Shuji Ogino

Associate Professor in the Department of Epidemiology

Department of Epidemiology

The Molecular Pathological Epidemiology Laboratory (The MPE Laboratory)

 

The Second International Molecular Pathological Epidemiology (MPE) Meeting

December 4-5, 2014

 Jimmy Fund Auditorium of Dana-Farber Cancer Institute (DFCI) in Boston, MA, USA

Please Register for this free, open meeting at this site (The MPE Lab Site at DFCI)

http://ogino-mpe-lab.dana-farber.org/

Agenda is also updated at this site.

http://www.globaleventslist.elsevier.com/events/2014/12/2nd-international-molecular-pathological-epidemiology-mpe-meeting/

  

Now “Molecular pathological epidemiology” is in Wikipedia.

http://en.wikipedia.org/wiki/Molecular_pathological_epidemiology

 

Research position available

I am seeking candidates for a position in my laboratory at Dana-Farber Cancer Institute, Harvard School of Public Health, Brigham and Women’s Hospital, and Harvard Medical School, in Boston, MA, USA.  I am currently the only one faculty member who holds appointments in both Department of Pathology (Harvard Medical School) and Department of Epidemiology at Harvard.  A position may be a postdoctoral fellow, technician or research assistant (either full-time or part-time), and whoever fits to this position may start soon or in the future.  My laboratory is The “Molecular Pathological Epidemiology” (MPE) Laboratory, which is a very unique, interdisciplinary multi-institutional laboratory. MPE is the emerging scientific field which I recently established as a distinct field (Ogino et al. J Natl Cancer Inst 2010; Ogino et al. Gut 2011; Ogino et al. Nat Rev Clin Oncol 2011; Field et al. JAMA 2013; etc).  We have been working on colorectal cancer, colorectal adenoma and polyp, pancreatic cancer, gastric cancer, and gastrointestinal neuroendocrine tumors.  For more information, please see below.  For postdoc candidates, I broadly seek candidates with background in pathology, epidemiology, biostatistics, bioinformatics, computational biology, molecular biology, and clinical medicine. Candidates with funding support will be highly considered. Our recent papers include R Nishihara et al. NEJM 2013; X Liao et al. NEJM 2012; E Barry et al. Nature 2013; R Straussman et al. Nature 2012; R Nishihara et al. JAMA 2013; ZR Qian et al. J Clin Oncol 2013; S Ogino et al. J Natl Cancer Inst 2013; A Kuchiba et al. J Natl Cancer Inst 2012; T Morikawa et al. JAMA 2011; T Morikawa et al. Cancer Res 2013; etc.   Please email me (sogi43@gmail.com) your CV or any inquiry.  Please pass this information to anyone who may be interested.  Please pardon me if I cannot reply to you because of too many responses or inquiries.

 

Research Theme 

Our research has two intersecting scientific themes.  One is scientific disciplinarity and the other is a focus on specific diseases (colorectal carcinoma, colorectal polyp, colorectal adenoma, pancreatic adenocarcinoma, neuroendocrine tumor, pancreatic endocrine tumor, carcinoid tumour).  Other diseases are studied on collaborative basis (esophageal carcinoma, gastro-esophageal GE junction carcinoma, Barrett’s esophagus) or on theoretical basis [non-neoplastic diseases such as obesity, inflammatory bowel diseases (IBD), ulcerative colitis, Crohn's disease, etc].  Our research is interdisciplinary, transdisciplinary and multidisciplinary in nature.  We are developing several emerging fields of biomedical and population health sciences, generating novel concepts, paradigms and research frameworks.  Please contact me (shuji_ogino[at]dfci.harvard.edu) if you are interested in collaborating with me in following emerging disciplines.

 

EMERGING SCIENTIFIC DISCIPLINES:

Molecular Pathological Epidemiology (MPE) (first described in S Ogino and M Stampfer. J Natl Cancer Inst 2010).  Please see further below for more detail.

Immuno-MPE (Immuno-epidemiology, immunoepidemiology, immuno-prevention, immunoprevention) is an integrative field of immunology and MPE for prevention and treatment of many diseases.  Innate and adaptive immunity plays major roles in human health and diseases including cancer.  The journal Science selected cancer immunotherapy as “the Breakthrough of the Year for 2013″.  Utilizing anti-tumor immunity is a promising strategy with definite advantages; our immune system can adapt enemies – tumor cells which are molecularly heterogeneous even intra-personally.  Recent studies show that the immune checkpoint mechanism such as the CTLA4 (CTLA-4) and PDCD1 (programmed cell death 1, PD-1) pathways can be blocked to treat multiple malignancies.  Experimental evidence also indicates a role of tumor metabolic alterations including upregulation of IDO1 (IDO), TDO2 (TDO) and ARG1, in evading host immune surveillance; hence, targeting tumor metabolic alterations may offer another mean for immunotherapy.  While immunotherapy is under intense investigation, strategies to prevent cancer through immune modulators (“immuno-prevention”) are also promising.  Diet and lifestyle can be routine immunoprevention strategy, since evidence indicates that modifiable factors such as vitamin D, ω-3 polyunsaturated fatty acid (PUFA) intake, physical activity, and aspirin use can influence not only cancer risk but also host immunity.  Thus, we need to consider environmental exposures, tumor molecular features and host immunity in cancer.  Although CRC has so far exhibited lack of response to checkpoint blockade by anti-CTLA4, anti-PDCD1 and anti-CD274 (PD-L1, programmed cell death 1 ligand 1) antibodies, we and others have shown that immune response to CRC is associated with better survival, and can be linked to specific molecular features such as microsatellite instability (MSI).  To harness host immunity for CRC prevention (e.g., lifestyle modification, cancer vaccine, etc.) and therapy, a better understanding of the key drivers of immune response / reaction to CRC is essential.  We plan to investigate many different immune cell types including helper T cell, memory T cell, regulatory T cell, cytotoxic T cell, suppressor T cell, B cell, plasma cell, natural killer cell (NK cell), other lymphocytes, myeloid derived suppressor cell (MDSC), neutrophil, eosinophil, basophil, macrophage, histiocyte, dendritic cell, etc.  We utilize our MPE analytical strategy to investigate the combined role of exposures and immunity in colorectal carcinogenesis and cancer progression.

Integrative Lifecourse Epidemiology – MPE.  Lifecourse epidemiology studies long-term effects of social and environmental exposures on health and diseases.  A key challenge in the models of lifecourse epidemiology is translating its empirical evidence into intervention planning especially among populations where the critical social and environmental exposures happened in the past or they are difficult to intervene.  Investigating molecular heterogeneity of disease and disease development process can help epidemiologists to identify modifiable factors at the ongoing disease development process caused by early-life exposures among adult populations.  The integrated model of lifecourse epidemiology and MPE can identify more effective interventions and the more appropriate timing in primary prevention.  When we are asked to plan a health promotion program for the community population, we need to identify the factors currently modifiable in the target population at any levels (i.e. from molecular and cellular to individual, to societal) in relation to the ongoing molecular pathological change.  The integrated model of lifecourse epidemiology and MPE can help us to accomplish this.

Integrative Social Epidemiology – MPE.  The MPE-based approach (e.g. molecular diagnostics and molecularly-targeted intervention) can potentially increase health disparity.  The interdisciplinary integration of MPE and social epidemiology can efficiently address the global cancer disparity together with molecular pathological insights.  This social-MPE integration may enable us to better understand biological consequences of unique personal life stories interacted with social environments at the molecular pathological level, and to identify better, fairer, and feasible intervention plans of socio-behavioral change and treatment.

Integrative Causal Inference – MPE.  Causal inference and MPE share a common goal of elucidating causality in the association between exposure and disease, and can synergize by virtue of complementary strengths of each field.  Mendelian randomization (MR) has been used in causal inference, and utilizes a genetic marker as an instrumental variable.  A genetic marker such as SNP may have effects on expression and/or function of the gene or neighboring genes.  Analysis of possible downstream consequences of the genetic variant may shed lights on pathogenic role of the variant.  Practically, molecular pathologic features of disease can be examined and fully integrated into MR design or any other causal inference models.

Integrative MPE – Health Communication Research (HCR).  The social-MPE integration can link social and behavioral factors to molecular signatures of cancer.  However, it remains to be a challenge to actually change behavior of each individual based on evidence.  The field of health communication is the study and practice of communicating health information (such as in public health campaigns, health education, and daily medical practice), and has recently been growing.  The purpose of disseminating health information is to influence personal health choices by improving health literacy.  Because effective health communication must be tailored for the audience and the situation, health communication research seeks to refine communication strategies to inform people about ways to enhance health and to avoid health risks.  MPE research has strengths of linking behavioral factors to molecular signatures of disease, and can work synergistically with health communication research to implement behavioral intervention tailored to individuals based on disease susceptibilities.


Integrative MPE – Comparative Effectiveness Research (CER)
.  The purpose of CER is to improve health care at both the individual and population levels by assisting in informed decision making.  As MPE indicates, each individual has unique susceptibilities to various diseases, and each patient has unique features of disease.  Essentially, a population consists of uniquely different individuals.  Hence, CER must assess impacts of this fundamental unique nature of individual and disease.  In MPE, molecular signatures of disease are used to subgroup patients based on similarities.  However, biological similarities which justify disease molecular subtyping may not be directly translated into similarities of effectiveness of intervention.  Hence, CER is needed when MPE research findings are utilized to maximize both efficacy and effectiveness in clinical medicine and public health.

 

Rationale, strengths and challenges of MPE

The relationship between exposures and molecular changes in tumors has been examined for decades (eg, smoking -> KRAS mutation), usually under the umbrella of “molecular epidemiology”.  However, this type of analysis needs a consideration of disease heterogeneity (eg, KRAS mutation present vs. absent), which necessitates a paradigm shift from conventional epidemiology.  Conventional epidemiology is based on the premise that individuals with a given disease (by name) are homogeneous and can be lumped together to analyze exposure associations.

 

Considering this paradigm shift, “Molecular Pathological Epidemiology (MPE)” (or Molecular Pathologic Epidemiology) has been coined for integrative (interdisciplinary and transdisciplinary) science (Ogino et al. J Natl Cancer Inst 2010; Ogino et al. Gut 2011; Ogino et al. Nat Rev Clin Oncol 2011; Ogino et al. Int J Epidemiol 2012; Ogino et al. Am J Epidemiol 2012).  MPE is conceptually defined as “epidemiology of molecular pathology and heterogeneity of disease” (Ogino et al. Oncogene 2014).  MPE encompasses ALL HUMAN DISEASES (Ogino et al. Mod Pathol 2013), and MPE research can be done in any epidemiology cohorts.  MPE of non-neoplastic diseases (such as obesity) is a possible future research area (Field et al. JAMA 2013).  I have been advancing the MPE field as the first “Molecular Pathological Epidemiologist (MPE-ist)” (Ogino et al. Am J Epidemiol 2012).  The power and promise of MPE has been well attested by our recent studies (eg, Morikawa et al. JAMA 2011; Liao et al. N Engl J Med 2012; Nishihara et al. JAMA 2013; Nishihara et al. N Engl J Med 2013, etc.).  As I am a unique faculty in pathology (Harvard Medical School) and epidemiology (Harvard School of Public Health), my long-term goal is to transform pathology and epidemiology into an integrative science for both education and research.

 

In MPE, we try to dissect complex interrelationship between; (1) environmental, dietary, lifestyle and genetic factors; (2) alterations in the tumor microenvironment and cellular molecules; and (3) disease pathways and evolution.  MPE encompasses all human diseases (most of which are complex multifactorial diseases), and takes into account genome, epigenome, methylome, transcriptome, proteome, metabolome, microbiome, metagenome, reactome, and interactome.  MPE is based on the “Unique Tumor Principle” (Ogino et al. Expert Rev Mol Diagn 2012) and more broadly, the “Unique Disease Principle” (Ogino et al. Mod Pathol 2013).  MPE design can be used as the next step of genome-wide association study (GWAS) (“GWAS-MPE Approach”; Ogino et al. Gut 2011; Garcia-Albeniz et al. Carcinogenesis 2013; Nan et al. J Natl Cancer Inst in press).  Other new concepts related to MPE include “Colorectal Continuum Paradigm / Theory / Hypothesis” (Yamauchi, Morikawa, et al. Gut 2012; Yamauchi, Lochhead, et al. Gut 2012), which underscores the importance of interplay of gut microbiota, host factors (diet, immunity, inflammation, etc.), and carcinogenesis.  This novel “Colorectal Continuum Paradigm” has a considerable impact on gastrointestinal research and clinical practice.  The “Etiologic Field Effect” (EFE) concept (Lochhead et al. Mod Pathol 2014) is an expansion of the conventional “field effect” paradigm, considering contribution of the exposome from environment as well as the interactome in the tumor microenvironment.  EFE is applicable to all steps of cancer evolution, while the traditional notion of fied effect only considers early phases of neoplasia.

 

The MPE paradigm has been in widespread use; e.g., Curtin et al. Pathol Res Int 2011; Hughes et al. PLoS ONE 2011; R Jacobs et al. Curr Opin Pharmacol 2012; Hughes et al. Int J Epidemiol 2012; Ku et al. Mod Pathol 2012; Rex et al. Am J Gastroenterol 2012; Koshiol et al. Ann Epidemiol 2012; Chia et al. Nat Rev Clin Oncol 2012; Spitz et al. Cancer Discovery 2012; Galon et al. J Tranl Med 2012; Rosty et al. Mod Pathol 2013; Lam et al. Cancer Epidemiol Biomarkers Prev 2013; Weijenberg et al. Curr Nutr Rep 2013; Buchanan et al. Cancer Epidemiol Biomarkers Prev 2013; Burnett-Hartman et al. Cancer Res 2013; Alvarez et al. World J Gastroenterol 2013; Hagland et al. Dig Surg 2013; Zaidi et al. Prog Lipid Res 2013; Hughes et al. Cancer Res 2013; Abbenhardt et al. Int J Mol Epidemiol Genet 2013; J Bae et al. Brit J Cancer 2013; Amirian et al. Infectious Agents and Cancer 2013; Ikramuddin and Livingston. JAMA 2013; Hoffmeister et al. Cancer Epidemiol Biomarkers Prev 2013; RF Araujo et al. Pathol Res Pract 2013; MM Esterhuyse et al. Expert Rev Mol Diagn 2013; Y Zhu et al. Brit J Cancer 2014; NJ Shaheen Am J Gastroenterol 2014; HR Hagland, et al. Cancer Lett 2014; J Brandstedt et al. BMC Cancer 2014; F Coppedè. Expert Rev Gastroenterol Hepatol 2014; F Bishehsari et al. World J Gastroenterol 2014; AJ Cross et al. Cancer 2014; BM Ryan et al. Cancer Epidemiol 2014; NL Bragazzi. Omics Group eBooks 2014; T Mikeska et al. Genes 2014; P Li, H Wu, et al. Gut 2014. 

MPE has been a topic in international meetings such as those of American Association for Cancer Research (AACR), Society for Epidemiology Research (SER), and American Society for Preventive Oncology (ASPO) (L Kuller et al. Am J Epidemiol 2013; M Epplein et al. Cancer Epidemiol Biomarkers Prev 2014).

 

 

We have been utilizing comprehensive MPE databases of two U.S. nationwide prospective cohort studies, the Nurses’ Health Study (N=121,000 followed since 1976) and the Health Professionals Follow-up Study (N=51,500 followed since 1986), as well as CALGB trials (Alliance for Clinical Trials in Oncology).  Our discoveries by the MPE approach include (to mention just several); influence of the tumor microenvironment on tumor phenotype (Straussman et al. Nature 2012); YAP1 (yes-associated protein 1; or YAP) in colorectal cancer (Barry et al. Nature 2013); Interaction between aspirin use and PIK3CA mutation in colorectal cancer (Liao et al. N Engl J Med 2012, which is replicated by Domingo et al. J Clin Oncol 2013); interactions between aspirin use and PTGS2 (cyclooxygenase-2, COX-2) expression in colorectal cancer (Chan et al. N Engl J Med 2007; Chan et al. JAMA 2009); aspirin use and BRAF mutation in colorectal cancer (Nishihara et al. JAMA 2013); endoscopy screening and post-colonoscopy colorectal cancer with CIMP and microsatellite instability MSI (Nishihara et al. N Engl J Med 2013); interactions between obesity (host energetics) and FASN (fatty acid synthase) expression in colorectal cancer (Ogino et al. J Clin Oncol 2008; Kuchiba et al. J Natl Cancer Inst 2012); interactions between host energetics and CTNNB1 (b-catenin) activation in colorectal cancer (Morikawa et al. JAMA 2011; Morikawa et al. Cancer Res 2013); LINE-1 (long interspersed nucleotide element-1) hypomethylation and colon cancer aggression (Ogino et al. J Natl Cancer Inst 2008) and colorectal cancer family history (Ogino et al. J Natl Cancer Inst 2013); one-carbon nutrients, alcohol and colon cancer risk according to TP53 (p53) status and LINE-1 methylation level (Schernhammer et al. Gastroenterology 2008; Schernhammer et al. Gut 2010); fusobacterium (microbiota) in colorectal cancer (Kostic et al. Genome Res 2012); CDK8 in colorectal cancer (Firestein et al. Nature 2008; Firestein et al. Int J Cancer 2010); VTI1A-TCF7L2  fusion (translocation) in colorectal cancer (Bass et al. Nat Genet 2011).  In summary, a better understanding of heterogeneity of carcinogenic processes and influences of exogenous and endogenous factors will further contribute to personalized prevention and treatment strategies.

 

To transform pathology and epidemiology by the integrative MPE field and concept, I recently launched three programs.  (1) The MPE Working Group (MPE WG) aims to establish standardized methodologies in MPE research.  The MPE WG currently consists of researchers in the MPE areas, including biostatistics experts such as Drs. Donna Spiegelman, Molin Wang and Bernard Rosner.  (2) International MPE Meeting (Molecular Pathological Epidemiology Meeting) aims to gather selected experts and discuss ways to advance this transdisciplinary science.  The first meeting in Boston on April 24, 2013 (my birthday) went very successfully.  The Second International MPE Meeting will be held in Boston (tentatively on December 4-5, 2014), to host a larger group of both epidemiologists and pathologists.  (3) The “STROBE-MPE” initiative (Ogino et al. Am J Epidemiol 2012) is an extension of STROBE, which stands for “STrengthening of the Reporting of OBservational Epidemiology” (von Elm et al. PLoS Med 2007), and is an international guideline for epidemiology research.  I always call for collaboration in this STROBE-MPE international initiative.  In addition, (4) I am a member of Education and Professional Development Committee (chaired by Dr. Jay Kaufman) of Society for Epidemiologic Research (SER) to address paucity of interdisciplinary education opportunities.  MPE was one of highlights in recent SER Meeting in 2013 (Kuller et al. Am J Epidemiol 2013; AJE Symposium Proceeding).

 

Another focus of my research (which is very much related to MPE) is epigenetics and epigenomics of colorectal cancer.  We have found that LINE-1 hypomethylation in colorectal cancer is associated with shorter survival (Ogino et al. J Natl Cancer Inst 2008), family history of colorectal cancer (Ogino et al. J Natl Cancer Inst 2013) and young age of onset (Baba et al. Mol Cancer 2010); and that it is preventable by high folate (leafy vegetables) and low/no alcohol intakes (Schernhammer et al. Gut 2010).  I have been characterizing the CpG island methylator phenotype (CIMP), a unique molecular phenotype in colorectal cancer.  My investigation led to the discovery of “CIMP-low (CIMP-L)” associated with KRAS mutation (Ogino et al. J Mol Diagn 2006), which has been confirmed by other investigators including Peter Laird’s group (Hinoue et al. Genome Res 2012).  We were the first to apply “structural equation modeling (SEM)” to epigenetic and genetic correlation structure analysis (Tanaka et al. Am J Pathol 2010).  We have been deciphering prognostic roles of CIMP, MSI, KRAS, BRAF and PIK3CA mutations, and immune reactions in colorectal cancer (Ogino et al. J Clin Oncol 2009; Ogino et al. Gut 2009; Ogino et al. Clin Cancer Res 2009; Nosho et al. J Pathol 2010; Ogino et al. Clin Cancer Res 2012; Liao et al. Clin Cancer Res 2012; Imamura et al. Clin Cancer Res 2012; Lochhead et al. J Natl Cancer Inst 2013; Ogino et al. J Natl Cancer Inst 2013).

 

Disease areas:  We focus on colorectal cancer and precursors (colon carcinoma, rectal carcinoma, adenocarcinoma, colon cancer, rectal cancer, anal cancer, aberrant crypt foci, hyperplastic polyp, sessile serrated adenoma, sessile serrated polyp, traditional serrated adenoma, tubular adenoma, tubulovillous adenoma, villous adenoma, high-grade dysplasia, intramucosal carcinoma, hamartoma, hamartomatous polyp, neoplasm, neoplasia, mixed polyp, etc.).  I am Advisor of Lower GI Panel of American Joint Commission on Cancer (AJCC) which makes colon and rectal cancer staging system.  We also investigate pancreatic cancer, neuro-endocrine tumor, carcinoid tumour, gastric carcinoma, gastroesophageal (GE) junction carcinoma, and other upper GI cancers in our collaborations.  In theoretical projects, we also deal with other cancers including leukemia, lymphoma, Hodgkin lymphoma, myeloma, myelodysplastic syndrome, sarcoma, melanoma, brain tumor, glioma, glioblastoma, astrocytoma, lung cancer, breast cancer, prostate cancer, liver cancer, hepatocellular carcinoma, gallbladder cancer, head and neck cancer, ovarian cancer, endometrial cancer, uterine cervical cancer, renal cell carcinoma, other kidney cancer, bladder cancer, and non-neoplastic diseases, including obesity, cardiovascular diseases, autoimmune diseases, inflammatory diseases, inflammatory bowel diseases, ulcerative colitis, Crohn’s disease, infectious diseases, neurological diseases, psychiatric diseases, ie, all kinds of human diseases and health conditions.  MPE can address disease and pathogenic heterogeneity across all illnesses

 

Education

1993 (MD) University of Tokyo

2001 (PhD) University of Tokyo

2010 (MS in Epidemiology) Harvard School of Public Health

 

Hospital and academic appointments, and other roles

1995-1997     Resident in Pathology, Allegheny General Hospital, Drexel University, Pittsburgh, PA

1997-1999     Resident in Pathology, Case Western Reserve University, Cleveland, OH

1999-2001     Molecular Pathology Fellow and Postdoctoral Fellow, University of Pennsylvania

2001-2004     Instructor in Pathology, Harvard Medical School, and Dana-Farber Cancer Institute

2001-              Pathologist, Brigham and Women’s Hospital, Boston, MA

2003-              Member, Cancer Epidemiology Program, Dana-Farber / Harvard Cancer Center

2003-              Member, Gastrointestinal Malignancies Program, Dana-Farber / Harvard Cancer Center

2004-2008     Assistant Professor of Pathology, Harvard Medical School, and Dana-Farber Cancer Institute

2008-              Associate Professor of Pathology, Harvard Medical School, and Dana-Farber Cancer Institute

2012-              Associate Professor, Department of Epidemiology, Harvard School of Public Health

2012-              Head, The Molecular Pathological Epidemiology Laboratory (The MPE Lab)

2012-              Leader, Molecular Pathological Epidemiology (MPE) Working Group

2013-              Chairperson, International Molecular Pathological Epidemiology (MPE) Meeting Series

 

Awards and Honors

2004 Executive Officer’s Award, from Association for Molecular Pathology (AMP)

2011 Ramzi Cotran Young Investigator Award, from United States and Canadian Academy of Pathology (USCAP)

2012 Meritorious Service Award, from Association for Molecular Pathology (AMP)

2014- Elected Member, American Society for Clinical Investigation (ASCI)

2014 “The Most Influential Scientific Minds: 2014″ by Thomson Reuters

2014- Member, FASEB (Federation of American Societies for Experimental Biology) Excellence in Science Award Committee

 

Office Address

Dana-Farber Cancer Institute

450 Brookline Ave., Room M422, Boston, MA 02215

Email: shuji_ogino[at]dfci.harvard.edu

 

Administrator / Secretary:

Tracy Baker; Tel: 617-632-1972; Fax: 617-582-8558

Email: tracy_baker@dfci.harvard.edu

 

 

Members of The Ogino Lab

[The MPE Laboratory - Interdisciplinary multi-institutional Lab - Dana-Farber Cancer Institute (DFCI), Brigham and Women's Hospital (BWH), Harvard Medical School (HMS), and Harvard School of Public Health (HSPH)]

 

Instructor in Medicine (Co-Leaders)

Reiko Nishihara, PhD, RN, MW, PHN (DFCI / HMS / HSPH) (Epidemiology)

Zhi Rong Qian, MD, PhD (DFCI / HMS) (Pathology)

 

Research fellows and other trainees (background, expertise)

Ruoxu Dou, MD, PhD (DFCI / HMS) (Surgery)

Kentaro Inamura, MD, PhD (DFCI / HMS) (Liaison from/to Curtis Harris Lab, NCI / NIH) (Pathology)

Sun A Kim, MD, PhD (DFCI / HMS) (Pathology)

Ting-Ting Li, MD (DFCI / HMS) (Gastroenterology)

Atsuhiro Masuda, MD, PhD (DFCI / HMS) (Gastroenterology)

Kosuke Mima, MD, PhD (DFCI / HMS) (GI Surgery)

Akihiro Nishi, MD, DrPH (Yale University / HSPH) (Liaison from Ichiro Kawachi Lab) (Social Epidemiology)

Yasutaka Sukawa, MD, PhD (DFCI / HMS) (Gastroenterology)

Juhong Yang, PhD (DFCI / HMS) (Endocrinology and Metabolism)

 

Associate Pathologist

Jonathan A Nowak, MD, PhD (BWH / HMS) GI Pathology Fellow and Molecular Genetic Pathology Fellow

 

Administrative and Research Assistant

Tracy Baker (DFCI)

 

Doctoral Students

Kathryn Fitzgerald, MS (HSPH ScD course in Epidemiology / Nutrition)

Akiko Hanyuda, MD (HSPH MPH (QM) course)

Mingyang Song, MD, MS (HSPH ScD course in Epidemiology / Nutrition)

 

Other Associated members

Gregory J Kirkner, MPH (BWH, Project Manager of the Nurses’ Health Study)

Kaori Sato, MS (DFCI, Biostatistician at Gastrointestinal Cancer Center)

Kana Wu, MD, PhD (HSPH, Senior Research Scientist)

Xuehong Zhang, MB, ScD (BWH/HMS, Instructor in Medicine)

Molecular Pathology Epidemiology, MD, PhD, MS (BWH, DFCI, HMS, HSPH) (Pathology and Epidemiology)

 

The Ogino Lab Alumni (past members)

Yoshifumi Baba (2008-2010); Mohan Brahmandam (2002-2006); Mami Cantor (2001-2005, 2009); Inga Dorfman (2005-2006); Kevin Golden (2009-2010); Marika Hayashi (2009-2010); Yu Imamura (2010-2013); Natsumi Irahara (2008-2009); Seungyoun Jung (2012-2013); Takako Kawasaki (2003-2008); Aya Kuchiba (2010-2013); Shoko Kure (2008-2009); Xiaoyun Liao (2010-2013); Paul Lochhead (2011-2012); Teppei Morikawa (2010-2012); Katsuhiko Nosho (2007-2010); Akiyo Ogawa (2006); Mutsuko Ohnishi (2007-2008); Ayano O’Reily (2009); Jeanne Shen (2011-2012); Sung Kwan Shin (2013-2014); Kaori Shima (2008-2011); Yuko Suemoto (2007-2008); Ruifang Sun (2011-2012); Maiko Suzuki (2010); Noriko Tanaka (Yamaguchi) (2009-2010); Saori Toyoda (2008-2009); Chong Xu (2002); Taiki Yamaji (2006); Mai Yamauchi (2010-2014); Mika Yasunari (2013-2014); Jing Zhou (2003)

 

 

Past Key Events in MPE

(March 5, 2010) Ogino and Stampfer (“Lifestyle Factors and Microsatellite Instability in Colorectal Cancer: The Evolving Field of Molecular Pathological Epidemiology” in J Natl Cancer Inst) introduced the field of “Molecular Pathological Epidemiology” in the literature.

(October 19, 2010) First invited lecture on MPE (by Shuji Ogino) outside the Harvard community, at The Jackson Laboratory Conference “Colon Cancer in Murine Models and Humans III” (Conference Chairperson, William F Dove), Bar Harbor, ME

(June 3, 2011) First invited lecture on MPE (by Shuji Ogino) outside of the USA at International Symposium on Physiology and Diseases of the Digestive Tract, Orford, QC, Canada

(March 23, 2012) First invited lecture on MPE (by Shuji Ogino) outside of North America at Seoul National University Cancer Hospital 1st Anniversary Symposium, Seoul, Korea

(April 12, 2012) First lecture on MPE, independently by another investigator (by Amanda I Phipps) at Fred Hutchinson Cancer Research Center and University of Washington, Seattle, WA

(July 3, 2012) First MPE Working Group Meeting was held at Harvard School of Public Health, Boston, MA

(August 8, 2012) First review article which mentioned MPE without citing any previous MPE article (by RJ Jacobs et al. Current Opin Pharmacol 2012;12:690-695)

(April 24, 2013) First International MPE Meeting (closed) was held in Boston, MA

(June 20, 2013) First lecture on MPE in an international epidemiology meeting (Society for Epidemiologic Research; at The AJE-Sponsored Symposium, chaired by Lewis H Kuller) in Boston, MA.  Symposium proceeding published by Kuller et al. in Am J Epidemiol 2013.

(October 29, 2013) First symposium on MPE (chaired by Shuji Ogino) (with 4 lectures by Shuji Ogino, Peter T Campbell, Celeste Leigh Pearce, and Lusine Yaghjyan, and a panel discussion) at Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research, National Harbor, MD

(November 4, 2013) First article on MPE of non-neoplastic diseases published in JAMA (Field et al. “The Merits of Subtyping Obesity: One Size Does Not Fit All”. JAMA 2013)

(February 10, 2014) “Molecular pathological epidemiology” became a stand-alone article in Wikipedia. http://en.wikipedia.org/wiki/Molecular_pathological_epidemiology