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WELCOME TO 2017 KASBP SPRING SYMPOSIUM
Korean American Society in Biotech and Pharmaceuticals (KASBP) welcomes you to 2017 KASBP Spring
Symposium, made possible by a generous support from Yuhan Co. Ltd. and Hanmi Pharmaceutical.
Built on a very successful event last year, 2017 KASBP Spring Symposium is coming back to Boston for the
second time. This event will promote and expand KASBP membership in the Greater Boston area and establish a
stronger and wider network amongst KASBP members in the northeast region. This symposium also provides an
opportunity for members to establish professional networks and share information and experiences in the pursuit
of excellence in pharmaceutical research and development.
The symposium organizing committee is also delighted to announce Dr. William C. Hahn as a keynote speaker.
Dr. Hahn is a world-renowned researcher in the field of cancer cell biology at Dana-Farber Institute and a
distinguished professor of medical oncology at Harvard University.
The committee is also proud and excited to present the outstanding list of speakers and panelists. Invited speakers
will share their experiences with cutting-edge science in early discovery research to the clinical trials in
biopharmaceutical research, which will be featured in detail during the three scientific sessions: 1) Immuno-
oncology / de novo protein design, 2) Korean industry innovation and translational research, 3) Diabetes research
and outcome trial as well as imaging technology for speech map. Invited panelist will participate in the discussion
with young scientists who are interested in pursuing a career in the industry. For the first time this year, the
committee is hosting a special event on Saturday night with three special guest presentations on biotechnology
venture opportunities and strategies. All sessions are carefully coordinated to enhance the understanding of topics
on biotechnology and pharmaceutical research, industry-academia alliance, and business development.
Continuing the tradition, KASBP-Yuhan and KASBP-Hanmi Fellowship Awards will be presented to young
scholars who will be selected among the graduate students and post-doctoral scholars in recognition for their
exceptional contribution to their respective research field.
We hope you to enjoy the cutting–edge science and have productive scientific exchanges with fellow scholars in
academia and members of pharmaceutical and biotechnology industries. More importantly, we hope the
symposium can serve as a fun and informative time to network with fellow Korean-American scientists.
With best wishes,
2017 KASBP Spring Symposium Organizing Committee
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2016-2017 KASBP OFFICERS
Title Name Affiliation
President JEONG, Jae Uk (정재욱) GSK
President Designated CHOE, Yun H. (최윤) Lucas & Mercanti
1st Vice President SUH, K. Stephen (서광순) Hackensack Med Center
2nd Vice President KIM, Sean (김승빈) Blueprint Medicines
Executive Director JIN, Yong Hwan (진용환) Samsung Biologics
Science Director Lee, Hyun-Hee (이현희) Merck
Program Director Hong, Peter (홍성원) Regeneron
Financial Director HWANG, Seongwoo (황성우) PTC Therapeutics
General Director CHOI, Suktae (최석태) Celgene
Web Director HEO, Jun Hyuk (허준혁) Merck
1st Membership Director KIM, Sahee (김사희) RevHealth, LLC
2nd Membership Director JEONG, Claire (정가영) GSK
Public Relations Director BANG, Hanseong (방한성) CMIC CMO USA Corp
YG Director YOU, Diana Dahea (유다혜) Rutgers University
Councilor MOON, Young-Choon (문영춘) PTC Therapeutics
Councilor LEE, Hak-Myung (이학명) Shire
Councilor KIM, Jae-Hun (김재훈) IFF
Councilor KIM, Youngsun (김영선) Adello Biologics
Councilor LIM, Sung Taek (임성택) Sanofi
Councilor KOH, Jong Sung (고종성) Genosco
Local Chapters
Boston Chapter President SHIN, Hyunjin (Gene) (신현진) Takeda
Boston Chapter Vice President LEE, Hyun-Hee (이현희) Merck
Boston Chapter General Director LEE, Dooyoung (이두영) Applied Biomath
Boston Chapter Treasurer KIM, Haley (김혜민) Takeda
Connecticut Chapter President KIM, Sung-Kwon (김성권) Alexion
DC Chapter President PARK, Sang Tae (박상태) Macrogen
DC Chapter Vice President SONG, Jeong Keun (송정근) L & J Biosciences
DC Chapter General Director KIM, Miha (김미하) Leidos Bimedical
DC Chapter Science Director LEE, Byung Ha (이병하) NeoImmuneTech
NJ Chapter President KIM, Youngsun (김영선) Adello Biologics
NJ Chapter Vice President JUNN, Eunsung (전은성) Rutgers University
Philadelphia Chapter President CHANG, KernHee (장건희) J&J
KASBP-SF
President MA, Sunghoon (마성훈) Exelixis
Vice President LIM, Hanjo (임한조) Genentech
Vice President YOO, Seung-Yun (유승연) Gilead
Executive Director JO, Hyunsun(조현선) Embedbio
Executive Director HWANG, Bum-Yeol (황범열) DuPont Pioneer
Science Director CHANG, Ji Hoon (장지훈) Amgen
Financial Director JEONG, Joon Won (정준원) Carmot
Public Relationship Director LIM, Min Young (임민영) ThermoFisher Scientific
General Director CHO, Hanna (조해나) Clovis Oncology
Web Director SOHN, Dongmin (손동민) UCSF
Councilor JOH, Danny (조현정) Sangamo
Councilor PARK, Chong Yon (박정연) UCSF
Councilor HAN, Wooseok (한우석) Novartis
Councilor KIM, Yong-Jae (김용재) Gilead
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SYMPOSIUM SCHEDULE AT A GLANCE
June 16 (Friday) June 17 (Saturday)
AM 7 7:30 – 8:30 AM Registration and
Breakfast
8:30 – 8:35 AM Opening Remarks 8
8:35 – 9:45 AM Scientific Session A
9
9:45 – 10:05 AM Sponsor Presentation
and Introduction of new KASBP chapters
10 10:05 –10:20 AM Coffee Break
10:20 –11:30 AM Scientific Session B
11
11:30 – 12:10 PM Fellowship Awards and
Presentations
PM 12 12:10 – 12:20 PM Group Photo
1 12:20 – 3:20 PM Lunch and Poster
Session 2
3 3:00-5:30 PM
Job Fair
-details will be available at
www.kasbp.org
3:20 – 5:05 PM Scientific Session C
4
5
5:30 – 6:30 PM
Registration and Networking
5:05– 5:10 PM Closing Remarks
6 Departure or Networking
Optional Dinner and Networking Session
(registeration required)
6:00 – 8:00 PM
6:30 – 7:50 PM
Opening & Congratulatory Remarks
and Dinner 7
8 7:50 – 8:45 PM
Keynote Presentation
8:45 – 9:00 PM
Sponsor Presentation
9 9:00 – 9:50 PM
Networking Session 1
10 9:50 – 10:40 PM
Networking Session 2 and Panel
Discussion: Pharma industry -
Academia
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SYMPOSIUM SCHEDULE IN DETAIL
June 16, 2017, Friday
Job Fair (details will be provided before the symposium at www. kasbp.org)
3:00 pm ~ 5:30 pm Contact: Suktae Choi (email: [email protected])
Registration & Networking
5:30 pm ~ 6:30 pm
Coordinators: Yun Choe (KASBP President-designated), Lucas & Mercanti
Sahee Kim, RevHealth, LLC
Opening & Congratulatory Remarks and Dinner
6:30 pm ~ 6:50 pm
Opening Remark
Jae Uk Jeong, KASBP President & GlaxoSmithKline
Congratulatory Remarks
Jong-Gyun Kim, Director, Head of Global Research Center, Yuhan Corporation
Jay S. Kim, School of Management, Boston University
Jung Hoon Woo, Director General of KHIDI USA
6:50 pm ~ 7:50 pm
Dinner
Toast: Tae-Ung Eom, President, Samyang Biopharmaceuticals Corp.
Keynote Presentation
7:50 pm ~ 8:45 pm
Coordinator: Sean Kim (2nd Vice president KASBP), Blueprint Medicines
Keynote Speaker:
William C. Hahn, Dana-Farber Cancer Institute, Harvard Medical School
“ Defining a Cancer Dependencies Map”
Sponsor Presentations
8:45 pm ~ 9:00 pm
Yuhan Corporation: Han-Joo Kim, Head, R&D Strategy and Partnering Team
Networking Sessions 1 & 2
9:00 pm ~ 9:50 pm & 9:50 pm ~ 10:40 pm
Organizer: Stephen Suh (1st Vice President, KASBP), Hackensack Med Center
Biology
A. Immuno-oncology/Autoimmune/Inflammatory
Moderators: Hyun-Hee Lee and Hyungwook Lim
B. Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative
Moderators: Alex Yi and Kern Chang
C. Cell and Gene Therapy/Viral infection/Rare disease
Moderators: K. Stephen Suh and Hakryul Jo
Chemistry
Moderators: Sungtaek Lim and Mooje Sung
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PK/PD/pre-clinical/Clinical Science/CMC:
Moderators: Sean Kim and Peter Hong
BD/Legal/VC:
Moderators: Hanseong Bang and Yun Choe
Pharmacy/YG
Moderators: Dahea You and Sahee Kim
Pharma industry – Academia
9:50 pm ~ 10:40 pm
Moderator: Hyunjin (Gene) Shin, Takeda
Panelists:
Min-Kyu Cho, Novartis
Dann Huh, Biogen
Seunghee Jo, Agios
Dooyoung Lee, Applied Biomath
Elizabeth Paik, CRISPR Therapeutics
Young Generation (YG) group networking
10:40 pm ~
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June 17, 2017, Saturday
Registration & Light Breakfast
7:30 am ~ 8:30 am
Opening Remarks
8:30 am ~ 8:35 am
KASBP-Boston Chapter President: Hyunjin Shin, Takeda
Session A -------- Chair: Jaekyoo Lee, Genosco
8:35 am ~ 9:45 am
A-1: “Induction of Anti-Tumor Immunity by Targeting TIGIT in Solid Cancer”
Angie Park, OncoMed Pharmaceuticals
A-2: "Evolution of Complex Molecular Mechanism Dissected by De Novo Protein Design -
Computationally Designed Transmembrane Antiporter of Zinc and Proton"
Nathan Joh, Amgen (Former NIH Fellow at UCSF)
Sponsor Talk
9: 45 am ~ 9:55 am
Osong Medical Innovation Foundation: Tae Gyu Lee
Introduction of New KASBP Chapters
9: 55 am ~ 10:05 am
SF Chapter President: Sunghoon Ma, Exelixis
NJ Chapter President: Youngsun Kim, Adello Biologics
Coffee Break
10:05 am ~ 10:20 am
Session B ------- Chair: Mooje Sung, Novartis
10:20 am ~ 11:30 am
B-1: “Korea as Active Life Science Innovation Hub in Asia”
Jungkue Lee, Bridge Biotherapeutics
B-2: “Drug Discovery; Translating Science into Medicine”
Taeyoung Yoon, Dong-A Socio R&D Center
Fellowship Award Ceremony & Presentation ----- Chair: Hyun-Hee Lee, Merck
11:30 am ~ 12:10 pm
Group Photo Session
12:10 pm ~ 12:20 pm
Lunch & Poster Session
12:20 pm ~ 3:20 pm
Session C -------- Chair: Dooyoung Lee, Applied BioMath
3:20 pm ~ 5:05 pm
C-1: “The Role of Obesity-Induced Inflammation in The Development of Insulin
Resistance and Type 2 Diabetes”
Jongsoon Lee, Joslin Diabetes Center, Harvard Medical School
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C-2: “New Developments in Diabetes Outcomes Trials: The New Crosstalk between Cardiologists and
Diabetologists”
Alexander Yi, Novartis
C-3: “Speech Map: a New Imaging and Analysis Technique to Quantify Speech Using MRI”
Jonghye Woo, Harvard University
Closing Remarks
5:05 pm ~ 5:10 pm
KASBP President: Jae Uk Jeong, GlaxoSmithKline
Dinner & Networking (optional / registration required)
6:00 pm ~ 8:00 pm
Special Presentations
Jay S. Kim, Boston University
Sung Ho Park, SV Investment
Derek Yoon, AJU IB Investment
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KEYNOTE SPEAKER ABSTRACT
Defining a Cancer Dependencies Map
William C. Hahn, Harvard Medical School
Biography:
Professor of Medicine, Harvard Medical School; 2001-present; Chief of the Division of Molecular and Cellular Oncology
(2010-present), and Chair of the Executive Committee for Research (2015-present) at the Dana-Farber Cancer Institute;
Institute Member of the Broad Institute of Harvard and MIT (2004-present); Postdoctoral Fellow, Whitehead Institute for
Biomedical Research (1997-2001); Resident and Fellow, Massachusetts General Hospital and Dana-Farber Cancer Institute
(1996-1999); M.D., Harvard Medical School (1994); Ph.D. Harvard University (1994), A.B. Biochemical Sciences, Harvard
College (1987).
Abstract:
Although we now have a draft view of the genetic alterations that occur in human cancer, the number of mutations found
at low frequency and the molecular heterogeneity of most cancers makes identifying genes that contribute to cancer
phenotypes challenging. Determining the function of genes altered in cancer genomes is essential to develop new
therapeutic approaches. To complement these genome characterization studies, we have used genome scale gain and loss
of function approaches to identify genes required for cell survival and transformation. Specifically, we have performed
systematic studies to interrogate rare alleles found altered in cancer genomes and used advances in synthetic gene
synthesis to prospectively interrogate all possible alleles of known cancer genes. In parallel, we have performed both
genome scale RNAi and CRISRP-Cas9 screens in more than 500 cell lines to identify differentially essential genes and the
context that specifies gene dependency. These studies allow us to begin to define a global cancer dependencies map.
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SCIENTIFIC SESSION – SPEAKERS BIO AND ABSTRACTS
Session A
A-1: Induction of anti-Tumor Immunity by Targeting TIGIT in Solid Cancer
Angie Park, OncoMed Pharmaceuticals
Biography
Senior Director, OncoMed Pharmaceuticals, Inc, 2016 – present; Director, OncoMed Pharmaceuticals, Inc, 2013-2015;
Associate Director, OncoMed Pharmaceuticals, Inc, 2010-2012; Sr. Scientist, OncoMed Pharmaceuticals, Inc, 2005-2009;
Research Investigator, University of Michigan Cancer Center, MI, 2001-2005; Post-doc, University of Michigan Cancer
Center, MI, 1996-2000, Post-doc, Vollum Institute, OHSU, Portland, OR, 1994-1996; Ph.D., Indiana University School of
Medicine, Dept of Biochemistry and Molecular Biology, Indianapolis, IN, 1987-1994.
Abstract
Using OncoMed’s rabbit MAP Trap platform, we have developed antibodies against checkpoint inhibitor TIGIT. Anti-
TIGIT antibodies can block PVR ligand binding and inhibit TIGIT signaling. Anti-TIGIT antibody induced tumor specific
T-cell responses, particularly of the Th1 type, increased antigen-specific CD8 response, and promoted a reduction in Treg-
mediated immune-suppressive activity, leading to tumor growth suppression and generation of long-term immunological
memory against tumors.
A-2: Evolution of Complex Molecular Mechanism Dissected by De Novo Protein Design - Computationally Designed
Transmembrane Antiporter of Zinc and Proton
Nathan Joh, Amgen
Biography
Scientist, Amgen, Thousand Oaks CA 2016 – present; Development Scientist, Bayer HealthCare, Berkeley CA, 2014 –
2016; NIH Postdoctoral Fellow, UCSF Dpt of Pharmaceutical Chemistry, 2011 – 2014; NIH Postdoctoral Fellow, UPenn
Dpt of Biochemistry and Biophysics, 2009-2011; PhD, Biochemistry and Molecular Biology, UCLA Dpt. Of Chemistry and
Biochemistry (2009)
Abstract
De-novo computational design appertains to achieving the desired function by building the protein from scratch. So, this
approach allows active testing of principles governing the protein structure, function and dynamics, in contrast to the passive
investigations involving traditional biochemical approaches, such as mutagenesis and protein chain truncation. Here, I
designed a 25-residue-long peptide, dubbed Rocker, that self-assembles into a tetrameric helical bundle that harnesses proton
concentration gradient to actively transport Zn(II) ions, and vice versa, across the lipid bilayer in vesicles. X-ray crystal
structures show the the intended peptide-peptide interface. Nuclear magnetic resonance shows stable, conformationally
dynamic tetrameric bundle. Rocker illuminates the possible evolutionary pathway for natural transporter proteins. How
protein design can be implemented in therapeutics development will also be discussed.
Session B
B-1: Korea as Active Life Science Innovation Hub in Asia
Jungkue Lee, Bridge Biotherapeutics
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Biography
Mr. James Junkgue Lee has served Bridge Biotherapeutics as CEO since its inception in September 2015. Prior to Bridge,
he founded Rexbio, specialized in discovery of monoclonal antibody for the treatment of pancreatic cancer. He co-founded
CrystalGenomics in 2000 and had played key roles in financing and business development until 2017. He started industry
career at LG Chemical Ltd (currently LG Life Sciences) 1993 after earning MS degree at Department of Chemistry, Seoul
National University.
Abstract
Korea has made steady and robust progress in research capability in academia and development capabilities in industry.
Recent global partnering of Korean biopharma companies with global pharma companies has proven Korea’s such improved
capabilities.
At the same time, VC industry and equity stock market have grown steadily for last two decade, supporting R&D focused
biotech companies have spun out of universities and local pharma companies. This 20-minute talk will provide several
examples research intensive local pharma companies and VC-backed biotech companies which are competing with global
biopharma companies, to recruit talent scientist and entrepreneurs from around the world. 1st generation biotech
entrepreneurs who started biotech around 2000 have been looking around to find novel sciences and talents domestically
and internationally, which will provide different opportunities to KASBP communities..
B-2: Drug Discovery; Translating Science into Medicine
Taeyoung Yoon, Dong-A Socio R&D Center
Biography
Senior Vice President, Don-A Socio R&D Center, 2012 – present; Senior Investigator, Novartis, Cambridge, MA, 2004-
2012; Neurogen Corp, CT, 1996-2004; PhD, Chemistry, Yale University, CT, 1989-1994; M.S. (1987) and B.S. (1985),
Chemistry, Seoul National University, Korea
Abstract
First-in-class drug discovery is a process through which novel target hypotheses are translated into innovative clinical
applications. During such a process, identification and optimization of ‘tool compounds’ is intertwined with increasing
levels of validation of the target concept. Taking as an example the recent success in global license-out of the MER
Tyrosine Kinase program, the speaker will elaborate further on what it takes to build a ‘discovery engine’ that can form the
foundation upon which to grow competitive in the global bio-pharmaceutical market.
Session C
C-1: The Role of Obesity-Induced Inflammation in The Development of Insulin
Resistance and Type 2 Diabetes
Jongsoon Lee, Joslin Diabetes Center, Harvard Medical School
Biography:
Assistant Professor, Harvard Medical School, Boston, MA, 2009–present; Assistant Investigator, Joslin Diabetes Center,
Boston, MA, 2006–present: Instructor, Harvard Medical School, 1999–2009; Research Associate, Joslin Diabetes Center,
MA, 1999–2006; Postdoctoral Research Fellow, Joslin Diabetes Center/Harvard Medical School, Boston, MA, 1995–1999;
Postdoctoral Research Associate, Boston University, School of Medicine, Boston, MA, 1993–1995; Ph.D. Biochemistry,
Department of Biochemistry, Boston University, School of Medicine, Boston, MA (1993); Research Scientist, Genetic
Engineering Institute, Korean Institute of Science and Technology, Seoul, Korea, 1986–1988; M.S. Biochemistry,
Department of Zoology, College of Natural Science, Seoul National University, Seoul, Korea (1985); B.A. Physiology,
Department of Zoology, College of Natural Science, Seoul National University, Seoul, Korea (1983).
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Abstract
Obesity is the major cause of the development of insulin resistance and Type 2 Diabetes. Recently, the notion that obesity-
induced inflammation mediates the development of insulin resistance in animal models and humans has been gaining strong
support. Furthermore, numerous studies have also shown that immune cells in local tissues, in particular in visceral adipose
tissue, play a major role in the regulation of obesity-induced inflammation. It has been shown that obesity disrupts the
immune balance by suppressing anti-inflammatory cells (e.g., regulatory T cells [Tregs]) while simultaneously activating
pro-inflammatory cells (e.g., adipose tissue macrophages [ATMs]). Many studies from the classical immunology field show
that complex cross-regulating interactions between different immune cell types control inflammation. However, the roles
these interactions play have not been studied extensively in the metabolism field. We have recently shown that natural killer
(NK) cells play a critical role in the development of obesity-induced inflammation and insulin resistance, in part by
controlling ATM activation and adipose tissue inflammation. Hence, our studies may provide important preclinical evidence
for the notion that obesity-induced inflammation regulated by adipose NK cells could be a therapeutic target for the
treatment of insulin resistance and Type 2 Diabetes.
C-2: New Developments in Diabetes Outcomes Trials: The New Crosstalk between Cardiologists and Diabetologists
Alexander Yi, Novartis
Biography
Senior Investigator II, Translational Medicine Expert, Novartis Institutes for BioMedical Research, Cambridge, MA 2013
– present; Instructor of Medicine, Division of Cardiology, Massachusetts General Hospital, Boston, MA 2013-2013;
Research Fellow in Medicine, Division of Cardiology, Massachusetts General Hospital, Boston, MA 2008-2012; Cardiology
Fellow, Division of Cardiology, Massachusetts General Hospital, Boston, MA 2006-2012; Residency, Internal Medicine,
New York Presbyterian Hospital-Weill Cornell Medical College, New York, NY 2003-2006; M.D., University of California,
San Francisco (2003); Ph.D., University of California, San Francisco (2001); B.S., Biology, Massachusetts Institute of
Technology (1994)
Abstract
Cardiovascular disease is a major life-threatening complication of patients with type 2 diabetes mellitus. Thus, the
publication of meta-analyses suggesting an increased risk of CV events associated with the thiazolidinedione rosiglitazone
caused great concern and led to a 2008 FDA guidance that new antidiabetic agents must rule out excess cardiovascular risk
prior to approval. Nearly a decade later, recent results of large placebo-controlled studies of SGLT2 inhibitors and GLP-1
agonists have demonstrated for the first time the potential for antidiabetic drugs to reduce the risk of heart disease and heart
failure. These positive results have spurred interest among cardiologists in the potential for diabetes medicines to reduce the
risk of cardiovascular disease in high risk diabetes patients.
C-3: Speech Map: a New Imaging and Analysis Technique to Quantify Speech Using MRI
Jonghye Woo, Harvard University
Biography
Assistant Professor, Harvard Medical School and Massachusetts General Hospital, Boston, MA, 2015-Present; Postdoctoral
Research Fellow and Faculty member, University of Maryland and Johns Hopkins University, Baltimore, MD, 2010-2014;
Research Associate, Cedars-Sinai Medical Center, Los Angeles, CA, 2009-2010; Ph. D., Electrical Engineering, University
of Southern California, Los Angeles (2009), M.S., Electrical Engineering, University of Southern California, Los Angeles
(2007); B.S. Electrical Engineering, Seoul National University, Seoul, South Korea (2005).
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Abstract
Quantitative measurement of functional and anatomical traits of 4D tongue motion in the course of speech remains a major
challenge inscientific research and clinical applications. In this talk, I will introduce MRI techniques including high-
resolution, diffusion, cine- and tagged-MRI and associated image/motion analysis techniques to measure tongue anatomy
and motion. I will then introduce a statistical multimodal atlas of 4D tongue motion using healthy subjects that enables a
combined quantitative characterization of tongue motion in a reference anatomical configuration. This atlas framework,
termed speech map, combines cine- and tagged-MRI to provide both the anatomic reference and motion information during
speech. Using this framework, the anatomic configuration of the tongue appears motionless, while the motion fields and
associated strain measurements change over the time course of speech. In addition, to form a succinct representation of the
highdimensional and complex motion fields, machine learning techniques are carried out to characterize the central
tendencies and variations of motion fields of our speech tasks. Our framework provides a platform to quantitatively and
objectively explain the differences and variability of tongue motion by illuminating internal motion and strain that have so
far been intractable. The findings are used to understand how tongue function for speech is limited by abnormal internal
motion and strain in tongue cancer and ALS (Amyotrophic Lateral Sclerosis) patients.
SPECIAL BREAK-OUT SESSION – SPEAKER BIO AND ABSTRACT
Boston’s bio innovation ecosystem
Jay S. Kim, Boston Univeristy
Biography
Dr. Jay Kim is Associate Professor of Operations and Technology Management at Boston University's Questrom School of
Business, where he teaches courses in operations management, global operations strategy, supply chain management, and
product innovation. He was the department chair in 1995-97, and the faculty director of the School’s various international
programs in 1997-2006. He was the research director of Global Manufacturing Futures Project in 1994-97. Professor
Kim’s research is focused on developing and implementing global operations and value chain strategies. Particularly, he
is investigating the complementary effects from two dominant forces of the 21st century economy that radically change
competitive requirements for global companies – accelerating technological innovations in a wide range of sectors and
vigorous economic development in emerging market countries. He has given lectures on global operations strategy, quality
improvement, value chain enhancement, and innovative business models to managers of various technology-intensive
companies, such as IBM, Raytheon, Johnson & Johnson, Carrier, Sanyo and Toshiba of Japan, and Korean conglomerates
like Daewoo, LG, SK, KEPCO, and Samsung. In 1997, he served as a special advisor for Chairman Kim Woo-Choong of
Korea's Daewoo Group.
Abstract
The speech focus on Boston’s bio innovation ecosystem that facilitates the translational development of scientific discovery
into commercial innovation. Using the examples of LabCentral and IBE (Institute for Biomedical Entrepreneurship), the
speaker discusses the business-side stories of B2B (bench to bedside) or L2M (lab to market) challenges faced by bio
researchers and scientists and presents opportunities for future innovators and entrepreneurs.
IPO Processes in KOSDAQ
Sung Ho Park, SV Investment Corporation
Biography
Mr. Sung Ho Park is the CEO of SV Investment Corporation (SVI), a Korean venture capital firm he founded in 2006. He
was the CEO of Hanwha-SV Meister SPAC from 2010 to 2013. Sung Ho has also served as a non-executive member of
the IPO Review Board for KOSDAQ. SVI was established as an equity investment company by leveraging the heritage
of SV Partners (formerly S-IPO), a consulting company he founded in 2000 specializing in IPO advisory. Over the past
decade, SVI has become a leading private equity and venture capital firm by focusing on investments in life sciences,
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electronic components, and telecommunications sectors. SVI primarily invests in South Korean enterprises as a direct
investor and has broadened its geographical reach and access via secondary investments outside of Korea, (e.g. Korea-China
Joint Investment Funds). Prior to founding the SV Group, Sung Ho was a senior fund manager at Hyundai Investment &
Securities Co., Ltd. Before his tenure at Hyundai Group, Sung Ho was a member of Investment Banking groups at Tongyang
Securities and Dongsuh Securities, where he managed IPOs and M&A transactions. Before his career in investment banking
and venture capital, Sung Ho was a licensed KICPA at Samil PricewaterhouseCoopers Korea. He consulted more than 20
companies on IPO listing and managed more than 15 M&A transactions. Sung Ho holds BA in Business Administration
from Sogang University
Abstract
In 1996, the KOSDAQ Securities Exchange was established as a new stock exchange independent from the Korea Stock
Exchange. Since then KOSDAQ has rapidly grown not only in terms of its total market capitalization but also in quality of
listed companies in terms of their financial performance, level of transparency and increased liquidity. In 2005, the
KOSDAQ introduced a new IPO track for enterprises and entrepreneurs developing unique and cutting-edge technology.
This new IPO review program has allowed qualified technology-based growth companies to receive a P&L waiver, a critical
part of traditional IPO review processes in Korea. This waiver has enabled qualified companies to be listed on KOSDAQ
before they could generate revenues. Over the following decade, this new system has overcome the challenges of risk and
transparency issues. Moreover, it has contributed to creating a more business-friendly environment by providing
opportunities for qualified technology-based enterprises and their private-stage investors to finance growth and corporate
development. Since 2005, 33 of 37 companies listed on KOSDAQ via this tech-based IPO program have come from the
bio/life sciences sector. SVI & SVP have been the leading advocates and pioneers of this new IPO program. This lecture
will help attendees to gain a greater understanding and potential of KOSDAQ IPO processes. Details of the regulations will
be explained using recent examples of technology-based IPOs on KOSDAQ
US Life Science Ecosystem
Derek (Dong Min) Yoon, Aju IB Investment US
Biography
Mr. Yoon is Partner at Aju IB Investment, one of leading venture capital firms in Korea. Based in Boston, Massachusetts,
Mr. Yoon oversees Aju IB’s international investments with focus on U.S. based life science companies and early stage start-
ups with novel science. Mr. Yoon also leads multiple cross-border strategic partnerships by leveraging his relationship with
various pharmaceutical companies in Korea. Currently, he is involved in multiple overseas venture capital fundraising
projects by interacting with Korean governmental institutional funds as well as various private investors in Asia.
Additionally, Mr. Yoon is a board member of Clearside Biomedical and Trefoil Therapeutics, and a board observer at several
other private biotechnology companies. Prior to joining Aju IB Investment, he spent more than fifteen years in alternative
(VC/PE) investments and healthcare corporate banking where he took numerous responsibilities in portfolio management,
deal structuring, and fundraising. His previous experience includes venture investment management at Kibo Capital, the
oldest venture fund in Korea; portfolio management at RBS Citizens Healthcare Banking Group; and venture accelerator
management at Berwind Private Equity, a multi-generational family office located in Harvard, Massachusetts. Mr. Yoon
earned his M.B.A. from Babson College, M.S.F. from Boston College and B.S. in Chemical Engineering from Yonsei
University in Seoul, Korea.
Abstract
The speech will provide analysis on US life science ecosystem to define key components of the ecosystem as well as role
of each component. The speaker will also share his professional experience with US-based VC investors and scientists/
researchers, which will conclude benchmark points and recommendations to Korea.
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POSTER SESSION – AWARDEE ABSTRACTS
2016 SPRING FELLOWSHIP AWARDEES
KASBP-HANMI FELLOWSHIP
KASBP-YUHAN FELLOWSHIP
Min-Kyung Choo, Ph.D
Harvard Medical School
Soo Seok Hwang, Ph.D
Yale University
Heeoon Han, Ph.D
University of Pennsylvania
Hanseul Yang
Rockefeller Univeristy
Ji-Hoon Park, Ph.D
NIH
Hong-Yeoul Ryu, Ph.D.
Yale University
HANMI AND YUHAN FELLOWSHIP AWARDEE ABSTRACTS
TLR sensing of bacterial spore-associated RNA triggers host immune responses with detrimental effects
Min-Kyung Choo, Yasuyo Sano, Changhoon Kim, Kei Yasuda, Xiao-Dong Li, Xin Lin, Mary Stenzel-Poore, Lena
Alexopoulou, Sankar Ghosh, Eicke Latz, Ian R. Rifkin, Zhijian J. Chen, George C. Stewart, Hyonyong Chong and Jin Mo
Park
Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA
02129, USA
The spores of pathogenic bacteria are involved in host entry and the initial encounter with the host immune system. How
bacterial spores interact with host immunity, however, remains poorly understood. Here, we show that the spores of Bacillus
anthracis (BA), the etiologic agent of anthrax, possess an intrinsic ability to induce host immune responses. This
immunostimulatory activity is attributable to high amounts of RNA present in the spore surface layer. RNA-sensing TLRs,
TLR7, and TLR13 in mice and their human counterparts, are responsible for detecting and triggering the host cell response
to BA spores, whereas TLR2 mediates the sensing of vegetative BA. BA spores, but not vegetative BA, induce type I IFN
(IFN-I) production. Although TLR signaling in itself affords protection against BA, spore RNA-induced IFN-I signaling is
disruptive to BA clearance. Our study suggests a role for bacterial spore-associated RNA in microbial pathogenesis and
illustrates a little known aspect of interactions between the host and spore-forming bacteria.
Transcription factor YY1 restrains differentiation and function of regulatory T cells by blocking Foxp3 expression
and activity
Hwang, Soo Seok
Department of Immunobiology, Yale University School of Medicine (P.I : Richard A. Flavell, Ph.D, FRS)
Regulatory T (Treg) cells are essential for maintenance of immune homeostasis. Foxp3 is the key transcription factor for
Treg cell differentiation and function; however, molecular mechanisms for its negative regulation are poorly understood.
Here we show that YY1 expression is lower in T reg cells than Tconv cells, and its overexpression causes a marked
reduction of Foxp3 expression and abrogation of suppressive function of T reg cells. YY1 is increased in Treg cells under
inflammatory conditions with concomitant decrease of suppressor activity in dextran sulfate-induced colitis model. YY1
inhibits Smad3/4 binding to and chromatin remodeling of the Foxp3 locus. In addition, YY1 interrupts Foxp3-dependent
target gene expression by physically interacting with Foxp3 and by directly binding to the Foxp3 target genes. Thus,
YY1 inhibits differentiation and function of T reg cells by blocking Foxp3.
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Anion Relay Chemistry: The Development of an Effective Diastereoselective [3+2] Annulation Tactic Exploiting an
Aldol/Brook Rearrangement/Cyclization Cascade
Heeoon Han, and Amos B. Smith III*
Department of Chemistry, University of Pennsylvania 231 S. 34th street, Philadelphia, PA 19104
An effective [3+2] annulation tactic for the construction of diverse bicyclic compounds possessing highly functionalized
cyclopentane rings has been developed exploiting ketone enolates as the initial nucleophile for Anion-Relay-Chemistry
(ARC). The protocol entails a highly diastereoselective Aldol/Brook rearrangement/cyclization cascade, thus providing
diverse bicyclic building blocks with high functional handles in one-pot to access biologically active natural products such
as capnellenes (4), lucinone (5), africanol (6) and rhodomollein (7) and analogues thereof.
Epithelial-Mesenchymal Micro-niches Govern Stem Cell Lineage Choices
Hanseul Yang,1 Rene C. Adam,1 Yejing Ge,1 Zhong L. Hua,1 and Elaine Fuchs1,2 1Robin Neustein Laboratory of Mammalian Development and Cell Biology2Howard Hughes Medical Institute,The
Rockefeller University, New York, NY 10065, USA
Adult tissue stem cells (SCs) reside in niches, which, through intercellular contacts and signaling, influence SC behavior.
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Once activated, SCs typically give rise to short-lived transit-amplifying cells (TACs), which then progress to differentiate
into their lineages. Here, using single-cell RNA-seq, we unearth unexpected heterogeneity among SCs and TACs of hair
follicles. We trace the roots of this heterogeneity to micro-niches along epithelial-mesenchymal interfaces, where
progenitors display molecular signatures reflective of spatially distinct local signals and intercellular interactions. Using
lineage tracing, temporal single-cell analyses, and chromatin landscaping, we show that SC plasticity becomes restricted in
a sequentially and spatially choreographed program, culminating in seven spatially arranged uni-lineage progenitors within
TACs of mature follicles. By compartmentalizing SCs into micro-niches, tissues gain precise control over morphogenesis
and regeneration: some progenitors specify lineages immediately, whereas others retain potency, preserving self-renewing
features established early while progressively restricting lineages as they experience dynamic changes in microenvironment.
Efficacy of a cell-permeable metformin analog on inhibiting mitochondrial respiration and preventing tumorigenesis
in a mouse model of Li-Fraumeni syndrome
Park, JH, Wang, P-y, and Hwang, PM
Laboratory of Cardiovascular and Cancer Genetics, NHLBI, NIH, Building 10-CRC, Room 5-5288, Bethesda, MD 20814
Rationale – Metformin, widely used to treat type 2 diabetes, has been associated with decreased incidence of cancer.
Mechanistically, metformin has pleiotropic cellular effects that include activation of AMPK and inhibition of mitochondrial
respiration. In a pilot study, we reported that patients with Li-Fraumeni syndrome, a hereditary cancer predisposition
disorder caused by germline p53 mutations, display evidence of increased mitochondrial metabolism (Wang PY et al, NEJM
2013). Moreover, we showed that both the genetic and metformin-mediated disruption of mitochondrial respiration in a
mouse model of LFS delayed tumorigenesis (Wang PY, …Park JH, et al, JCI 2017). Because metformin requires organic
cation transporters to cross the cell membrane, we reasoned that a membrane-permeable analog of metformin HL156A (Ju,
KD et al, AJPRP, 2016) that potently inhibits respiration and crosses the blood brain barrier merited further study to
determine its efficacy in preventing cancer.
Objective – To test whether the metformin analog HL156A would attenuate de novo tumorigenesis in a mouse model of
LFS at treatment doses that correspond to its inhibition of mitochondrial respiration.
Methods and results – We first examined the effect of HL156A on mitochondrial respiration in HCT116 human colon cancer
cells. Compared to metformin, HL156A caused relatively acute inhibition of respiration likely due to its cell permeable
nature. Lactate release was concomitantly increased, consistent with a compensatory increase in glycolysis associated with
inhibition of oxidative phosphorylation. The potencies of HL156A and metformin in inhibiting cell growth were assessed
by a viability assay in HCT116 cells. The IC50 of HL156A and metformin were ~50 µM and ~1200 uM, respectively,
representing a ~24-fold higher potency of HL156A compared with metformin. The cytostatic effect of these compounds
was dependent on mitochondrial function as non-respiring SCO2-/- HCT116 cells were relatively resistant to growth
inhibition.
To test the in vivo efficacy of HL156A in cancer prevention, a LFS mouse model with knockin of the p53 R172H mutation
was treated with HL156A in drinking water at 0.2 or 0.4 mM which corresponds to a daily dose of 15 or 30 mg/kg,
respectively. As positive control, LFS mice were also treated with metformin (7.6 mM) in drinking water which we
previously reported to increase their cancer-free survival. Because LFS mice develop thymic lymphomas, we measured
oxygen consumption in freshly dissociated thymic cells after 4 wk of treatment. Treatment with 0.4 mM HL156A resulted
in a similar degree of inhibition of mitochondrial respiration as 7.6 mM metformin. After confirming inhibition of respiration
in vivo, LFS mice were treated with HL156A at 0.4 or 0.6 mM in drinking water and monitored for cancer-free survival.
Interestingly, treatment with 0.4 mM HL156A increased the median survival time of LFS mice by 20%, comparable to the
effect of metformin, while the higher dose of 0.6 mM failed to improve survival likely due to some cytotoxicity.
Conclusions – In comparison to metformin, HL156A was more potent at inhibiting mitochondrial respiration both in vitro
and in vivo although it showed similar efficacy at preventing cancer in LFS mice. The membrane transporter-independent
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uptake and blood-brain barrier permeability of HL156A may confer additional advantages for chemoprevention in humans
that are not apparent using a mouse model that develops mostly thymic lymphomas. Further studies may be helpful to
determine the merits of HL156A or other derivatives of metformin in preventing cancer.
Acknowledgements - Compound HL156A was kindly provided by Sung-wuk Kim, ImmunoMet, Houston, TX.
Loss of the SUMO protease Ulp2 triggers a specific multichromosome aneuploidy
Hong-Yeoul Ryu (Hong Yeol Rhu),1 Nicole R. Wilson,1 Sameet Mehta,2 Soo Seok Hwang,3
and Mark Hochstrasser1 1Department of Molecular Biophysics and Biochemistry, 2Yale Center for Genome Analysis, 3Department of Immunobiology,
Yale University, New Haven, Connecticut 06520, USA
Post-translational protein modification by the small ubiquitin-related modifier (SUMO) regulates numerous cellular
pathways, including transcription, cell division, and genome maintenance. The SUMO protease Ulp2 modulates many of
these SUMO-dependent processes in budding yeast. From whole-genome RNA sequencing (RNA-seq), we unexpectedly
discovered that cells lacking Ulp2 display a twofold increase in transcript levels across two particular chromosomes:
chromosome I (ChrI) and ChrXII. This is due to the two chromosomes being present at twice their normal copy number. An
abnormal number of chromosomes, termed aneuploidy, is usually deleterious. However, development of specific
aneuploidies allows rapid adaptation to cellular stresses, and aneuploidy characterizes most human tumors. Extra copies of
ChrI and ChrXII appear quickly following loss of active Ulp2 and can be eliminated following reintroduction of ULP2,
suggesting that aneuploidy is a reversible adaptive mechanism to counteract loss of the SUMO protease. Importantly,
increased dosage of two genes on ChrI—CLN3 and CCR4, encoding a G1-phase cyclin and a subunit of the Ccr4–Not
deadenylase complex, respectively—suppresses ulp2Δ aneuploidy, suggesting that increased levels of these genes underlie
the aneuploidy induced by Ulp2 loss. Our results reveal a complex aneuploidy mechanism that adapts cells to loss of the
SUMO protease Ulp2.
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POSTER SESSION –ABSTRACTS
Genomic resistance patterns to second-generation androgen blockade in paired tumor biopsies of metastatic
castrate-resistant prostate cancer
G. Celine Han1,2,4#, Justin Hwang1,2#, Stephanie A. Mullane1,2,4, Zhenwei Zhang1, David Liu1,2, Carrie Cibulskis2, Glenn C.
Gaviola3, Varand Ghazikhanian3, Rana R. McKay5, Glenn J. Bubley6, Scott L. Carter1,2, Steven P. Balk6, William C.
Hahn1,2,3, Mary-Ellen Taplin1,3*, Eliezer M. Van Allen1,2,3,4*
1Dana-Farber Cancer Institute, Boston, MA, 2Broad Institute of Harvard and MIT, Cambridge, MA. 3Brigham and Women’s
Hospital, Boston, MA, 4Center for Cancer Precision Medicine, Dana-Farber Cancer Institute, Boston, MA, 5University of
California San Diego, La Jolla, CA, 6Beth Israel Deaconess Medical Center, Boston, MA; #Co-first author, *Co-senior
author
Background Recent “next generation” androgen deprivation therapies (ADT), such as abiraterone and enzalutamide, have
improved survival in patients with castrate-resistant prostate cancer (CRPC). Despite therapy, most patients develop
resistance to these agents. We investigated the genetic basis of tumor evolution and clinical resistance to next generation
ADT in CRPC by using whole exome sequencing (WES) on paired pretreatment and post-resistance biopsies from CRPC
patients.
Methods Matched “trios” of germline, pre-treatment and post-resistant tumor samples were obtained from 7 patients treated
with abiraterone (n=4) and enzalutamide (n=3) and WES was performed. Clinical data, including PSA and radiographic
measurements, was used to classify patients as intrinsically resistant or initially responsive to treatment. Quality control,
mutation and indel calling, copy number variation identification were performed using analytical pipelines at the Broad
Institute. Tumor purity and ploidy were inferred, and phylogenetic analysis was performed using ABSOLUTE and Phylogic,
respectively to identify resistance associated alterations in the context of clinical phenotypes.
Results We identified multiple putative mechanisms and genetic categories of resistance to next generation ADT in CRPC.
Abiraterone resistant tumors harbored alterations in AR and MYC, while enzalutamide resistant tumors had cell cycle
pathway alterations. Experimentally, overexpressing cell cycle kinases promoted enzalutamide resistance, which was
mitigated through CDK4/6 blockade.
Conclusion This study outlines an approach to identify clinical genetic resistance mechanisms of next generation ADT in
CRPC through integration of genomic data from serial biopsies, clinical patient outcomes, and preclinical functional
screening. These findings confirm previously known potential resistance mechanisms, such as AR and MYC activation, and
inform therapeutic sequence and combination strategies in genomically selected advanced CRPC.
Establishing a CRISPR-based platform to study schizophrenia-associated genes in human neurons
Seok-Man Ho1,3,5, Brigham J. Hartley1,5, Natalie Barretto1,2,5 and Kristen J. Brennand1,2,4,5#
Departments of 1Psychiatry, 2Neuroscience, 3Developmental and Stem Cell Biology, 4Genetics and Genomics, 5Friedman
Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029
Schizophrenia (SZ) is a complex genetic neuropsychiatric disease inherited via both common and rare polygenic risk factors.
SZ genome wide association studies (GWAS) have identified many SZ-associated single nucleotide polymorphisms (SNPs)
positioned in the putative enhancer regions of neuronal genes, suggesting a link between these SNPs, their respective
neighboring gene(s), and SZ risk. Recently, the CommonMind Consortium (CMC) examined gene expression in post-
mortem brains, identifying five genes with the strongest correlation between genotype and brain expression levels: FURIN,
SNAP91, CLCN3, TSNARE1 and CNTN4 (herein referred to as the "CMC genes"); however, the functional role of these
five genes in post-mitotic human neurons remains unresolved. We recently adapted a scalable CRISPR activation and
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interference (CRISPRa and CRISPRi, respectively) platform to NGN2-induced excitatory neurons, enabling robust and
combinatorial manipulation of CMC gene expression in human excitatory neurons. Specifically, we generated CRISPRa
(dCas9-VPR) and CRISPRi (dCas9-KRAB) stable NPC lines to achieve consistent expression of dCas9-effectors, and then
validated lentiviral-expressed gRNAs for each gene in NGN2-neurons generated from 3 control individuals. RNAseq-based
comparison of excitatory neurons with altered expression of CMC genes is underway, facilitating a greater understanding
of how perturbed expression of these CMC genes may contribute to SZ risk. In parallel, multi-electrode array and calcium
imaging experiments are evaluating the functional effect of manipulating these CMC genes in excitatory neurons. Our goal
is to better understand the link between these CMC genes, neuronal activity and SZ risk.
Anti-PD-L1 VHHs as a monitoring and a cytokine-delivery reagent for dense pancreatic tumors
Hee-Jin Jeong
Department of Cancer Immunology and Virology, Dana Farber Cancer Institute, 450 Brookline Avenue, Boston, MA 02215,
USA
Treatment for pancreatic cancer is limited by the dense stroma surrounding tumors and an immunosuppressive tumor
microenvironment. To generate therapies more able to overcome these barriers, we developed single domain antibodies
against PD-L1, and fused these to IL-2 and IFNg. Targeted delivery of each cytokine reduced tumor burden by 50%, while
isotype control conjugated cytokines or blockade of PD-L1 alone showed little effect. Targeted delivery of IL-2 increased
intratumoral CD8 T cells, while IFNg reduced MDSCs and reprogrammed intratumoral macrophages. We exploit the near-
ubiquitous expression of PD-L1 by tumors to focus immune therapies on the tumor microenvironment, and propose that
this may be a general technique for delivering combination immunotherapy to the tumor microenvironment, while greatly
reducing the risk of systemic toxicities.
Structural Basis of Transcription Arrest by Coliphage HK022 Nun in an Escherichia coli RNA Polymerase
Elongation Complex
Jin Young Kang, Paul Dominic B Olinares, James Chen, Elizabeth A Campbell, Arkady Mustaev, Brian T Chait, Maxwell
E Gottesman, and Seth A Darst
The Rockefeller University, 1230 York Avenue, New York, NY10065, United States
Coliphage HK022 Nun blocks superinfection by coliphage λ by stalling RNA polymerase (RNAP) translocation specifically
on λ DNA. To understand how Nun blocks RNAP translocation in molecular view, we determined structures of Escherichia
coli RNAP ternary elongation complexes (TECs) with and without Nun by single particle cryo-electron microscopy. Nun
tightly binds to the TEC by taking advantage of gaps between the RNAP and the nucleic acids. The C-terminal segment of
Nun interacts with the RNAP β and β’ subunits inside the RNAP active site cleft as well as with nearly every element of the
nucleic-acid scaffold, essentially crosslinking the RNAP and the nucleic acids to prevent translocation, a mechanism
supported by the effects of Nun amino acid substitutions. The nature of Nun interactions inside the RNAP active site cleft
suggests that RNAP clamp opening is required for Nun to establish its interactions, explaining why Nun stalls transcription
on pause sites.
Pathway dependence and drug synergism in NF1-associated malignant peripheral nerve sheath tumors using the
zebrafish model
Dong Hyuk Ki, A.Thomas Look
Dana-Farber Cancer Institute and Boston Children’s Hospital
Background: Malignant peripheral nerve sheath tumors (MPNSTs) are very aggressive and often metastatic soft tissue
sarcomas, which are frequently found in patients who have neurofibromatosis type 1 (NF1). Currently, surgical excision is
the only curative therapy for MPNST, although many patients have unresectable or metastatic tumors at diagnosis and the
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recurrence rate after surgery is high. Chemotherapy regimens are only partially effective and associated with significant
toxicity that can severely reduce quality of life.
Objective: To develop a faithful in vivo MPNST transplantation assay to determine drug efficacy and host toxicity to identify
promising drugs and drug combinations. Our long range goal is to define active combinations of three or more non-cross
resistant drugs that exhibit synergistic and sustained tumor cell cytotoxicity at dosages tolerable to the developing recipient
zebrafish.
Methods: Primary MPNSTs were harvested from sox10:mCherry;nf1a+/-;nf1b-/-;p53m/m zebrafish and the cells were
mechanically dispersed. Approximately 100-120 MPNST cells were implanted into embryos at 2 day post-fertilization (dpf),
either into the posterior aspect of the yolk cell or into the pericardium. Twenty-four hours after implantation, the
fluorescent tumor cross-sectional area was imaged and MEK, Hsp90, mTOR, topoisomerase inhibitors at various
concentrations, or DMSO vehicle were added to the fish water. The transplanted embryos were incubated for 4 days in
the vehicle or each individual drug. Quantitative assessment of the cross-sectional area of remaining fluorescent tumor
cellswas performed at 7 dpf and fish were raised in the absence of drug and imaged every 7days to assess the durability of
the response.
Results: The pericardial transplantation assay proved superior, because the tumor cells formed an easily quantifiable mass
in a region that lacks non-specific fluorescence and the tumor cells grew vigorously in vehicle treated fish over the 4-day
incubation period. Drugs in clinical use for MPNST such as PD-0325901, ganetespib, and AZD2014 showed drug responses
at their maximum tolerated doses in the pericardial implantation assay, and topotecan elicited the best cytotoxic response
against transplanted MPNST cells.
Conclusion: We developed a robust in vivo pericardial transplantation model to test drug efficacy using our zebrafish model
of MPNST. We identified topotecan as a promising anti-tumor drug for NF1-associated MPNST, and we are now assessing
FDA approved drugs to identify those that synergize with topotecan to induce sustained MPNST cell death at tolerable
dosages for the host.
Funding Source: Department of Defense Neurofibromatosis Research Program Investigator-Initiated Research Award, NF1
Research Consortium, CTF Drug Discovery Initiative (DDI) Award. The Latsis family fellowship of the Boston Children’s
Hospital Neurofibromatosis program
Bimodality-based top-down clustering of single-cell RNA sequencing data reveals hierarchical structure of the cell
type
Junil Kim1,2, Julia Wang1,2, Diana Stanescu1,4, Maria Golson1,2, Doris Stoffers1,3, Klaus Kaestner1,2, and Kyoung Jae Won1,2 1Institute for Diabetes, Obesity and Metabolism, Perelman School of Medicine, 2Department of Genetics, 3Department of
Medicine, University of Pennsylvania, 4Division of Endocrinology and Diabetes, The Children’s Hospital of Philadelphia
Single-cell RNA sequencing (scRNA-seq) is useful for identifying multiple cell types in heterogeneous cell composition.
Several clustering algorithms successfully visualize predefined cell types as representative marker genes from scRNA-seq
data, but it is still hard to classify cells without marker gene information. To address this problem, we developed a new
clustering algorithm adopting bimodality and top-down hierarchical approach. Our algorithm first identifies gene groups
which share consistent or contrasting bimodal membership, and then identifies cell clusters according to the membership
pattern of the gene group. We applied our algorithm to single-cell gene expression data of the 1,083 human pancreatic cells
and hierarchically clustered the pancreatic cells into seven cell types (alpha, beta, pp, delta, duct, acinar, and mesenchyme)
without marker gene information. We show that our clustering algorithm is more accurate than both bottom-up hierarchical
clustering and t-distributed stochastic neighbor embedding followed by density-based spatial clustering of applications with
noise.
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Flip-flop transcriptional regulation by FoxP3
Ho-Keun Kwon, Hui-Min Chen, Diane Mathis* and Christophe Benoist*
Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, and Evergrande
Center for Immunologic Diseases, Harvard Medical School and Brigham and Women’s Hospital, Boston MA 02115, USA
FoxP3, the key lineage-determining factor of Treg cells, activates or represses a range of transcriptional targets to determine
the many facets of Treg function, in concert with a number of transcriptional cofactors. To understand how FoxP3 juggles
these activities, we constructed a set of 130 mutants spanning the protein, evaluating impacts on DNA binding, cofactor
interactions, chromatin binding and transcriptional activation, and assessing relevance by CRISPR-based genome editing
in mice. Computational integration of binding and transcription results, supported by biochemical dissection of multi-
molecular complexes, showed that mutations affected these functions in a variegated and non-modular manner, with
different mutation footprints for classic targets of the Treg signature vs those typical of tissue Tregs. We demonstrated that
FoxP3 partakes in two dominant complexes of opposite function, activating when partnered with RelA, Ikzf2 and Kat5,
repressing when paired with Ezh2 and Ikzf3. Yet different interactions underpin transcriptional programs of tissue-Tregs.
Mutations with partial effects yielded mice with normal numbers of Tregs in the steady-state context, but of reduced fitness
under stress and autoimmune challenge, suggesting that similar mild FoxP3 variants may have unappreciated consequence
in human pathology.
Novel role of miR-29 in pancreatic cancer autophagy and its therapeutic potential
Jason J Kwon1, Jeffrey A Willy2, Ronald C Wek1,2, Murray Korc2,3,4,5, Xiao-Ming Yin6, and Janaiah Kota1,4,5
1Department of Medical and Molecular Genetics, Indiana University School of Medicine (IUSM), Indianapolis, IN, USA, 2Department of Biochemistry and Molecular Biology, IUSM, Indianapolis, IN, USA, 3Department of Medicine, IUSM,
Indianapolis, IN, USA, 4The Melvin and Bren Simon Cancer Center, IUSM, Indianapolis, IN, USA., 5Center for Pancreatic
Cancer Research, Indiana University and Purdue University-Indianapolis (IUPUI), Indianapolis, IN, USA, 6Department of
Pathology and Laboratory Medicine, IUSM, Indianapolis, IN, USA
Pancreatic Ductal Adenocarcinoma (PDAC) is one of the most lethal human malignancies with a five-year survival rate of
8% and is often undiagnosed until it has metastasized. These advanced tumors display resistance to current therapeutic
modalities. The lack of effective therapies and early detection reinforces the need to understand molecular mechanisms
associated with PDAC to develop novel therapies. We found consistent downregulation of miR-29 in pancreatic cancer cells,
and its restored expression sensitized chemotherapeutic resistant pancreatic cancer cell lines to gemcitabine, leading to
reduced cancer cell viability and increased cytotoxicity. Furthermore, reintroduction of miR-29 blocked autophagy flux,
evidenced by an accumulation of autophagosomes and autophagy substrate, p62, and decreased autophagosome-lysosome
fusion. In addition, miR-29 decreased TFEB and ATG9A expression, which are critical for lysosomal function and
autophagosome trafficking respectively. Subsequent knockdown of TFEB or ATG9A expression alone or in combination
resulted in inhibition of autophagy similar to miR-29 overexpression. Finally, miR-29 reduced migration, invasion, and
anchorage independent growth of pancreatic cancer cells. Collectively, our findings indicate that miR-29 functions as a
potent autophagy inhibitor that sensitizes pancreatic cancer cells to gemcitabine and decreases their invasive potential. Our
data provides evidence for the use of miR-29 as a novel therapeutic agent to target PDAC.
Electrophysiological and transcriptome profiling of hyperexcitable motor neurons derived from ALS patient iPSC
identifies downregulation of a potassium channel subtype
Seungkyu Lee1,2, Ole Wiskow3, Sulagna Ghosh3, Kasper Roet1,3, Xuan Hwang1,3, Bruce P. Bean2, Brian J. Wainger4, Kevin
Eggan3, and Clifford J. Woolf1,2
1 F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA 02115, USA, 2 Department of Neurobiology,
Harvard Medical School, Boston, MA 02115, USA, 3Department of Stem Cell and Regenerative Biology, Harvard University,
Cambridge, MA 02138, USA, 4 Department of Neurology, Massachusetts General Hospital, Charlestown, MA 02129, USA
- 22 -
Amyotrophic lateral sclerosis (ALS) is associated with motor neuron hyperexcitability. The hyperexcitability phenotype
was recapitulated in spinal motor neurons derived from ALS patient iPSC lines that harbor SOD1 and FUS mutations and
C9orf72 repeat expansions. The inhibition of this hyperexcitability using the potassium channel (Kv7) opener retigabine
reduces motor neuron cell death, supporting a pathogenic role (Wainger et al., Cell Reports, 2014). However, the
mechanisms involved in the hyperexcitability remain elusive. To identify the mechanism we have recently developed patch-
seq and patch-RT-qPCR techniques for linking neuronal excitability and gene expression at the single cell level, collecting
RNA after whole cell patch clamp recordings from motor neurons and performing single cell next generation sequencing
and high-throughput multiplex qPCR, respectively. Single cell gene expression profiling in functionally characterized
neurons was performed on HB9::GFP sorted iPSC-derived motor neurons from an ALS patient carrying the SOD1 A4V
mutation (39b) and isogenic control motor neurons with the mutation corrected (39b-cor). We found by whole cell current
clamp recording that 39b motor neurons have larger cell sizes and robust hyperexcitability compared to 39b-cor motor
neurons. Both single cell RNA-seq and ion channel targeted multiplexed high throughput qPCR analysis independently
show a significant down-regulation of a K channel in hyperexcitable ALS motor neurons from this patient in two
independent batches of motor neurons from the same line. These results suggest the reduced expression of a K channel as a
molecular mechanism for the increased excitability in familial ALS.
Targeting lytic and quiescent herpes simplex virus 1 genomes with CRISPR/Cas9
Hyung Suk Oh1, Magdalena Angelova1, Werner Neuhausser3, Kevin Eggan2, 3 and David M. Knipe1
1Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, United States of
America, 2Department of Stem Cell and Regenerative Biology, Harvard Stem Cell Institute, Harvard University, Cambridge,
Massachusetts, United States of America, 3Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard,
Cambridge, Massachusetts, United States of America
Herpes simplex virus (HSV) 1 can undergo lytic replication or establish latency following primary infection. Although there
are several anti-HSV drugs that target lytic infection, no treatment is available to target latent HSV genomes and prevent
reactivation. Here we evaluated the use of the CRISPR (Clustered regularly-interspaced short palindromic repeats)/Cas9
system to target HSV lytic and latent genomes. To study lytic infection, we established human foreskin fibroblast (HFF)
cell lines stably expressing Cas9 and guide RNAs (gRNAs) targeting essential HSV-1 genes, and infected the cells with
HSV-1. Cas9/gRNA expression reduced viral yield by 2-4 logs compared to a control cell line expressing Cas9 alone. We
showed that Cas9/gRNA induced mutations in HSV genomes earlier than 6 hpi, and the mutations accumulated over the
viral replication. Interestingly, replicating HSV genomes are more prone to editing than non-replicating HSV genomes. To
test the ability of CRISPR/Cas9 system to target latent genomes, we established a quiescent infection in HFFs with
replication-defective HSV-1 d109. We transduced quiescently infected cells with lentiviruses encoding Cas9/gRNA
targeting essential viral genes, followed by reactivation with wildtype HSV-1. We observed that reactivation of d109 from
quiescent infection was reduced by 2-5 logs by single gRNAs or combinations of gRNAs compared to the Cas9 control
without gRNA. Additionally, we showed by deep sequencing that quiescent HSV-1 genomes could be efficiently targeted
and edited by Cas9/gRNA. This study demonstrates that the CRISPR/Cas9 system can efficiently target lytic and latent
HSV genomes.
Enhanced Histone Acetylation Up-Regulates MDR1 and BCRP Transporters in Human Blood-Brain Barrier Cells
Dahea You1, Xia Wen2,3, Ayeshia Morris1, Jason R. Richardson4, Lauren M. Aleksunes2,3. 1Joint Graduate Program in Toxicology, Rutgers University, Piscataway, NJ, 2Environmental and Occupational Health
Sciences Institute, Rutgers University, Piscataway, NJ, 3Department of Pharmacology and Toxicology, Rutgers University,
Piscataway, NJ, 4Northeast Ohio Medical University, Rootstown, OH
Multidrug Resistance Protein 1 (MDR1, ABCB1) and the Breast Cancer Resistance Protein (BCRP, ABCG2) expressed at
the blood-brain barrier (BBB) are key efflux transporters that extrude chemicals from the BBB and regulate the efficacy
and/or toxicity of chemicals in the brain. Prior studies in cancer cells have pointed to the ability of histone deacetylase
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(HDAC) inhibitors to modulate the expression and function of MDR1 and BCRP. However, whether or not such regulation
occurs at the BBB is not known. Here we sought to test whether HDAC inhibitors could potentially alter expression and
function of MDR1 and BCRP at the BBB. To test this, we treated immortalized human brain capillary endothelial
(hCMEC/D3) cells, a model of the BBB, with six different HDAC inhibitors, valproic acid (VPA), sodium butyrate (NaB),
romidepsin, apicidin, suberoylanilide hydroxamic acid (SAHA), and trichostatin A (TSA), and assessed for expression and
function of MDR1 and BCRP. HDAC inhibition following treatment was confirmed by increased levels of acetylated histone
H3 protein. After 12 h of treatment, VPA, apicidin, SAHA, and TSA up-regulated MDR1 mRNA levels between 50% and
200%. All six HDAC inhibitors significantly induced BCRP mRNA levels between 100% and 270%. Similarly, the protein
expression of MDR1 and BCRP transporters was up-regulated about two-fold at 24 h. Interestingly, these effects have been
observed at clinically-relevant concentrations of HDAC inhibitors. Enhanced MDR1 expression corresponded with reduced
intracellular accumulation of the substrate rhodamine 123. Collectively, these results demonstrate that HDAC inhibitors up-
regulate MDR1 and BCRP transporters at the BBB by modifying histone acetylation. The clinical use of HDAC inhibitors
may enhance efflux transporter activity at the BBB and restrict access of xenobiotics to the brain.
Mechanisms of transcription factor-mediated direct reprogramming of mouse embryonic stem cells to trophoblast
stem-like cells
Catherine Rhee1,2, Samuel Beck1,2, Bum-Kyu Lee1,2, Lucy LeBlanc1,2, Haley O Tucker1,2, and Jonghwan Kim1,2,3,* 1Department of Molecular Biosciences, 2Institute for Cellular and Molecular Biology, 3Center for Systems and Synthetic
Biology, The University of Texas at Austin, Austin, TX, 78712
Direct reprogramming can be achieved by forced expression of master transcription factors. Yet how such factors mediate
repression of initial cell-type-specific genes while activating target cell-type-specific genes is unclear. Through embryonic
stem (ES) to trophoblast stem (TS)-like cell reprogramming by introducing individual TS cell-specific “CAG” factors (Cdx2,
Arid3a, Gata3), we interrogate their chromosomal target occupancies, modulation of global transcription, and chromatin
accessibility at the initial stage of reprogramming. From the studies, we uncover a sequential, two-step mechanism of
cellular reprogramming in which repression of pre-existing ES cell-associated gene expression program is followed by
activation of TS cell-specific genes by CAG factors. Therefore, we reveal that CAG factors function as both decommission
and pioneer factors during ES to TS-like cell fate conversion.
DNA aptamers that recognize the altered tertiary structure of mutant huntingtin modulate its activity
Baehyun Shin1, 2, Hyejin Oh1, 2, Gwen E. Owens3, Roy Jung1, 2, Hyeongseok Lee4, Seung Kwak5 , Ramee Lee5, Daniel J.
Lavery5, Susan L. Cotman1, 2, Jong-Min Lee1, 2, Marcy E. MacDonald1, 2, Ji-Joon Song4, Ravi Vijayvargia1, 2 and Ihn Sik
Seong1, 2 1Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA 02114, USA, Department of Neurology,
Harvard Medical School, Boston, MA 02114, USA, 3Division of Biology and Biological Engineering, California Institute of
Technology, Pasadena, CA, USA, 4Department of Biological Sciences, KAIST Institute for the BioCentury, Korea Advanced
Institute of Science and Technology (KAIST), Daejeon 305-701, Republic of Korea, 5CHDI Foundation, Princeton NJ 08540,
USA.
Purpose: Huntington’s disease (HD) is a dominant CAG trinucleotide repeat expansion disorder, caused by an elongated
polyglutamine tract in huntingtin. We found its polyglutamine tract size influences both huntingtin’s structure and function,
including modulating its activity in stimulating polycomb repressive complex 2 (PRC2). These observations strongly imply
that small molecules that preferentially bind to mutant rather than normal huntingtin can be found and that, in doing so they
may selectively influence the impact of the longer polyglutamine tract on mutant huntingtin activity.
Materials & Methods: To provide an initial proof for the concept of small molecule-binding as a route to directly alter the
impact of the expanded polyglutamine tract on mutant huntingtin, we have screened a library of single stranded DNA
- 24 -
aptamers for mutant huntingtin specific binders, using highly purified human recombinant huntingtin with polyglutamine
tract lengths of either 23- or 78-residues. This biochemical strategy has yielded a specific set of aptamers that exhibit
differential binding affinities to mutant and normal huntingtin. In this study, we have evaluated the aptamers’ binding sites
and potential ability to modulate the effects of polyglutamine tract length on huntingtin structure and PRC2-stimulating
activity in HD human neural progenitor cells (hNPCs).
Results: We identified forty-five DNA aptamers that preferentially bind to Q78-huntingtin compared to Q23-huntingtin.
Four representative aptamers (MS1,2,3,4) comprise guanine rich sequences forming G-quadruplex structures and bind
predominantly to the CTD-II carboxyl-terminal sub-domain of mutant huntingtin. All four aptamers, particularly MS3 at
low concentration, were found to decrease the enhanced PRC2 stimulating activity conferred by the expanded polyglutamine
tract (Panel A). After incubating HD hNPCs (HD60) and normal hNPCs (HD17) lysates with biotinylated MS3 followed
by pull-down with streptavidin-conjugated beads, we observed a 2.5 fold more efficient pull-down of endogenous huntingtin
in HD60 compared to HD17 (Panel B). Moreover, MS3 transfection into HD60 showed the co-localization with cellular
mutant huntingtin (Panel C) and resulted in a significant decrease in the abnormally elevated PRC2 activity in mutant cells
without affecting the level in HD17 (Panel D).
Conclusion: Our DNA aptamers are a novel biochemical probe for detecting the subtle structural changes specific to mutant
huntingtin and provide a first proof-of-principle to directly modulate mutant huntingtin activity.
Supported by R01ES021800, P30ES005022.
- 25 -
Developing Computational Algorithms for Identifying Important Gene Sets for Thyroid Tumour from Genomic
Data
Yejin Esther Yun, Edwin Wang, Ralf Paschke, Markus Eszlinger
University of Calgary Cumming School of Medicine, Department of Biochemistry and Molecular Biology, Alberta
Children's Hospital Research Institute, Arnie Charbonneau Cancer Research Institute, Calgary, Alberta, Canada
Thyroid nodules are very commonly observed in adults but only a small percentage of the nodules is associated with
malignant tumour. With the advanced diagnostic technology and the enhanced surveillance, an accuracy of diagnostic
testing is of importance for thyroid cancer treatment. Although the fine needle aspiration biopsy is a standard diagnostic
tool to differentiate the malignant and benign tumour, it is invasive to perform such biopsy and still 20% of the results are
indeterminate. Therefore, patient genetic information guided diagnosis has become a necessity to improve patient outcome.
Several studies have been done to unravel driver mutations and to use them for diagnostic testing. However, there were
some cases that are not explained by known driver gene mutations. In order to overcome the challenge, a computational
algorithm will be developed to discover the relationship between the genetic variants and thyroid cancer by identifying
important gene sets that contribute in the background of the known driver mutations.
Funding agency: Alberta Innovates: Health Solutions
- 26 -
PAST FELLOWSHIP AWARDEES
KASBP-DAEWOONG FELLOWSHIP
2006 민재기 New York University, 김 한 Princeton University, 박혜진 Rutgers University
2007 문지숙 Harvard University, 박성연 Rutgers University, 이석근 Columbia University
2008 이흥규 Yale University, 김정환 Rutgers University, 강민식 Columbia University
2009 박진아 Harvard University, 최재민 Yale University, 김덕호 Johns Hopkins University
2010 기정민 Rockefeller University 김형욱 NIH, 안세진 Harvard University
2011 한무리 University of California, LA, 장환종 Boston College
2012 장정호 Columbia University, 최재우 Oregon State University
2013 JangEun Lee (University of Pennsylvania), Eun Chan Park (Rutgers University)
2014 Kimberly H. Kim (Harvard University), Seung Koo Lee (Weill Cornell Medical College), Min-Sik Kim (Johns
Hopkins University)
2015 Jiyeon Kim (UT Southwestern), Sun Mi Park (Memorial Sloan-Kettering Center), Byeong Seon Kim (University
of Pennsylvania)
2016 Sang Bae Lee (Columbia University), Junil Kim (University of Pennsylvania), Ho-Keun Kwon (Harvard Medical
School)
KASBP-GREEN CROSS FELLOWSHIP
2011 조한상 Harvard Medical School, 강성웅 Johns Hopkins University,
김미연 Columbia University, 소재영 Rutgers University, 황성용 NIEHS/NIH
2012 조원진 Drexel University, 강효정 Yale University, 이정현 Columbia University, 이용재 Yale University,
윤재현 NIH
2013 Yunjong Lee (Johns Hopkins University), Jun-Dae Kim (Yale University)
Bae-Hoon Kim (Yale University) Ja Young Kim-Muller (Columbia University)
2014 Catherine Rhee (University of Texas at Austin), Ji-Seon Seo (The Rockefeller University) Sehyun Kim (New York
University)
2015 Young-Su Yi (New York University), Hee-Woong Lim (University of Pennsylvania), Bloria Bora Kim (The
Pennsylvania State University)
2016 Eui Tae Kim (University of Pennsylvania), Kihyun Lee (Weill Cornell Medical Science)
KASBP-HANMI FELLOWSHIP
2011 안형진 Rockefeller University, 조창훈 Abramson Research Center
2012 김유나 University of North Carolina, 태현섭 Yale University, 이인혜 NIH
2013 이주희 Memorial Sloan-Kettering Cancer Center, 이경륜 Rutgers University 이만률 Indiana University
2014 Young Chan Cha (Wistar Institute), Min-Kyu Cho (New York University) Lark Kyun Kim (Yale University), Yu
Shin Kim (Johns Hopkins University)
2015 Seonil Kim (New York University), Peter B. Kim (Yale University)
2016 Sungwhan Oh (Harvard Medical School), Won-Gil Lee (Yale University), Hee-Jin Jeong (Harvard Medical School)
- 27 -
KASBP-YUHAN FELLOWSHIP
2011 김기영 Boston University, 심중섭 Johns Hopkins University
2012 허예민 University of Michigan, 방숙희 University of Pennsylvania, 백정호 Columbia University
2013 Dong Jun Lee (University of Chicago), Ingyu Kim (Yale University), Ja Yil Lee (Columbia University)
2014 Seouk Joon Kwon (Rensselaer Polytech Institute), Jeongmin Song (Yale University), Jae-Hyun Yang (Harvard
Medical School), Wan Seok Yang (Columbia University)
2015 Min-Joon Han (Harvard Medical School), Minjung Kang (Cornell University)
2016 Ki Su Kim (Harvard Medical School), Hongjae Sunwoo (Harvard Medical School), Seo-Young Park (University of
Massachusetts)
KASBP-ST PHARM FELLOWSHIP
2016 Jung-Eun Jang (New York University), Byungsu Kwon (MIT)
KASBP FELLOWSHIP
2009 최상호 NIH
2010 김상령 Columbia University, 윤태숙 Rutgers University, 허은미 Cal. Tech.
2015 (Spring) Mi Jung Kim (Duke University)
2015 (Fall) Minyoung Park (The Rockefeller University)
KASBP-KSEA FELLOWSHIP
2013 Sung In Lim (University of Virginia)
2014 Keun-woo Jin (Temple University)
KASBP-KUSCO FELLOWSHIP
2008 김현호 National Institutes of Health, 온택범 Harvard Medical School, 주원아 Wistar Institute
KASBP-KRICT FELLOWSHIP
2009 신승식 Rutgers University, 정은주 Columbia University, 백규원 University of Pennsylvania
KASBP-KHIDI FELLOWSHIP
2010 배재현 Yale University, 조희연 Boston College
Preliminary Program
For more information, please visit www.kasbp.org
2017 SPRING SYMPOSIUM ATTENDEES
Last Name
First Name Korean Affiliate Area Group Discussion
1. Ahn Kyonghoon 안경훈 Daewoong pharmaceutical company KR Respiratory/metabolic/cardiovascular/Neurogenerative
2. Aoyagi kazuko Celerion NJ Respiratory/metabolic/cardiovascular/Neurogenerative
3. Baek Kyuwon 백규원 AMO Lifescience KR Cell and Gene Therapy/Viral infection/Rare disease
4. Baek Jonathan 백인환 대원제약 주식회사 KR BD/Legal/VC:
5. Bang Hanseong 방한성 CMIC CMO USA NJ BD/Legal/VC:
6. Barker Thomas Foley Hoag LLP DC BD/Legal/VC:
7. Cha Bumjoon 차범준 University of Massachusetts Lowell MA Cell and Gene Therapy/Viral infection/Rare disease
8. Chang Hemmie 장혜미 Foley Hoag MA BD/Legal/VC:
9. Chang Jintae 장진태 CORESTEM KR Cell and Gene Therapy/Viral infection/Rare disease
10. Chang Dong-Eun 장동은 CJ Research Center America MA BD/Legal/VC:
11. Chang Kern 장건희 Janssen R&D PA Respiratory/metabolic/cardiovascular/Neurogenerative
12. Cho Jaemin 조재민 KCRN Research MD PK/PD/pre-clinical/Clinical Science:
13. Cho Min-Kyu 조민규 Novartis MA Chemistry
14. Choe Yun H. 최윤 Lucas and Mercanti, LLP NJ BD/Legal/VC:
15. Choi AHyun 최아현 Univ. of Massachusetts, Medical School MA Immuno-oncology/Autoimmune/Inflammatory
16. Choi Yong Jin 최용진 UC Berkeley CA Cell and Gene Therapy/Viral infection/Rare disease
17. Choi Sungwook 최성욱 U mass medical school MA BD/Legal/VC:
18. Choi Jun Young 최준영 Nitto Avecia MA
19. Choi Younggi 최영기 FORMA Therapeutics CT Chemistry
20. Choi Suktae 최석태 Celgene Inc NJ PK/PD/pre-clinical/Clinical Science:
21. Choo Min-Kyung 추민경 MGH MA
22. Chung Seungwon 정승원 AbbVie IL Chemistry
23. Chung Jaeyoon 정재윤 Boston University MA Respiratory/metabolic/cardiovascular/Neurogenerative
24. Chung WonWoo 정원우 MCPHS Universty MA Pharmacy
25. Chung Kyung Hyun 정경훈 MCPHS MA PK/PD/pre-clinical/Clinical Science:
26. Chung HaeWon 정해원 The University of Texas at Austin TX Cell and Gene Therapy/Viral infection/Rare disease
27. Doh Hyounmie 도현미 Dong-A ST
KOREA
Immuno-oncology/Autoimmune/Inflammatory
28. Eo Jinsu 어진수 Center for engineering in medicine MA
29. Eom Tae Ung 엄태웅 Samyang Biopharmaceuticals Corp. KR
30. HAHM Sean 함성원 The Yakup Shinmoon KR
31. Hahn William Dana-Farber Cancer Institute MA BD/Legal/VC:
32. Hailey Jeong 정혜연 MCPHS University MA BD/Legal/VC:
33. Han Heeoon 한희운 University of Pennsylvania PA
34. Han Celine Garam 한가람 Dana-Farber Cancer Institute MA Immuno-oncology/Autoimmune/Inflammatory
35. Han Sangyeul Cell Signaling Technology MA Immuno-oncology/Autoimmune/Inflammatory
36. Ho Seok-Man 호석만 Icahn School of Medicine at Mount Sinai NY Respiratory/metabolic/cardiovascular/Neurogenerative
37. Hong Peter 홍성원 Regeneron Pharmaceuticals NY PK/PD/pre-clinical/Clinical Science:
38. Huh Jeongho 허정호 Greencross Corp. KR
39. Hwang So-Young 황소영 Genosco MA
40. Hwang Ji Young 황지영 Geisel School of Medicine at Dartmouth NH Immuno-oncology/Autoimmune/Inflammatory
41. Hwang Soo Seok 황수석 Yale University School of Medicine CT Immuno-oncology/Autoimmune/Inflammatory
42. Hwang Seongwoo 황성우 PTC Therapeutics NJ Chemistry
43. Hyun Grace 현은지 MCPHS University MA Pharmacy
44. IM WEON BIN 임원빈 DONGA ST KR Chemistry
Last Name
First Name Korean Affiliate Area Group Discussion
45. Im Eunju 임은주 Nathan S. Kline Institute, NYU Medical center NY Respiratory/metabolic/cardiovascular/Neurogenerative
46. In Hwa Chung 정인화 Sungwun pharmacopia KR Immuno-oncology/Autoimmune/Inflammatory
47. JEONG HEE-JIN 정희진 Dana-Farber Cancer Institute MA
48. JEONG HEYKYEONG 정혜경 Temple University PA Respiratory/metabolic/cardiovascular/Neurogenerative
49. Jeong Jae Uk 정재욱 GSK PA BD/Legal/VC:
50. Jin Joon Yung 진준영 CJ CheilJedang MA BD/Legal/VC:
51. Jo Seunghee 조승희 Agios Pharmaceuticals MA Cell and Gene Therapy/Viral infection/Rare disease
52. Jo Hakryul Agios Pharmaceutical Inc. MA Cell and Gene Therapy/Viral infection/Rare disease
53. Joh Nathan Amgen CA
54. Jung Young Chun 정영춘 Zafgen Inc. MA Chemistry
55. Kang Unbeom 강운범 Dana-Farber Cancer Institute MA PK/PD/pre-clinical/Clinical Science:
56. Kang Young Bok 강영복 Mass General Hospital MA Immuno-oncology/Autoimmune/Inflammatory
57. Kang Pilsoo 강필수 Genzyme MA Cell and Gene Therapy/Viral infection/Rare disease
58. Kang Jungwook 강정욱 Rutgers Univ. School of Pharmacy NJ Pharmacy
59. Kang Jin Young 강진영 Rockefeller University NY Immuno-oncology/Autoimmune/Inflammatory
60. Ki Dong Hyuk 기동혁 Dana-Farber Cancer Ins./Harvard M. S. MA
61. Kim Ah Ram 김아람 Boston Children's Hospital MA Cell and Gene Therapy/Viral infection/Rare disease
62. Kim Alexander 김지혁 Boston College MA Pharmacy
63. Kim Hyungchul 김형철 Novartis MA
64. KIM Paul T. Foley Hoag LLP DC BD/Legal/VC:
65. Kim Younghoon 김영훈 Sanofi-Genzyme MA Cell and Gene Therapy/Viral infection/Rare disease
66. Kim Jungeun 김정은 MCPHS university MA Pharmacy
67. Kim Minji 김민지 Curis, Inc MA BD/Legal/VC:
68. Kim YeonJin 김연진 Harvard School of Dental Medicine MA Immuno-oncology/Autoimmune/Inflammatory
69. Kim Eunkyung 김은경 Genosco MA PK/PD/pre-clinical/Clinical Science:
70. Kim Judith Rubin and Rudman LLP MD BD/Legal/VC:
71. Kim Jong-Gyun 김종균 Yuhan Corporation KR Immuno-oncology/Autoimmune/Inflammatory
72. KIM BUMJUN 김범준 Northeastern University MA Pharmacy
73. Kim Jia 김지아 Stony Brook University NY Cell and Gene Therapy/Viral infection/Rare disease
74. Kim Junil 김준일 University of Pennsylvania PA Cell and Gene Therapy/Viral infection/Rare disease
75. Kim Sung ki 김성기 MCPHS university MA Pharmacy
76. Kim Yongmin 김용민 MCPHS Pharmacy MA Pharmacy
77. Kim Sahee 김사희 RevHealth NJ Pharmacy
78. Kim Sehoon 김세훈 Merck MA Immuno-oncology/Autoimmune/Inflammatory
79. Kim Mi-Sook 김미숙 Takeda MA
80. Kim Sung-Kwon 김성권 Alexion Pharmaceuticals CT Immuno-oncology/Autoimmune/Inflammatory
81. Kim Dae-Shik 김대식 Eisai Inc MA Chemistry
82. KIM KYOUNGTAE 김경태 Nieman Foundation of Journalism HARVARD MA Immuno-oncology/Autoimmune/Inflammatory
83. kim Youngjin 김영진 rockefeller university NY Pharmacy
84. Kim Joonyul 김준열 Proximity Biosciences LLC AL BD/Legal/VC:
85. Kim Han-Joo 김한주 Yuhan Corporation
OTHER
Respiratory/metabolic/cardiovascular/Neurogenerative
86. Kim Youngsun 김영선 Adello Biologics NJ BD/Legal/VC:
87. Kim Hai-Young 김혜영 Merck MA Immuno-oncology/Autoimmune/Inflammatory
88. Kim Leo Incyte Corporation DE Immuno-oncology/Autoimmune/Inflammatory
89. Kim Jisu 김지수 Massachusetts college of pharmacy MA Pharmacy
90. Kim Min-woo 김민우 Zafgen Inc. NJ Chemistry
91. Kim Young Woo 김영우 Access Bio NJ Immuno-oncology/Autoimmune/Inflammatory
Last Name
First Name Korean Affiliate Area Group Discussion
92. Kim Jae-Hun 김재훈 IFF NJ Chemistry
93. Kim Bae-Hoon 김배훈 HHMI at Yale School of Medicine CT Cell and Gene Therapy/Viral infection/Rare disease
94. KOH JONG SUNG 고종성 GENOSCO MA BD/Legal/VC:
95. Koo Jaseok Yale School of Medicine CT
96. Kwon Byungsu 권병수 MIT chemistry MA Chemistry
97. Kwon Jason 권재혁 Indiana University School of Medicine IN Cell and Gene Therapy/Viral infection/Rare disease
98. Kwon Sam 권상열 Vesta Pharmaceuticals, Inc. IN
99. Kwon Hokeun 권호근 Harvard Medical School MA Immuno-oncology/Autoimmune/Inflammatory
100. Kwon Eunjeong 권은정 MGH MA
101. Lee Young Eun 이영은 Monell Chemical Senses Center PA Chemistry
102. Lee Hyun-Hee 이현희 Merck MA Immuno-oncology/Autoimmune/Inflammatory
103. Lee Myung Yeol 이명렬 Amolifescience KR Cell and Gene Therapy/Viral infection/Rare disease
104. Lee Hak-Myung 이학명 Shire MA
105. Lee Dooyoung 이두영 Applied BioMath MA PK/PD/pre-clinical/Clinical Science:
106. Lee Jeongwook 이정욱 Wyss Institute, Harvard University MA Immuno-oncology/Autoimmune/Inflammatory
107. Lee Jongsoon 이종순 Joslin Diabetes Center/Harvard M Medical School MA Respiratory/metabolic/cardiovascular/Neurogenerative
108. Lee Sam 이상엽 CRScube America Inc. MD BD/Legal/VC:
109. Lee Kyungjin 이경진 STP America Research NJ Chemistry
110. Lee HeaYeon 이혜연 Northeastern University NY Respiratory/metabolic/cardiovascular/Neurogenerative
111. LEE JAEKYOO 이재규 GENOSCO MA BD/Legal/VC:
112. Lee Joonsoo 이준수 Shire MA
113. Lee Tae Gyu 이태규 Osong New Drug Development Center KR Immuno-oncology/Autoimmune/Inflammatory
114. Lee James Jungkue 이정규 Bridge Biotherapeutics, Inc KR BD/Legal/VC:
115. Lee Hwaseong 이화성 Samyang Biopharmaceuticals Corp. KR
116. Lee Seung-Mi 이승미 Rutgers University NJ Pharmacy
117. Lee Seungkyu 이승규 Boston children's hospital MA Respiratory/metabolic/cardiovascular/Neurogenerative
118. Lim Sungtaek 임성택 Sanofi Pharmaceuticals MA Chemistry
119. Lim Hyungwook 임형욱 Novartis MA Immuno-oncology/Autoimmune/Inflammatory
120. Lim Hanjo 임한조 Genentech CA PK/PD/pre-clinical/Clinical Science:
121. Ma Sunghoon 마성훈 Exelixis CA Chemistry
122. Moon Ji Yoon 문지윤 MCPHS Worcester MA Pharmacy
123. Moon Young-Choon 문영춘 PTC Therapeutics NJ Chemistry
124. Nam Gyeongsug 남경숙 Daewoong pharmaceutical company KR Immuno-oncology/Autoimmune/Inflammatory
125. Nam Spencer 남성한 SV Investment Corporation MA
126. Oh Chris Chigon 오치곤 ENVIGO KR PK/PD/pre-clinical/Clinical Science:
127. Oh Hyungsuk 오형석 Harvard Medical School MA Cell and Gene Therapy/Viral infection/Rare disease
128. Paik Ik-Hyeon 백익현 WAVE Life Sciences, Inc. MA Cell and Gene Therapy/Viral infection/Rare disease
129. Park Soo-Hee 박수희 Novartis MA Respiratory/metabolic/cardiovascular/Neurogenerative
130. Park Sangho 박상호 Merck & Co MA Immuno-oncology/Autoimmune/Inflammatory
131. Park Angie Inkyung 박인경 OncoMed Pharmaceuticals CA Immuno-oncology/Autoimmune/Inflammatory
132. Park Daniel 박종호 Rutgers University NJ Pharmacy
133. PARK JAHA 박자하 Boston University MA BD/Legal/VC:
134. Park JiYoung 박지영 Rutgers University NJ Pharmacy
135. Park Jinkyu 박진규 Internal Medicine, Yale University CT
136. Park Keun Woo 박근우 burke-cornell medical research institute NY Respiratory/metabolic/cardiovascular/Neurogenerative
137. Park Jeehae 박지혜 Harvard Medical School MA Cell and Gene Therapy/Viral infection/Rare disease
138. PARK SUNGHO 박성호 SVinvestment KR
Last Name
First Name Korean Affiliate Area Group Discussion
139. Park YoungSeoub 박영섭 Green Cross KR Immuno-oncology/Autoimmune/Inflammatory
140. Park Jihoon 박지훈 National Institutes of Health MD Immuno-oncology/Autoimmune/Inflammatory
141. Park Min 강민 STP America Research NJ
142. Park Jeonghan 박정한 STP America Research NJ Chemistry
143. Park Hee Dong 박희동 LG Chem, Life Science BU KR Respiratory/metabolic/cardiovascular/Neurogenerative
144. Park Dong Ho 박동호 Massachusetts Eye and Ear Infirmary MA Immuno-oncology/Autoimmune/Inflammatory
145. Park Seung-Yeol 박승열 BWH MA Immuno-oncology/Autoimmune/Inflammatory
146. Park Jiyoung 박지영 University of Pennsylvania PA Cell and Gene Therapy/Viral infection/Rare disease
147. Park Jonghoon 박종훈 Life Sciences Company, LG Chem KR Immuno-oncology/Autoimmune/Inflammatory
148. Park Jaehong 박재홍 Takeda Oncology MA Immuno-oncology/Autoimmune/Inflammatory
149. Rhu Hong Yeol 류홍열 Yale University CT
150. Shim Jaehoon 심재훈 Boston children's hospital MA Cell and Gene Therapy/Viral infection/Rare disease
151. Shin Jaeyoun 신재윤 Columbia University NY Chemistry
152. Shin Baehyun 신배현 MGH/Harvard Medical School MA Respiratory/metabolic/cardiovascular/Neurogenerative
153. Shin Seung-Wook 신승욱 L&J Biosciences, Inc MD Respiratory/metabolic/cardiovascular/Neurogenerative
154. Shin Hyunjin 신현진 Takeda MA
155. Song HoJuhn 송호준 Genosco MA Immuno-oncology/Autoimmune/Inflammatory
156. Song JK 송정근 L&J Bioscience MD PK/PD/pre-clinical/Clinical Science:
157. Suh Hyunsuk 서현석 Pfizer MA
158. Suh Kathryn MCPHS NJ Pharmacy
159. Suh Byung-Chul 서병철 GENOSCO MA Chemistry
160. Suh K. Stephen Hackensack Meridian Health NJ Cell and Gene Therapy/Viral infection/Rare disease
161. suh Sandy Exeltis NJ Immuno-oncology/Autoimmune/Inflammatory
162. Sung Moo Je 성무제 Novartis MA Chemistry
163. Um Moonkyoung 엄문경 law firm MA BD/Legal/VC:
164. Won Yougun 엄유근 Harvard Medical School MA BD/Legal/VC:
165. Won Kwang-Ai 원광애 LG Chem Life Science R&D CA Immuno-oncology/Autoimmune/Inflammatory
166. Woo Jonghye 우종혜 MGH MA Respiratory/metabolic/cardiovascular/Neurogenerative
167. Yang Eun-Jin 양은진 Decision Resources Group MA BD/Legal/VC:
168. Yang Garp Yeol 양갑열 STP America Research NJ
169. Yang Hanseul 양한슬 The Rockefeller University NY Cell and Gene Therapy/Viral infection/Rare disease
170. Yi B. Alexander 이병두 Novartis MA Respiratory/metabolic/cardiovascular/Neurogenerative
171. Yi Michael 이용민 Celerion Inc. KR PK/PD/pre-clinical/Clinical Science:
172. yim yeong shin 임영신 MIT MA Respiratory/metabolic/cardiovascular/Neurogenerative
173. Yoon Seongkyu 윤성규 University of Massachusetts Lowell MA Cell and Gene Therapy/Viral infection/Rare disease
174. Yoon Chan 윤석찬 Rutgers University NJ Pharmacy
175. Yoon Taeyoung 윤태영 Dong-A ST KR
176. Yoon Derek 윤동민 Aju IB Investment MA BD/Legal/VC:
177. You Kwontae 유권태 Broad Institute MA Immuno-oncology/Autoimmune/Inflammatory
178. You Dahea 유다혜 Rutgers University NJ PK/PD/pre-clinical/Clinical Science:
179. Yu Mikyung 유미경
Brigham and Women's Hospital/ Havard Medical School
MA
180. Yun Esther 윤예진 University of Calgary CA Cell and Gene Therapy/Viral infection/Rare disease
181. Yun Jeong-Ho 윤정호 YPSO-FACTO MA Chemistry