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Ludwig Institute Consolidated Financial Report for 2012
Ludwig Institute for Cancer Research Ltd Statutory Financial Statements 2012 Ludwig Institute for Cancer Research Ltd, Zurich Report of the Statutory Auditor on the Financial Statements to the General Meeting of Shareholders Financial Statements 2012 KPMG AG Zurich, May 14, 2013 - 8 - Ludwig Institute for Cancer Research Ltd - 9 - Ludwig Institute for Cancer Research Ltd - 10 - Ludwig Institute for Cancer Research Ltd Balance Sheet as at December 31, 2012 USD CHF 2012 2011 2012 2011 Assets Current assets Liquid funds (Notes 1 & 2) 22,138,495 15,385,587 20,265,932 14,387,043 Fixed term deposits (Notes 1 & 2) 6,439,223 14,765,382 5,894,618 13,806,828 Other receivables - Third parties 2,640,414 3,461,456 2,417,059 3,236,845 External funding 3,888,612 3,411,279 3,559,672 3,189,902 Prepayments and accrued income 3,120,349 2,681,977 2,856,387 2,507,918 Total current assets 38,227,093 39,705,681 34,993,668 37,128,536 Fixed assets Financial fixed assets - Investments (Note 4) 7,080,599 5,103,000 6,481,635 4,771,815 Other (Notes 1 & 5) 1,517,679 1,987,090 1,389,319 1,858,180 Total fixed assets 8,598,278 7,090,090 7,870,954 6,629,995 Total assets 46,825,371 46,795,771 42,864,622 43,758,531 Liabilities and Net worth Current liabilities Accounts payable - third parties (Note 7) 8,873,562 10,624,684 8,122,981 9,935,143 Accruals (Note 1) 6,507,197 7,514,082 5,956,785 7,026,474 Provisions (Notes 1 & 8) 5,839,674 5,860,811 5,345,653 5,480,518 Deferred income (Notes 1 & 10) 6,887,424 10,096,102 6,304,919 9,441,140 Total current liabilities 28,107,857 34,095,679 -
Tyler Jacks, Phd President, Break Through Cancer; Founding Director, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Tyler Jacks, PhD President, Break Through Cancer; Founding Director, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology www.breakthroughcancer.org Dr. Tyler Jacks, the President of Break Through Can- Dr. Jacks is an elected member of the National Acad- cer, has dedicated his life to cancer research. He emy of Sciences, the National Academy of Medicine, is the Founding Director of the Koch Institute for the American Academy of Arts and Sciences, and Integrative Cancer Research at the Massachusetts was a member of the inaugural class of Fellows of Institute of Technology, the David H. Koch Profes- the AACR Academy. In 2015, Dr. Jacks received the sor of Biology, and Co-director of the Ludwig Cen- Killian Faculty Achievement Award, the highest honor ter for Molecular Oncology. From 2001 – 2007, he the MIT faculty can bestow upon one of its members. served as director of the Koch Institute’s predeces- In 2016, Dr. Jacks co-chaired the Blue-Ribbon Panel sor, the MIT Center for Cancer Research, and was for (then) Vice President Joe Biden’s Cancer Moon- a long-standing Investigator of the Howard Hughes shot Initiative. He was also chair of the National Medical Institute (1994-2021). Dr. Jacks received his Cancer Advisory Board of the National Cancer Insti- bachelor’s degree in Biology from Harvard College, tute during the Obama administration. and his doctorate from the University of California, Dr. Jacks serves on the Board of San Francisco, where he trained with Nobel Laure- Directors of Amgen and Thermo ate Harold Varmus. He was a postdoctoral fellow Fisher Scientific. -
Ludwig Institute Consolidated Financial Report for 2019
Ludwig Institute for Cancer Research Ltd, Zurich Report of the Statutory Auditor on the Consolidated Financial Statements to the General Meeting of Shareholders Consolidated Financial Statements 2019 KPMG AG Zurich, May 22, 2020 KPMG AG Audit Räffelstrasse 28 PO Box Telephone +41 58 249 31 31 CH-8045 Zurich CH-8036 Zurich Internet www.kpmg.ch Report of the Statutory Auditor to the General Meeting of Shareholders of Ludwig Institute for Cancer Research Ltd, Zurich Report of the Statutory Auditor on the Consolidated Financial Statements As statutory auditor, we have audited the accompanying consolidated financial statements of Ludwig Institute for Cancer Research Ltd, which comprise the balance sheet, income statement, statement of cash flows, statement of capital changes and notes for the year ended December 31, 2019. Board of Directors’ Responsibility The board of directors is responsible for the preparation of the consolidated financial statements in accordance with Swiss GAAP FER and the requirements of Swiss law. This responsibility includes designing, implementing and maintaining an internal control system relevant to the preparation of consolidated financial statements that are free from material misstatement, whether due to fraud or error. The board of directors is further responsible for selecting and applying appropriate accounting policies and making accounting estimates that are reasonable in the circumstances. Auditor’s Responsibility Our responsibility is to express an opinion on these consolidated financial statements based on our audit. We conducted our audit in accordance with Swiss law and Swiss Auditing Standards. Those standards require that we plan and perform the audit to obtain reasonable assurance whether the consolidated financial statements are free from material misstatement. -
Francisco J. Sánchez-Rivera
Francisco J. Sánchez-Rivera Memorial Sloan Kettering Cancer Center Sloan Kettering Institute Zuckerman Research Building 417 East 68th Street - Z-1119 New York, NY 10065 Tel: 939-292-5555 E-mail: [email protected] Education Fall 2008 - Winter 2016 Massachusetts Institute of Technology Department of Biology Ph.D. in Biology Fall 2003 - Spring 2008 University of Puerto Rico, Mayagüez, PR Department of Biology B.S. in Microbiology Research January 2016 - Present Memorial Sloan Kettering Cancer Center - Sloan Kettering Institute Postdoctoral fellow in the laboratory of Dr. Scott W. Lowe Main Project: Dissecting the biological impact of mutational heterogeneity using mouse models and genome engineering June 2009 - January 2016 Department of Biology at MIT and David H. Koch Institute for Integrative Cancer Research Graduate student in the laboratory of Dr. Tyler Jacks Thesis title: Constructing and deconstructing cancer using CRISPR-Cas9 Main projects: 1) Modeling cancer in vivo using the CRISPR-Cas9 system. 2) CRISPR screens for uncovering genotype-specific cancer drug targets. 3) Molecular mechanisms dictating tumor-specific responses to p53 restoration. June 2008 - August 2008 Whitehead Institute for Biomedical Research Summer student researcher in the laboratory of Dr. Harvey F. Lodish Project: The role of histone deacetylases in enucleation of cultured mouse fetal erythroblasts. June 2007 - August 2007 Department of Biology at MIT Summer student researcher in the laboratory of Dr. Stephen P. Bell Project: Identification of dominant negative helicase mutants by insertional mutagenesis of the yeast replicative helicase Mcm2-7. January 2006 - May 2008 University of Puerto Rico, Mayagüez Campus Department of Biology Undergraduate researcher in the laboratory of Dr. -
The Role of HIF-1Α in Sarcoma Metastasis and Response to Radiation Therapy
The Role of HIF-1α in Sarcoma Metastasis and Response to Radiation Therapy by Minsi Zhang Department of Pharmacology and Cancer Biology Duke University Date:_______________________ Approved: ___________________________ David Kirsch, Supervisor ___________________________ Mark Dewhirst ___________________________ Christopher Kontos ___________________________ Kenneth Poss ___________________________ Jeffrey Rathmell Dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Pharmacology and Cancer Biology in the Graduate School of Duke University 2015 ABSTRACT The Role of HIF-1α in Sarcoma Metastasis and Response to Radiation Therapy by Minsi Zhang Department of Pharmacology and Cancer Biology Duke University Date:_______________________ Approved: ___________________________ David Kirsch, Supervisor ___________________________ Mark Dewhirst ___________________________ Christopher Kontos ___________________________ Kenneth Poss ___________________________ Jeffrey Rathmell An abstract of a dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Pharmacology and Cancer Biology in the Graduate School of Duke University 2015 Copyright by Minsi Zhang 2015 Abstract The degree of intratumoral hypoxia is clinically correlated to poor response to therapy and increased incidence of distal spread in various cancer subtypes. Specifically, the transcription factor Hypoxia Inducible Factor-1α (HIF- 1α), which is accumulated in cells in response to a hypoxic microenvironment, is implicated in poor disease outcome associated with intratumoral hypoxia. Using novel genetically engineered mouse models of primary soft tissue sarcoma, I show that in vivo genetic deletion of HIF-1α specifically in tumor cells 1) decreases the incidence of lung metastases by limiting sarcoma collagen deposition, and 2) improves sarcoma response to radiation therapy by limiting the inflammatory response and metabolic adaptations. -
Don Cleveland Shows How Research in Neuroscience Is Leading to New Approaches to Treat Brain Cancer
18 INTERDISCIPLINARY RESEARCH Ludwig Cancer Research has a long tradition of nurturing investigators who see connections among different fi elds. The work of Ludwig scientist Don Cleveland shows how research in neuroscience is leading to new approaches to treat brain cancer. 19 TECHNIQUE TO VANQUISH DISEASE IN NERVOUS SYSTEM APPLIED TO CANCER Richard Smith, a neurologist who has a roster of patients with neurodegenerative disease, would not leave Ludwig scientist Don Cleveland alone. Cleveland’s laboratory at Ludwig San Diego had the means to test an idea to help people with Don Cleveland amyotrophic lateral sclerosis (ALS, also called Lou Gehrig’s disease), whom Smith saw regularly at his San Diego clinic. “He was relentless in badgering me,” recalls Cleveland of their interactions in 2005. The idea was to silence a gene that is mutated in a proportion of inherited ALS cases, caused by mutation in SOD-1 (superoxide dismutase 1), in the hope that quelling the bad gene could also quell disease. To silence the gene, Smith suggested using an antisense oligonucleotide, a small piece of single-stranded DNA. It was designed to destroy the gene’s mRNA, a molecular intermediary between the gene and the protein it encodes. Smith proposed testing the oligonucleotide in animals with a pump that would infuse the DNA drug directly into the cerebrospinal fl uid, essentially bathing the brain and spinal cord in it. To work, the drug needed to be taken up by the motor neurons. Cleveland didn’t think this would happen. But Smith, who later spent two years in Cleveland’s lab working on the project, argued that they had nothing to lose. -
LUDWIG LINK | NOVEMBER 2013 Irector of Communications Irector Steinhardt Achel Positive
LUDWIG LINK NOVEMBER 2013 IN THIS ISSUE 3 | Oxford Report 11 | Irv Weissman Q&A News from the Ludwig A conversation with the scientific retreat Ludwig Stanford director Continued inside > LUDWIG LINK | NOVEMBER 2013 1 LUDWIG LINK NOVEMBER 2013 LETTER Fall is an ideal time to refresh the mind and engage in creative new thinking and direction. TABLE OF CONTENTS And last month started off on a high note, with a Ludwig retreat Meeting Notes 3 in Oxford that packed three Getting to know you days with information sharing 3 Abracadabra and networking. The caliber 4 of the content, speakers and attendees was amazing Company News in itself. It was an unparalleled opportunity to foster 4 interactions and collaborations among some of the most Well designed 4 distinguished researchers from around the world. News Roundup 5 The passion was palpable from the presentations to the Buyer beware 5 coffee breaks and after-hour conversations. Off-site Dark horse 5 meetings encourage out-of-the-box thinking because Don’t delete 6 being in unfamiliar surroundings can break old habits Sn(i)ps 7 and generate energy, leading to fresh ideas and deeper Fickle finger of cell fate 7 LUDWIG LINK | NOVEMBER 2013 thinking. The splice of life 8 Eats, shoots and leaves 9 And the feedback couldn’t have been more positive. “The retreat offered me an incredible opportunity to Ask a Scientist 10 foster new and deeper collaborations with other Ludwig labs. It felt like the cancer biologist’s version of AC/DC’s Q&A with Irv Weissman 11 greatest hits album!” said Adriel Cha of Ludwig Stanford. -
Susceptibility to Astrocytoma in Mice Mutant for Nf1 and Trp53 Is Linked to Chromosome 11 and Subject to Epigenetic Effects
Susceptibility to astrocytoma in mice mutant for Nf1 and Trp53 is linked to chromosome 11 and subject to epigenetic effects Karlyne M. Reilly*†, Robert G. Tuskan*, Emily Christy‡§, Dagan A. Loisel‡§, Jeremy Ledger‡, Roderick T. Bronson¶, C. Dahlem Smithʈ, Shirley Tsang**, David J. Munroe**, and Tyler Jacks‡§ *Mouse Cancer Genetics Program, National Cancer Institute, Frederick, MD 21702; ‡Department of Biology and Center for Cancer Research and §Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02169; ¶Department of Pathology, Harvard Medical School, Boston, MA 02115; and Laboratories of ʈAnimal Sciences Program and **Molecular Technology, Science Applications International Corporation, Frederick, MD 21702 Edited by Bert Vogelstein, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD, and approved July 9, 2004 (received for review February 21, 2004) Astrocytoma is the most common malignant brain tumor in hu- tumors such as astrocytoma (8, 9), although this observation is mans. Loss of the p53 signaling pathway and up-regulation of the as likely due to the particular mutant allele of NF1 (10) as to ras signaling pathway are common during tumor progression. We genetic or environmental risk factors. Astrocytomas are also have shown previously that mice mutant for Trp53 and Nf1 frequently associated with mutations in Tp53 in sporadic cases develop astrocytoma, progressing to glioblastoma, on a C57BL͞6J (11, 12) or in LFS patients carrying germline mutations in the strain background. In contrast, here we present data that mice Tp53 gene (5) (Trp53 in the mouse). Although there are no clear mutant for Trp53 and Nf1 on a 129S4͞SvJae background are highly data in patients that genetic background affects the risk of resistant to developing astrocytoma. -
The David H. Koch Institute for Integrative Cancer Research at MIT
The David H. Koch Institute for Integrative Cancer Research at MIT The David H. Koch Institute for Integrative Cancer Research was announced on October 9, 2007. By combining the faculty of the (now former) MIT Center for Cancer Research (CCR) with an equivalent number of distinguished engineers drawn from various MIT departments, the Koch Institute will continue CCR’s tradition of scientific excellence while also seeking to directly promote innovative ways to diagnose, monitor, and treat cancer through advanced technology. Among the engineering faculty there will be remarkable diversity, as the Electrical Engineering and Computer Science, Materials Science and Engineering, Biological Engineering, Chemical Engineering, and Mechanical Engineering departments will be represented in the Koch Institute. For three decades, CCR has been a mainstay of MIT’s—and the nation’s—efforts to conquer cancer. Its faculty has included five Nobel Prize winners, and the wealth of fundamental discoveries that have emerged under its aegis have helped shape the face of molecular biology. Under the banner of the Koch Institute, the future promises to hold even more astounding advances. Within the Koch Institute we will not directly provide clinical care for cancer patients but discoveries made by Koch Institute scientists and engineers will have a broad impact on how the disease is detected and managed. Applying our great strengths in science and technology, and working closely with our clinical collaborators, Koch Institute researchers will be tireless in unraveling the complexities of this disease and bringing new discoveries—and new hope—to patients. The Koch Institute includes more than 40 laboratories and more than 500 researchers located at our headquarters and across the MIT campus. -
Conference Program and Schedule
02_BCR_front.qxd:Layout 1 9/15/09 2:23 PM Page 11 Conference Program and Schedule Thursday, October 8, 2009 1:30 p.m.-3:45 p.m. Session 2: Mouse Models of Cancer Imperial Ballroom 8:00 a.m.-9:00 a.m. Continental Breakfast Chairperson: Guillermina Lozano, UT M. D. Anderson Stanbro Room Cancer Center, Houston, TX The regulation of p53 tumor suppressing activities* Guillermina Lozano 9:00 a.m.-12:00 p.m. Session 1: Genes and Pathways in Cancer Studying tumor evolution in mouse models of cancer* Imperial Ballroom Tyler Jacks, David H. Koch Institute for Integrative Cancer Research at MIT, Cambridge, MA Chairperson: Robert A. Weinberg, Whitehead Institute for Biomedical Research, Cambridge, MA Dissecting tumor suppressor gene networks in vivo* Scott W. Lowe, Cold Spring Harbor Laboratory, Molecular characterization of circulating tumor cells Cold Spring Harbor, NY Daniel A. Haber, Massachusetts General Hospital, Charlestown, MA From chromosome engineering to chromatin remodeler: 3:45 p.m.-4:30 p.m. Special Lecture: CHD5 is a tumor suppressor mapping to human 1p36* Host-Germline Genetics Alea A. Mills, Cold Spring Harbor Laboratory, Imperial Ballroom Cold Spring Harbor, NY Single nucleotide polymorphisms in the p53 pathway* New cancer targets emerging from studies of the VHL tumor Arnold J. Levine, Institute for Advanced Study, Princeton, NJ suppressor gene William G. Kaelin, Jr., Dana-Farber Cancer Institute, Boston, MA 4:30 p.m.-4:45 p.m. Coffee Break PI3-Kinase and cancer metabolism* Stanbro Room Lewis C. Cantley, Beth Israel Deaconess Medical Center, Boston, MA 4:45 p.m.-5:30 p.m. -
Development and Characterization of Immunogenic Genetically Engineered Mouse Models of Pancreatic Cancer
Development and characterization of immunogenic genetically engineered mouse models of pancreatic cancer By Laurens J. Lambert MSc, Medical Biology Radboud University, 2014 Submitted to the Department of Biology in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy at the MASSACHUSETTS INSTITUTE OF TECHNOLOGY September 2020 © 2020 Massachusetts Institute of Technology. All rights reserved. Signature of Author………………………………………………………………………………. Laurens J. Lambert Department of Biology June 16, 2020 Certified by………..………………………………………………………………………………. Tyler Jacks David H. Koch Professor of Biology Investigator, Howard Hughes Medical Institute Thesis Supervisor Accepted by………………………………………………………………………………………. Stephen Bell Uncas and Helen Whitaker Professor of Biology Investigator, Howard Hughes Medical Institute Co-Director, Biology Graduate Committee 2 Development and characterization of immunogenic genetically engineered mouse models of pancreatic cancer By Laurens J. Lambert Submitted to the Department of Biology on June 16, 2020 in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy in Biology Abstract Insights into mechanisms of immune escape have fueled the clinical success of immunotherapy in many cancers. However, pancreatic cancer has remained largely refractory to checkpoint immunotherapy. To uncover mechanisms of immune escape, we have characterized two preclinical models of immunogenic pancreatic ductal adenocarcinoma (PDAC). In order to dissect the endogenous antigen-specific T cell response in PDAC, lentivirus encoding the Cre recombinase and a tumor specific antigen LSL-G12D/+; flox/flox (SIINFEKL, OVA257-264) was delivered to Kras Trp53 (KP) mice. We demonstrate that KP tumors show distinct antigenic outcomes: a subset of PDAC tumors undergoes clearance or editing by a robust antigen-specific CD8+ T cell response, while a fraction undergo immune escape. -
LUDWIG LINK | JULY 2014 Director of Communications Director Steinhardt Rachel Sincerely, Reading! Happy More Prizes
LUDWIG LINK 2014 | JULY IN THIS ISSUE LUDWIG 8 | News Roundup 14 | Q&A Bird virus boosts Peter Gibbs of Ludwig LINK effectiveness of Melbourne-WEHI on immunotherapy effort inspiration and science JULY 2014 Continued inside > 1 LUDWIG LINK JULY 2014 LETTER Antoine-Augustin Parmentier got one in 1773 for identifying a vegetable that could ease TABLE OF CONTENTS famines, and popularized the potato in France. About a Awards and distinctions 3 century and a half later, Charles Cancer’s worst enemy 3 Lindbergh got one for flying Turbocharged team 3 from New York to Paris, and Inspired immunotherapist 4 revolutionized the business of aviation. More recently, A new chief 4 the X Prize Foundation used one to kick off a commercial Nonpareil class 5 space race. Meeting notes 6 A prize is what each of them got. Prizes inspire human achievement at least as much as they celebrate it. And Omne trium perfectum 6 they give the rest of us an opportunity to tip our collective hats to the intrepid, the inspired and the awe-inspiring. News roundup 7 Real hope for real change 7 In this issue you’ll read about 13 Ludwig scientists who Of birds and men 8 dared to ask big questions. Each of the awards won by our Developmental disorders 8 LUDWIG LINK 2014 | JULY researchers this year recognizes significant contributions Clairvoyant 9 to cancer research or therapy. Taken together, they serve Making headway 10 as testament to the high caliber of Ludwig research and DNA detectives 10 the dedication of its scientists. Break repair 11 The nuclear option 12 We also asked three young Ludwig researchers from around the world how prizes impact science.