About

Shuji Ogino, MD, PhD, MS, is a Professor of Pathology at Harvard Medical School and the Chief of the Molecular Pathological Epidemiology (MPE) Program at Brigham and Women’s Hospital. He also holds the position of Professor of Epidemiology at Harvard T.H. Chan School of Public Health and is an Associate Member of the Broad Institute of MIT and Harvard. Dr. Ogino established the International Molecular Pathological Epidemiology (MPE) Meeting Series in 2013 and serves as its Chair/Co-Chair. His research focuses on the integrative science of MPE, studying the interactive roles of environment, microbiome, immunity, and tumor in carcinogenesis. He conducts multifaceted studies using large-scale prospective cohort studies, notably discovering the link between fiber-poor, inflammatory diets and higher incidence of colorectal cancer enriched with Fusobacterium nucleatum, as well as the suppressive effect of F. nucleatum on T-cell-mediated antitumor immunity. His transdisciplinary scientific contributions have earned him numerous awards and honors.

Research topics

• Biology
• Genetics
• Medicine
• Political Science
• Cancer research
• Oncology
• Internal medicine
• Public relations
• Computational biology
• Bioinformatics
• Engineering
• Virology
• Immunology
• Engineering ethics
• Endocrinology
• Nursing

Selected publications

• Spatially organized multicellular immune hubs in human colorectal cancer

  Cell · 2021 · 786 citations

  • Biology
  • Cancer research
  • Immunology
  DOI

• Genetic architectures of proximal and distal colorectal cancer are partly distinct

  Gut · 2021 · 79 citations

  • Biology
  • Genetics
  • Bioinformatics

  OBJECTIVE: An understanding of the etiologic heterogeneity of colorectal cancer (CRC) is critical for improving precision prevention, including individualized screening recommendations and the discovery of novel drug targets and repurposable drug candidates for chemoprevention. Known differences in molecular characteristics and environmental risk factors among tumors arising in different locations of the colorectum suggest partly distinct mechanisms of carcinogenesis. The extent to which the contribution of inherited genetic risk factors for CRC differs by anatomical subsite of the primary tumor has not been examined. DESIGN: To identify new anatomical subsite-specific risk loci, we performed genome-wide association study (GWAS) meta-analyses including data of 48 214 CRC cases and 64 159 controls of European ancestry. We characterised effect heterogeneity at CRC risk loci using multinomial modelling. RESULTS: ) and that were not reported by previous GWASs for overall CRC risk. Multiple lines of evidence support candidate genes at several of these loci. We detected substantial heterogeneity between anatomical subsites. Just over half (61) of 109 known and new risk variants showed no evidence for heterogeneity. In contrast, 22 variants showed association with distal CRC (including rectal cancer), but no evidence for association or an attenuated association with proximal CRC. For two loci, there was strong evidence for effects confined to proximal colon cancer. CONCLUSION: Genetic architectures of proximal and distal CRC are partly distinct. Studies of risk factors and mechanisms of carcinogenesis, and precision prevention strategies should take into consideration the anatomical subsite of the tumour.

  PublisherOA PDFDOI

• The urgent need for integrated science to fight COVID-19 pandemic and beyond

  Journal of Translational Medicine · 2020 · 162 citations

  • Political Science
  • Political Science
  • Public relations

  The COVID-19 pandemic has become the leading societal concern. The pandemic has shown that the public health concern is not only a medical problem, but also affects society as a whole; so, it has also become the leading scientific concern. We discuss in this treatise the importance of bringing the world's scientists together to find effective solutions for controlling the pandemic. By applying novel research frameworks, interdisciplinary collaboration promises to manage the pandemic's consequences and prevent recurrences of similar pandemics.

  DOI

• Adiposity, metabolites, and colorectal cancer risk: Mendelian randomization study

  BMC Medicine · 2020 · 177 citations

  • Medicine
  • Internal medicine
  • Oncology

  BACKGROUND: Higher adiposity increases the risk of colorectal cancer (CRC), but whether this relationship varies by anatomical sub-site or by sex is unclear. Further, the metabolic alterations mediating the effects of adiposity on CRC are not fully understood. METHODS: We examined sex- and site-specific associations of adiposity with CRC risk and whether adiposity-associated metabolites explain the associations of adiposity with CRC. Genetic variants from genome-wide association studies of body mass index (BMI) and waist-to-hip ratio (WHR, unadjusted for BMI; N = 806,810), and 123 metabolites from targeted nuclear magnetic resonance metabolomics (N = 24,925), were used as instruments. Sex-combined and sex-specific Mendelian randomization (MR) was conducted for BMI and WHR with CRC risk (58,221 cases and 67,694 controls in the Genetics and Epidemiology of Colorectal Cancer Consortium, Colorectal Cancer Transdisciplinary Study, and Colon Cancer Family Registry). Sex-combined MR was conducted for BMI and WHR with metabolites, for metabolites with CRC, and for BMI and WHR with CRC adjusted for metabolite classes in multivariable models. RESULTS: ) was associated with 1.09 (95% CI = 0.97, 1.22) times higher CRC odds. WHR (per 0.07 higher) was more strongly associated with CRC risk among women (IVW OR = 1.25, 95% CI = 1.08, 1.43) than men (IVW OR = 1.05, 95% CI = 0.81, 1.36). BMI or WHR was associated with 104/123 metabolites at false discovery rate-corrected P ≤ 0.05; several metabolites were associated with CRC, but not in directions that were consistent with the mediation of positive adiposity-CRC relations. In multivariable MR analyses, associations of BMI and WHR with CRC were not attenuated following adjustment for representative metabolite classes, e.g., the univariable IVW OR for BMI with CRC was 1.12 (95% CI = 1.00, 1.26), and this became 1.11 (95% CI = 0.99, 1.26) when adjusting for cholesterol in low-density lipoprotein particles. CONCLUSIONS: Our results suggest that higher BMI more greatly raises CRC risk among men, whereas higher WHR more greatly raises CRC risk among women. Adiposity was associated with numerous metabolic alterations, but none of these explained associations between adiposity and CRC. More detailed metabolomic measures are likely needed to clarify the mechanistic pathways.

  DOI

• Landscape of somatic single nucleotide variants and indels in colorectal cancer and impact on survival

  Nature Communications · 2020 · 93 citations

  • Biology
  • Genetics
  • Cancer research

  Colorectal cancer (CRC) is a biologically heterogeneous disease. To characterize its mutational profile, we conduct targeted sequencing of 205 genes for 2,105 CRC cases with survival data. Our data shows several findings in addition to enhancing the existing knowledge of CRC. We identify PRKCI, SPZ1, MUTYH, MAP2K4, FETUB, and TGFBR2 as additional genes significantly mutated in CRC. We find that among hypermutated tumors, an increased mutation burden is associated with improved CRC-specific survival (HR = 0.42, 95% CI: 0.21-0.82). Mutations in TP53 are associated with poorer CRC-specific survival, which is most pronounced in cases carrying TP53 mutations with predicted 0% transcriptional activity (HR = 1.53, 95% CI: 1.21-1.94). Furthermore, we observe differences in mutational frequency of several genes and pathways by tumor location, stage, and sex. Overall, this large study provides deep insights into somatic mutations in CRC, and their potential relationships with survival and tumor features.

  DOI

• Genome-wide Modeling of Polygenic Risk Score in Colorectal Cancer Risk

  The American Journal of Human Genetics · 2020 · 225 citations

  • Medicine
  • Oncology
  • Internal medicine
  DOI

Recent grants

• NIH Grant K07CA122826

  NIH · $634k · 2011

• Interdisciplinary Epidemiologic Consortium to Investigate T-cell Response in Colorectal Cancer

  NIH · $3.6M · 2020–2026

• NIH Grant R01CA151993

  NIH · $2.6M · 2015

• NIH Grant R13CA203287

  NIH · $20k · 2018

• Accelerating Transdisciplinary Epidemiology of Colorectal Cancer

  NIH · $6.0M · 2019–2022

Frequent coauthors

• Charles S. Fuchs

  3683 shared

• Andrew T. Chan

  Brigham and Women's Hospital

  3448 shared

• Edward L. Giovannucci

  Harvard University

  2448 shared

• Jeffrey A. Meyerhardt

  1782 shared

• Mingyang Song

  Massachusetts General Hospital

  1670 shared

• Reiko Nishihara

  1510 shared

• Marios Giannakis

  Dana-Farber Cancer Institute

  1373 shared

• Kana Wu

  1262 shared

Awards & honors

• Many awards and honors

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