medical Sciences (1979); Papanicolaou Award for Scientific Achievement (1979); Lewis S. Rosenstiel Award in Basic Medical Research (1980); Genetics Society of America Medal (1981); Ernst Jung Gold Medal for Medicine (1990); John Scott Award for Scientific Achievement (1994); March of Dimes Prize in Developmental Biology (1996); American Cancer Society National Medal of Honor for Basic Research (1997); Pearl Meister Greengard Prize (2008); Albert Szent-Györgyi Prize for Progress in Cancer Research (2011). Academies: National Academy of Sciences (1973); Fellow, American Association for the Advancement of Science (1976); Honorary Fellow, American Gynecological and Obstetrical Society (1980); American Philosophical Society (1982); Fellow, American Academy of Arts and Sciences (1982); Pontifical Academy of Sciences (1986). Degrees: Doctor of Science, New York Medical College (1980); Medical College of Pennsylvania (1980); Northwestern University (1982); Hunter College (1986); Doctor of Humane Letters, Holy Family College (1988). Summary of scientific research Beatrice Mintz discovered the underlying relationship between development and cancer. She first showed that development is based on an orderly hierarchical succession of increasingly specialized small groups of precursor or "stem" cells, expanding clonally. She proposed that cancer involves a regulatory aberration in this process, especially in the balance between proliferation and differentiation. -
Therapeutic Cloning Gives Silenced Genes a Second Voice
NEWS p1007 Tricky Fix: p1009 Bohemian p1010 Better than A vaccine for cocaine brain: Neuroscientist Prozac: What’s next in addiction poses John Hardy bucks antidepressant drug ethical dilemmas. the trends. development? Therapeutic cloning gives silenced genes a second voice As controversy continues on therapeutic experiments in Xenopus embryos, is the removal silencing may not be permanent.” cloning to create human embryos, applying the of methyl groups from specific regions of DNA. Jaenisch and his colleagues have also shown technique—also known as somatic cell nuclear This may be a necessary step in the epigenetic that nuclei from a skin cancer cell can be repro- transfer—in animals is generating important reprogramming of the nucleus, the researchers grammed to direct normal development of a insights into disease development. suggest in the October Nature Cell Biology. mouse embryo—meaning that removal of the Some scientists are using the approach to As cells differentiate, they accrue many epigenetic alterations is enough to restore cells study epigenetic alterations—chromosomal other types of epigenetic alterations, such as to normal (Genes Dev.18,1875–1885; 2004).An modifications that do not alter the DNA the addition of phosphates or removal of earlier study reported similar results with brain sequence—which can cause cancer. “A acetyl groups from histones, or chromosomal tumor cells (Cancer Res. 63, 2733–2736; 2003). principal question in cancer research is what proteins, and trigger changes in chromatin Based on such findings, pharmaceutical part of the cancer cell phenotype comes from structure. Defects in these processes have been companies are racing to develop and test ‘epige- genetic defects and what part is epigenetic,”says linked to cancer and other diseases. -
Liberal Arts Science $600 Million in Support of Undergraduate Science Education
Janelia Update |||| Roger Tsien |||| Ask a Scientist SUMMER 2004 www.hhmi.org/bulletin LIBERAL ARTS SCIENCE In science and teaching— and preparing future investigators—liberal arts colleges earn an A+. C O N T E N T S Summer 2004 || Volume 17 Number 2 FEATURES 22 10 10 A Wellspring of Scientists [COVER STORY] When it comes to producing science Ph.D.s, liberal arts colleges are at the head of the class. By Christopher Connell 22 Cells Aglow Combining aesthetics with shrewd science, Roger Tsien found a bet- ter way to look at cells—and helped to revolutionize several scientif-ic disciplines. By Diana Steele 28 Night Science Like to take risks and tackle intractable problems? As construction motors on at Janelia Farm, the call is out for venturesome scientists with big research ideas. By Mary Beth Gardiner DEPARTMENTS 02 I N S T I T U T E N E W S HHMI Announces New 34 Investigator Competition | Undergraduate Science: $50 Million in New Grants 03 PRESIDENT’S LETTER The Scientific Apprenticeship U P F R O N T 04 New Discoveries Propel Stem Cell Research 06 Sleeper’s Hold on Science 08 Ask a Scientist 27 I N T E R V I E W Toward Détente on Stem Cell Research 33 G R A N T S Extending hhmi’s Global Outreach | Institute Awards Two Grants for Science Education Programs 34 INSTITUTE NEWS Bye-Bye Bio 101 NEWS & NOTES 36 Saving the Children 37 Six Antigens at a Time 38 The Emergence of Resistance 40 39 Hidden Potential 39 Remembering Santiago 40 Models and Mentors 41 Tracking the Transgenic Fly 42 Conduct Beyond Reproach 43 The 1918 Flu: Case Solved 44 HHMI LAB BOOK 46 N O T A B E N E 49 INSIDE HHMI Dollars and Sense ON THE COVER: Nancy H. -
Changes in Expression of Putative Antigens Encoded by Pigment
Proc. Natl. Acad. Sci. USA Vol. 92, pp. 10152-10156, October 1995 Medical Sciences Changes in expression of putative antigens encoded by pigment genes in mouse melanomas at different stages of malignant progression (albino locus/brown locus/slaty locus/silver locus) SETH J. ORLOW*, VINCENT J. HEARINGt, CHIE SAKAIt, KAZUNORI URABEt, BAO-KANG ZHOU*, WILLYS K. SILVERSt, AND BEATRICE MINTZO§ *Ronald 0. Perelman Department of Dermatology and Department of Cell Biology, New York University School of Medicine, New York, NY 10016; tLaboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; and tInstitute for Cancer Research, Fox Chase Cancer Center, Philadelphia, PA 19111 Contributed by Beatrice Mintz, July 25, 1995 ABSTRACT Cutaneous melanomas of Tyr-SV40E trans- This problem might be overcome by identifying changes in genic mice (mice whose transgene consists of the tyrosinase the antigenic profile associated with melanoma progression promotor fused to the coding regions of simian virus 40 early such that the design of a treatment protocol could encompass genes) strikingly resemble human melanomas in their devel- all the melanoma cells. Such a characterization in the case of opment and progression. Unlike human melanomas, the human melanoma would be complicated by genetic differences mouse tumors all arise in genetically identical individuals, among individuals, especially as the genetic background, as thereby better enabling expression of specific genes to be well as allelic differences at pigment gene loci themselves, can characterized in relation to advancing malignancy. The prod- influence the expression and interactions of these genes (11, ucts of pigment genes are of particular interest because 12). -
About Whitehead Institute for Biomedical Research Selected
About Whitehead Institute for Biomedical Research Selected Achievements in FOUNDING VISION Biomedical Science Whitehead Institute is a nonprofit, independent biomedical research institute with pioneering programs in cancer research, developmental biology, genetics, and Isolated the first tumor suppressor genomics. It was founded in 1982 through the generosity of Edwin C. "Jack" Whitehead, gene, the retinoblastoma gene, and a businessman and philanthropist who sought to create a new type of research created the first genetically defined institution, one that would exist outside the boundaries of a traditional academic human cancer cells. (Weinberg) institution, and yet, through a teaching affiliation with the Massachusetts Institute of Technology (MIT), offer all the intellectual, collegial, and scientific benefits of a leading Isolated key genes involved in diabetes, research university. hypertension, leukemia, and obesity. (Lodish) WHITEHEAD INSTITUTE TODAY True to its founding vision, the Institute gives outstanding investigators broad freedom Mapped and cloned the male- to pursue new ideas, encourages novel collaborations among investigators, and determining Y chromosome, revealing a accelerates the path of scientific discovery. Research at Whitehead Institute is unique self-repair mechanism. (Page) conducted by 22 principal investigators (Members and Fellows) and approximately 300 visiting scientists, postdoctoral fellows, graduate students, and undergraduate Developed a method for genetically students from around the world. Whitehead Institute is affiliated with MIT in its engineering salt- and drought-tolerant teaching activities but wholly responsible for its own research programs, governance, plants. (Fink) and finance. Developed the first comprehensive cellular LEADERSHIP network describing how the yeast Whitehead Institute is guided by a distinguished Board of Directors, chaired by Sarah genome produces life. -
Rudolf Jaenisch
Rudolf Jaenisch CURRICULUM VITAE Date of Birth: April 22, 1942 Place of Birth: Wolfelsgrund, Germany Citizenship: United States Education: M.D. 1967, University of Munich, Germany Associations, Memberships and Honors: Member, National Academy of Sciences Fellow, American Academy of Arts and Sciences Member, International Society for Stem Cell Research Member, American Association for the Advancement of Science Member, German Academy of Natural Sciences Leopoldina Associate Member, European Molecular Biology Organization Editorial Board, Developmental Dynamics, 1992-2000 Editorial Board, Development, 1989-1998 Editorial Board, Molecular Reproduction and Development, 1988-1996 1996 Boehringer Mannheim Molecular Bioanalytics Prize 2001 First Peter Gruber Foundation Award in Genetics 2002 Robert Koch Prize for Excellence in Scientific Achievement 2003 Charles Rodolphe Brupracher Foundation Cancer Award 2006 Max Delbrück Medal for Molecular Medicine 2007 Vilcek Foundation Prize for Achievements of Prominent Immigrants 2008 Meira and Shaul G. Massry Prize Professional Experience: 9/68-1/70 Postdoctoral Fellow, Max Planck Institute for Biochemistry, Munich, Germany; research on replication and transcription of E. coli phages M13 and PhiX174. 2/70-2/72 Postdoctoral Fellow with Dr. Arnold Levine, Department of Biochemistry, Princeton University, Princeton, New Jersey. Research on replication, transcription, and transformation with SV40 virus. 2/72-10/72 Visiting Fellow with Dr. Beatrice Mintz, Institute for Cancer Research, Fox Chase, Philadelphia, Pennsylvania Research on the in vitro cultivation and reimplantation of isolated mouse embryos; micromanipulation techniques. 11/72-1/76 Assistant Research Professor, The Salk Institute, La Jolla, CA 1/76-1/77 Associate Research Professor, The Salk Institute, La Jolla, CA Research on the interaction of viruses with early mammalian embryos, generation of first transgenic mice. -
The Wonderful World of Gene Editing Using CRISPR/Cas9
Sponsored by Rheumatic Diseases Core Center (P30-AR048311) & Comprehensive Arthritis, Musculoskeletal, Bone and Autoimmunity Center (CAMBAC) Please come to the Research in Progress Seminar Series WONDERFUL WORLD OF TECHNOLOGY event featuring Thomas M. Ryan, PhD Associate Professor, Biochemistry & Molecular Genetics The Wonderful World of Gene Editing Using CRISPR/Cas9 Thursday, Feb 5, 2015 12:00 – 1:00 PM SHEL 515, 1825 University Blvd. Raw data welcome! You provide the science, and we’ll provide the food. The Wonderful World of Gene Editing Using CRISPR/Cas9 2/5/2015 Thomas M. Ryan, PhD Biochemistry and Molecular Genetics Regenerative Medicine Patient Transplant back Somatic Cell into patient Biopsy Derive Isogenic In vitro Pluripotent differentiation Stem Cells Corrected Repair DNA Stem Cells lesion Gene Correction by Homologous Recombination in Pluripotent Stem Cells Mouse: Homologous recombination (HR) methodology in murine ES cells is relatively straight forward. Gene targeting (knockouts, knockins, etc.) using targeting constructs with 5’ and 3’ homology regions flanking a selectable marker have been used to modify the mouse genome for over 25 years. Human: Gene correction by HR has proven much more difficult in human ES/iPS cells. Their slower growth and lower plating efficiencies have resulted in only a handful of genes to be targeted by standard techniques. Newer gene correction methods with higher efficiencies are needed. Humanized Hb Mouse Model: Human gA Globin Knock-In LCR ey h0 h1h2 maj min g A hyg CRE ey h0 h1 h2 g A LCR gAKI Mario Capecchi, Martin Evans, and Oliver Smithies were awarded the Noble Prize for Physiology and Medicine in 2007 for this “Gene Targeting” technique. -
Administration of Barack Obama, 2011 Remarks on Presenting The
Administration of Barack Obama, 2011 Remarks on Presenting the National Medal of Science and the National Medal of Technology and Innovation October 21, 2011 Welcome, everybody. Please have a seat. It is a great pleasure to be with so many outstanding innovators and inventors. And I'm glad we could convince them all to take a day off—[laughter]—to accept our Nation's highest honor when it comes to inventions and innovation, and that is the National Medals of Science and the National Medals of Technology and Innovation. It's safe to say that this is a group that makes all of us really embarrassed about our old science projects. [Laughter] You know, the volcano with the stuff coming out—[laughter]— with the baking soda inside. Apparently, that was not a cutting-edge achievement— [laughter]—even though our parents told us it was really terrific. But thanks to the men and women on the stage, we are one step closer to curing diseases like cancer and Parkinson's. Because of their work, soldiers can see the enemy at night and grandparents can see the pictures of their grandchildren instantly and constantly. Planes are safer, satellites are cheaper, and our energy grid is more efficient, thanks to the breakthroughs that they have made. And even though these folks have not sought out the kind of celebrity that lands you on the cover of People magazine, the truth is that today's honorees have made a bigger difference in our lives than most of us will ever realize. When we fill up our cars, talk on our cell phones, or take a lifesaving drug, we don't always think about the ideas and the effort that made it all possible. -
From Blastomeres to Somatic Cells: Reflections on Cell Developmental Potential in Light of Chimaera Studies – a Review
Animal Science Papers and Reports vol. 35 (2017) no. 3, 225-240 Institute of Genetics and Animal Breeding, Jastrzębiec, Poland From blastomeres to somatic cells: reflections on cell developmental potential in light of chimaera studies – a review Krystyna Żyżyńska-Galeńska*, Anna Piliszek, Jacek A. Modliński Department of Experimental Embryology, Institute of Genetics and Animal Breeding, Polish Academy of Sciences, Jastrzębiec, 05-551 Magdalenka, Poland (Accepted June 10, 2017) Mammalian development is a process, whereby cells from a totipotent zygote gradually lose their potency, i.e. their ability to differentiate, in the environment of the developing embryo. An ideal model for testing the real potential of cells is the experimental production of chimaeras. The first experimentally produced mammalian (murine) chimaeras were created by Tarkowski [1961] and since then many new methods of chimaera production have been developed, including injecting cells into the blastocyst’s cavity or into cleaving embryos. This review describes how different cell types, depending on the developmental stage or culture conditions, manifest their potential to contribute to chimaeras. Cell developmental potential has been analysed in pluripotent blastomeres, which can contribute to all embryonic and extra-embryonic lineages, albeit differently depending on their developmental stage. This is the case in blastocyst lineages, with various developmental potentials depending on the surrounding cells, and in more differentiated cells from different stages of pregnancy, which in some cases may colonise chimaeric animal tissue. Cell potential has also been analysed in embryonic stem and embryonal carcinoma cells, which are pluripotent and efficiently contribute to chimaeras; in multipotent fetal and adult stem cells, which can also participate in chimaera formation; and in somatic mouse embryonic fibroblasts (MEFs), which can also be reprogrammed in the environment of the cleaving embryo. -
Blanche Capel, Phd FASEB Board of Directors
Blanche Capel, PhD FASEB Board of Directors Blanche Capel, PhD, is a James B. Duke Professor of Cell Biology at Duke University Medical Center, where she began her research laboratory in 1993. Her graduate training was in mouse genetics and stem cell biology with Beatrice Mintz at Fox Chase Cancer Center and the University of Pennsylvania, followed by postdoctoral research in the Lovell-Badge laboratory at the National Institute for Medical Research, Mill Hill, London, leading to the discovery of Sry, the male sex determining gene in mammals. Work from the Capel laboratory is prominent in the field of primary sex determination and the cell fate and patterning decisions that underlie the development of the early bipotential mammalian gonad into either testis or ovary. Dr. Capel’s work on signaling pathways in the gonad led to the widely accepted current model that sex determination results from antagonism between the male and female transcriptional and cell signaling networks. She pioneered organ culture techniques for studying the organogenesis of the testis and ovary, and was among the first to develop live imaging to explore the critical role of the vasculature in the morphogenesis of the gonad. Recently, she has used systems-biology and mouse genetics approaches to characterize the global transcriptional network underlying gonad fate, and has investigated the conservation of these mechanisms in the red-eared slider turtle, in which sex determination is thermally regulated. Other work in her laboratory aims to understand how the intracellular program in germ cells, in combination with regulation from their niche, leads to the transition of germ cells from a pluripotent state into pro-spermatogonia. -
III IIHIIII USOO5550316A United States Patent (19) 11 Patent Number: 5,550,316 Mintz 45) Date of Patent: Aug
III IIHIIII USOO5550316A United States Patent (19) 11 Patent Number: 5,550,316 Mintz 45) Date of Patent: Aug. 27, 1996 54) TRANSGENIC ANIMAL MODEL SYSTEM M Bradlet al. (1991) Proc Natl AcadSci, USA 88:164-168. FOR HUMAN CUTANEOUS MELANOMA K N Broadley et al (1989) Laboratory Investigation 61:571-575. 75) Inventor: Beatrice Mintz, Elkins Park, Pa. Hesketh (1995) The Oncogene Facts Book, pp. 32-42. (73) Assignee: Fox Chase Cancer Center, Strojek et al (1988) Genetic Engineering: Principles and Philadelphia, Pa. methods, 10:238. Loudon et al (1993) Clin Exp Pharmacol Physiol 20: 21 Appl. No.: 11,060 283-288. 22 Filed: Jan. 29, 1993 Primary Examiner-Jacqueline M. Stone Related U.S. Application Data Assistant Examiner-Bruce R. Campell Attorney, Agent, or Firm-Pennie & Edmonds 63 Continuation-in-part of Ser. No. 636,798, Jan. 2, 1991, abandoned. 57) ABSTRACT (51 Int. CI.' ................ C12N 15/00; A01K 67/00 52) U.S. Cl. ..................... 800/2; 800/DIG. 1; 435/172.3; The present invention relates to transgenic animal model 536/23.1; 536/23.72; 536/24.1; 424/9.2 systems for human cutaneous melanoma. It is based, at least Field of Search ................................... 800/2, DIG. 1; in part, on the discovery that, in susceptible transgenic mice, (58) accelerated formation of melanoma tumors occurred near 435/172.3; 536/23.1, 23.72, 24.1; 424/9 the wound borders of skin grafts carrying the Tyr-SV40E References Cited transgene, indicating that factors present during wound (56) healing facilitate the formation of cutaneous melanoma in PUBLICATIONS susceptible tissue. -
Normal Genetically Mosaic Mice Produced from Malignant
Proc. Nat. Acad. Sci. USA Vol. 72, No. 9, pp. 3585-589, September 1975 Cell Biology Normal genetically mosaic mice produced from malignant teratocarcinoma cells (embryonal carcinoma/teratoma/embryoid body core cells/blastocyst injection/allophenic mice) BEATRICE MINTZ AND KARL ILLMENSEE Institute for Cancer Research, Fox Chase, Philadelphia, Pennsylvania 19111 C6ntributed by Beatrice Mintz, June 26, 1975 ABSTRACT Malignant mouse teratocarcinoma (or em- The most rigorous test possible for developmental totipo- bryonal carcinoma) cells with a normal modal chromosome tency would be significant contributions of the carcinoma number were taken from the "cores" of embryoid bodies cells to the normal differentiation of virtually all tissues in a grown only in vivo as an ascites tumor for 8 years, and were mouse. For this to occur, the initially malignant cells would injected into blastocysts bearing many genetic markers, in order to test the developmental capacities, genetic constitu- presumably have to be brought into association with early tion, and reversibility of malignancy of the core cells. Ninety- embryo cells so that the latter could provide an organiza- three live normal pre- and postnatal animals were obtained. tional framework appropriate for normal development. The Of 14 thus far analyzed, three were cellular genetic mosaics experiment is analogous to production of allophenic mice with substantial contributions of tumor-derived cells in many (6). developmentally unrelated tissues, including some never The projected teratoma studies in this laboratory involve seen in the solid tumors that form in transplant hosts. The tissues functioned normally and synthesized their specific the use of mutagenized embryonal carcinoma cells for ex- products (e.g., immunoglobulins, adult hemoglobin, liver pro- perimental analyses of genetic regulatory systems in mam- teins) coded for by strain-type alleles at known loci.