Academic Background
•1967–1973: Medical studies at the Universities of Marburg and Münster
•1973: Medical Internship
•1975: Research Assistant, Institute for Cytobiology, Münster
•1976–1983: Residency in Pathology
•1983: Board Certification in Pathology
•1984: Appointed Privatdozent (Senior Lecturer) in Pathology, University of Münster
•1987: Full Professor of Pathology, University of Münster
•1993: Professor of Pathology and Director, Institute of Pathology, University of Magdeburg
•2017: Emeritus Status

Professional Memberships
•International Skeletal Society
•German Society of Pathology
•International Academy of Pathology
•German Society for Osteology
•European Society of Pathology
•Executive Editor, Pathology Research and Practice until 2025

Presidencies
•President, German Division of the International Academy of Pathology (1997–2001)
•Congress President, German Society of Pathology (2014)

Academic Administration
•Associate Medical Director (1997–1998)
•Vice Dean, Faculty of Medicine, University of Magdeburg (1998–1999)
•Dean, Faculty of Medicine, University of Magdeburg (2000–2008)
•Member, Executive Board, Association of Medical Faculties in Germany (2008–2011)

Editorial Work
•Co-editor of the textbook General Pathology and Fundamentals of Special Pathology (Elsevier) 14th edition published in November 2023
•Executive Editor, Pathology Research and Practice until 2025

Research Focus
•Bone Tumors:
◦Conventional and molecular diagnostics
◦Translational biology
◦Clinical aspects
•Gastrointestinal Tumors:
◦Inflammation and carcinogenesis

Current positions (with position start year)
•2001: Pathologist, Brigham and Women’s Hospital
•2012: Member (Cancer Immunology Program), Dana-Farber Harvard Cancer Center
•2015: Professor of Pathology, Harvard Medical School
•2015: Professor (Epidemiology), Harvard T.H. Chan School of Public Health
•2016: Chief of Molecular Pathological Epidemiology (MPE) Program, Brigham and Women’s Hospital
•2017: Associate/Affiliate Member, Broad Institute of MIT and Harvard
•2024: Global Fellow, Institute of Science Tokyo
•2024: American Cancer Society Professor

Awards and honors
•1999: The CAP (College of American Pathologists) Foundation Scholars Award Designee
•2004: Executive Officer’s Award, Association for Molecular Pathology (AMP)
•2011: Ramzi Cotran Young Investigator Award, United States and Canadian Academy of Pathology
•2012: Meritorious Service Award, Association for Molecular Pathology (AMP)
•2014: The Most Influential Scientific Minds in 2014 by Thomson Reuters (Web of Science)
•2014-2023: Member, FASEB Excellence in Science Award Committee
•2014-present: Elected Member, American Society for Clinical Investigation (ASCI)
•2015-2022: Highly Cited Researcher by Clarivate Analytics (Web of Science)
•2015-2022: Outstanding Investigator Award, National Cancer Institute, NIH, USA
•2018: Mentor-of-the-Year Runner-up Prize, Dana-Farber Cancer Institute 
•2018: Outstanding Investigator Award, American Society for Investigative Pathology (ASIP)
•2019: Gregory Derringer Grand Rounds Lecturer at Indiana University
•2019-2021: Invited Nominator for Nobel Prize in Physiology or Medicine 2019, 2020, 2021
•2019-2025: Funded Co-Investigator, Cancer Grand Challenge Award, Cancer Research UK
•2023: The 24th Annual Kornel L. Terplan Memorial Lecturer at the University at Buffalo
•2024: Keynote Lecturer, ESMO (European Society of Medical Oncology) Congress
•2024-present: American Cancer Society Clinical Research Professor Award
•
Scientific innovations and contributions
1. Creation of molecular pathological epidemiology (MPE) as an integrative field
Leveraging my unique interdisciplinary expertise, I have created and conceptualized the transdisciplinary science of MPE (Ogino et al. J Natl Cancer Inst 2010; Gut 2011; Annu Rev Pathol 2019; Inamura et al. Gut 2022) to unleash the full potential of the integrated research approach.  Based on the paradigm of the seamlessly unified field of MPE, several new concepts and fields have emerged as below.  Without integrated expertise in molecular pathology and epidemiology, it is difficult to appreciate the true power of the MPE approach.  Hence, the value and influence of MPE tend to be underestimated. 

Our proof-of-principle project utilized the prospective cohort design including a longitudinal exposure data collection integrated with data on colorectal cancer (CRC) incidence plus tumor tissue biomarkers.  We created the prospective cohort incident-tumor biobank method (PCIBM) as explained in the next section (Ugai et al. Lancet Reg Health Eur 2025; Ogino et al., Lancet Reg Health Am, online). 

Our first prospective MPE study (Chan et al. New Engl J Med 2007) using the PCIBM successfully linked long-term aspirin use with decreased incidence of PTGS2-positive CRC and drew much attention.  As of 2025 (18 years later), no other group has been able to conduct a similar prospective analysis, attesting to the unique value of this and subsequent PCIBM-based studies of ours.  We could also link long-term excessive alcohol and low folate intake with increased incidence of LINE-1 hypomethylated CRC (Schernhammer et al. Gut 2010). In the list of my innovations below, we successfully linked high-level vitamin D status with decreased incidence of tumor-infiltrating lymphocyte (TIL)-high colorectal carcinoma (Song et al. Gut 2016). We could also link the prudent diet pattern with decreased incidence of CRC containing abundant Fusobacterium nucleatum, a putative pathogen (Mehta et al. JAMA Oncol 2017). Despite much attention that these studies drew, no other group has been able to conduct similar prospective analyses.  These PCIBM-based MPE studies that examined long-term exposures in relation to tumor incidence plus characteristics are exceptionally unique.  My contribution to these scientific innovations has been unparalleled.  In the next point #2, why examining long-term time-varying exposures is important is explained more in detail.

2. Creation of the prospective cohort incident-tumor biobank method (PCIBM)
The somatic mosaicism phenomenon indicates that all of us, including cancer-free young people, have mutant clones / preneoplasia and that tumorigenesis is a decades-long process. However, a vast majority of tumor profiling studies focus on diagnosed tumors but cannot examine long-term time-varying risk factors exposures, which play substantial roles in tumorigenesis. Such a patient-focused study design also misses a decades-long window for effective prevention. Thus, our PCIBM, which is a longitudinal prospective cohort study combined with incident tumor profiling, is very unique and powerful.

The importance of long-term influence of exposures on tumor development is increasingly recognized (Ugai et al. Nat Rev Clin Oncol 2022; Ogino et al. Ann Oncol 2024). We have built a tumor tissue biobank of CRC/precancer cases that have occurred in the Nurses’ Health Study (NHS), NHS II, and Health Professionals Follow-up Study. There were substantial challenges in establishing such a biobank, as incident tumors in the prospective cohort studies had happened in different geographic areas at variable, unpredictable time points. Our creation of the PCIBM has enabled the novel style of studies and has exerted a substantial impact.

3. Conceptualization of the GWAS-MPE approach
Although genome-wide association studies (GWAS) have revealed numerous risk loci for many diseases, a major issue of typical GWAS is that biologically and etiologically heterogeneous disease subtypes with differing risk associations are typically lumped together into one disease entity.  Hence, deep disease phenotyping, especially molecular pathological characterization, has been recognized as one of the important post-GWAS strategies. I conceptualized the GWAS-MPE approach (Ogino et al. Gut 2011) for the use of molecular pathology technologies to further investigate causal mechanisms and refine effect estimates of risks for specific disease subtypes.  We have published proof-of-concept studies (Nan et al. JNCI 2013; Garcia-Albeniz et al. Carcinogenesis 2013; Khalili et al. Carcinogenesis 2015).

4. Conceptualization of the unique tumor principle and the unique disease principle
I explicitly conceptualized the uniqueness of each tumor (Ogino et al. Expert Rev Mol Diagn 2012), which led to the unique disease principle (Ogino et al. Mod Pathol 2013). Disease processes are influenced by many factors (including exogenous exposures and endogenous factors such as genomic variation) that differ from person to person, and some of these factors can be heterogeneous from place to place across body sites, even within one individual. Hence, each disease process is unique, necessitating the precision medicine approach.

5. Integration of pharmacoepidemiology into MPE
Under the precision medicine paradigm, each patient has a unique pathologic process influenced by pharmacological, environmental, microbial, dietary, and lifestyle factors.  Hence, multi-level research methods that can comprehensively analyze many of these variables are needed.  Our integrative research enabled us to make seminal discoveries of potential benefits of aspirin to prevent and treat colorectal carcinomas with PTGS2 (cyclooxygenase-2) overexpression (Chan et al. NEJM 2007; Chan et al. JAMA 2009), PIK3CA mutations (Liao et al. NEJM 2012) and lower-level tumor CD274 (PD-L1) expression (Hamada et al. J Clin Oncol 2017).  I have proposed the integration of pharmacoepidemiology into the MPE framework ("pharmaco-MPE") to improve our understanding of drug effects at the molecular, cellular, individual, and population levels (Ogino et al. NPJ Precis Oncol 2017).  The integrative pharmaco-MPE approach can provide insights into the interactive role of medications, exposures, and molecular pathology, thereby guiding the development of precision medicine.

6. Creation of the colorectal continuum model
Gastroenterology research and practice have been based on the long-standing dogma of the dichotomy (proximal vs. distal colorectum) model.  My laboratory made a seminal discovery of continuously increased prevalence of key molecular characteristics of colorectal carcinomas [i.e., microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and BRAF mutation] across colorectal subsites from the rectum to ascending colon (Yamauchi, Morikawa, et al. Gut 2012).  Based on these findings, I created the colorectal continuum model (Yamauchi, Lochhead, et al. Gut 2012), which underscores the pathogenic importance of the interplay of gut microbiota and host factors (diet, immunity, etc.) and has had substantial impacts on gastroenterology, oncology, epidemiology, and pathology. These two papers still draw much attention even 14 years after publications.

7. Creation, management, and leading of the International Molecular Pathological Epidemiology (MPE) Meeting Series
I created the International Molecular Pathological Epidemiology (MPE) Meeting Series (www.mpemeeting.org ) in 2013. The meeting series represents a forum open to the research community with considerable growth.  I served as the Chair or a Co-Chair for six meetings. We published proceedings (Ogino et al. Cancer Causes Cont 2015; Campbell et al. Cancer Causes Cont 2017; Campbell et al. Cancer Causes Cont 2019; Song et al. Cancer Causes Cont 2022).  The seventh meeting, rebranded as “Integrative Pathobiology-in-Population Sciences (IPPS): The 7th International MPE Meeting” will be held in Boston, MA, USA, in June 2027. Our primary goals have been to provide unique educational and networking opportunities and to promote transdisciplinary population sciences.

8. Conceptualization of the etiologic field effect model The concept of MPE has been integrated into the conventional field effect model to create the etiologic field effect model (Lochhead et al. Mod Pathol 2015).  This new model can encompass not only somatic molecular changes but also various environmental exposures and accompanying microenvironmental changes. Each of exposure factors make an “etiologic field” in tissue that can influence the proliferation and survival of neoplastic cells, thereby facilitating tumor development and progression. This concept is useful in designing precision cancer prevention strategies. This etiologic field effect model receives increasing recognitions in recent years, given the fact that most carcinogens or cancer risk factors do not appear to directly cause somatic DNA mutational signatures.

10. Development of statistical frameworks and methods to address etiologic heterogeneity
In a traditional epidemiological framework, cases of one disease entity are often considered a uniform outcome with an assumption that those cases share a common etiology. The underlying principle of MPE indicates that a disease is a fundamentally heterogeneous process differing from person to person (i.e., the unique disease principle) and that the assumption of a common etiology in all cases with the disease does not hold. Hence, we have developed new analytical approaches that can deal with heterogeneous cases with one disease entity. For instance, we developed analytic methods to study disease subtype heterogeneity for binary, ordinal, and non-ordinal categorical subtypes (Wang et al. Stat Med 2016) as well as methods to deal with multiple disease subtyping markers simultaneously (Wang et al. Am J Epidemiol 2015). We have also developed methods to address missing subtyping data (Nevo et al. Lifetime Data Anal 2018; Nevo et al. Biostatistics 2020) and continuous disease subtypes (Li et al. Cancers 2022). User-friendly software to implement the various techniques is publicly available. 

11. Integration of MPE into the causal inference framework and models. 
Both MPE and causal inference are subspecialty fields of epidemiology that share a common goal of elucidating causality in an association between exposure and disease. We have conceived that the two fields can synergize by virtue of the complementary strengths of each field.  We have illustrated how the MPE paradigm can easily solve epidemiological paradoxes (Nishihara et al. Eur J Epidemiol 2015). We have implemented the inverse probability weighting (IPW) method into MPE research to address selection bias due to tissue data availability (Liu et al. Eur J Epidemiol 2018).  The integrative field of MPE causal inference has substantial potential in addressing causality in medical and public health sciences (Nevo et al. Int J Epidemiol 2021). 

12. Creation of the integrative field of lifecourse MPE
The concept of MPE has been integrated into lifecourse epidemiology to create the integrative field of lifecourse-MPE (Nishi et al. Am J Prev Med 2015). This new model can address the effects of various exposures during lifecourse (from early life, encompassing prenatum, infancy, childhood, and adolescence, to adulthood) on the molecular pathology of disease and can possibly help develop strategies of lifestyle modification and intervention in early life. This integrative lifecourse MPE approach will advance research on early-onset cancers, as early-life exposures appear to play pathogenic roles in the rising global incidence of early-onset cancers in many body sites (Akimoto et al. Nat Rev Clin Oncol 2021; Ugai et al. Nat Rev Clin Oncol 2022). 

13. Creation of the integrative field of social MPE
Although the evolving transdisciplinary field of MPE can advance biomedical and health research, the use of state-of-the-art technologies may increase racial, ethnic, and socioeconomic disparities. To address this, we have integrated social science and MPE (Nishi et al. Expert Rev Mol Diagn 2016, Dai et al. Expert Rev Mol Diagn 2021). This integrative field, termed social MPE, can address global health inequalities and elucidate the biological effects of social environments, behaviors, and networks.  The interdisciplinary approach of social MPE aims to utilize advancements in molecular medicine to benefit individuals in all societal settings in the world.

14. Integration of immunology into MPE, encompassing immunogenomics
Immunology-MPE represents an integrative field of immunology, molecular pathology, and epidemiology (Ogino et al. Gut 2018; Ogino et al. Annu Rev Pathol 2019). Diet and lifestyle can be routine immunoprevention strategies, as some modifiable factors can influence not only cancer risk but also host immunity. We need to integrate analyses of environmental exposures, tumor molecular features, microbiota, and host immunity in cancer.  We can utilize MPE analytical (epidemiologic and statistical) strategies and the PCIBM to investigate the combined role of long-term exposures and immunity in disease pathogenesis and progression. My laboratory has spearheaded to conduct proof-of-principle studies in this increasingly recognized area (e.g., Khalili et al. Carcinogenesis 2015; Song et al. Gut 2016; Song et al. JAMA Oncol 2016; Cao et al. Gastroenterology 2016; Liu et al. Gastroenterology 2017; Yang et al. Cancer Prev Res 2019; Hamada et al. J Natl Cancer Inst 2019; Ugai et al. J Natl Cancer Inst 2022; Ugai et al. Innovation Med 2024). 

15. Integration of microbiology and microbiomics into MPE
Microbiology-MPE is an integrative field of microbiology, microbiomics, molecular pathology, and epidemiology (Hamada et al. J Pathol 2019; Inamura et al. Gut 2022). Microorganisms (collectively, the microbiome) play an essential role in human health and diseases.  Analyses of the microbiota in biospecimens, including stools, tissue, and body fluids, combined with immunology-MPE strategies for the exposome and immunity, can generate a wealth of information on disease etiologies and pathogenesis.  This has been demonstrated by our studies using the PCIBM (Mehta et al. JAMA Oncol 2017; Liu et al. Clin Gastroenterol Hepatol 2018; Arima et al. Gastroenterology 2022; Kawamura et al. Ann Surg 2024; Wang et al. Gastroenterology 2024; Ugai et al. Gut Microbes 2025). Microbiology-MPE is a critical interdisciplinary discipline to address the global rise of early-onset cancers (Mima et al. Gut Microbes 2023). 

16. Computational pathology: in situ single-cell analyses, bioinformatics, machine learning, and Bayesian analysis models using artificial intelligence (AI)
We have developed in situ single-cell assays using multispectral immunofluorescence combined with machine learning algorithms (Fujiyoshi et al. EBioMedicine 2020; Borowsky et al. Clin Cancer Res 2021; Vayrynen et al. Cancer Immunol Res 2021; Vayrynen et al. J Immunother Cancer 2021; Vayrynen et al. Cancer Immunol Res 2022). We have developed and used AI-based bioinformatic tools to quantify immune response (Vayrynen et al. Clin Cancer Res 2020) and discover previously unrecognized tissue features that can predict tumor aggressiveness (Tsai et al. Nat Commun 2023).  We have also leveraged advanced Bayesian analysis methods to construct risk prediction models that use a wide variety of variables (Zhao et al. NPJ Precis Oncol 2023). We have created novel computational microgeometric method called TIPC to decipher tumor-immune interplay (Lau et al. PLoS Comp Biol 2025). We seamlessly integrate bioinformatics and computational pathology into the MPE paradigm. 

17. Setting future directions for early-onset cancer (EOC) research: Quantitative global data analyses in combination with the MPE approach and multi-omics in mixed-method research
To address the uncertainty of the global trend of early-onset cancer incidence, we leveraged the GLOBOCAN data to analyze the incidence trend of 14 different cancer types which showed a recent rise in young adults (Ugai et al. Nat Rev Clin Oncol 2022). Literature data analyses indicate that early-life risk factor exposures might play a role in the recent rise of early-onset cancer (Akimoto et al. Nat Rev Clin Oncol 2021; Ugai et al. Nat Rev Clin Oncol 2022). In addition, our research on tumor molecular and immunological features can shed light on pathogenic heterogeneity and biological aggressiveness of early-onset colorectal cancer (Akimoto et al. Cancers 2021; Ugai et al. Cancer Immunol Immunother 2022; Ugai et al. Am J Gastroenterol 2023; Ugai et al. J Gastroenterol 2023).  We are further characterizing tumor molecular changes in early-onset colorectal cancer using a large consortium setting. The microbiology and microbiomics should be integrated into early-onset cancer research (Mima et al. Gut Microbes 2023), as most of the rising early-onset cancer types relate to the digestive system, implying the importance of diets, nutrition, and the oral/intestinal microbiota. My vision for future research direction in this area is summarized (Ogino et al. Ann Oncol 2024). The first flagship paper on the overview of mixed-method EOC research is under preparation.  PCIBM-based studies (see point #2) can be leveraged to study EOC etiologies (Ogino et al. Eur J Epidemiol 2026).

18. Creation and leading of the Gene Product Nomenclature Consortium (GPNC)
The current lack of a standardized nomenclature system for gene products (e.g., proteins) has resulted in a haphazard, counterproductive labeling system.  Not surprisingly, different names are often used for the same gene product (e.g., NKX2-1 and TTF-1 for the NKX2-1 gene product), while the same name is sometimes used for unrelated gene products (e.g., TTF1 for the TTF1 product and the NKX2-1 product).  Such ambiguity causes not only potential harm to patients, whose treatments increasingly rely on laboratory tests for multiple gene products, but also miscommunication and inefficiency, both of which hinder the progress of broad scientific areas.  To mitigate this confusion, I led a project team that recommended standardizing human protein nomenclature through the use of a Human Genome Organisation (HUGO) Gene Nomenclature Committee (HGNC) gene symbol (Fujiyoshi et al. Proc Natl Acad Sci USA 2021).  Working with the HGNC led by Dr. Elspeth Bruford, I established the Gene Product Nomenclature Consortium (GPNC) for the standardization of the nomenclature systems of gene products in 2021 and have been serving its founding Chairperson.  The consortium calls for action across all biomedical communities and scientific and medical journals to standardize the nomenclature of gene products using HGNC gene symbols to enhance accuracy in scientific and public communication. To standardize protein nomenclature, the GPNC now works along with the Nomenclature Committee of the International Union of Biochemistry and Molecular Biology (IUBMB), for which I serve as a member.  The goals of these initiatives are to avoid confusion in data sciences and address the educational need for the entire research and clinical practice areas in chemical, biological, medical, and health sciences.