About

Kenneth Buetow is a human genetics and genomics researcher who leverages computational tools to understand complex traits such as cancer, liver disease, and obesity. He currently serves as the director of the Computational Sciences and Informatics program for Complex Adaptive Systems at Arizona State University (CAS@ASU). He is a professor in the School of Life Sciences within ASU’s College of Liberal Arts and Sciences, and also holds the position of director of the Center for Evolution and Medicine. Additionally, he is the director of bioinformatics and data management for the National Biomarker Development Alliance. Professor Buetow previously served as the Founding Director of the Center for Biomedical Informatics and Information Technology within the National Institutes of Health’s National Cancer Institute. His educational background includes a Ph.D. and M.S. in Human Genetics from the University of Pittsburgh and a B.A. in Biology from Indiana University. His research activity involves developing and applying computational and bioinformatics approaches to understand complex biological traits and diseases, with a focus on cancer and other complex conditions. He is actively involved in various research collaborations, advisory committees, and initiatives related to biomedical informatics, data management, and health solutions.

Research topics

• Political Science
• Biology
• Genetics
• Cancer research
• Oncology
• Bioinformatics
• Medicine
• Computational biology

Selected publications

• APOE4 is associated with elevated blood lipids and lower levels of innate immune biomarkers in a tropical Amerindian subsistence population

  eLife · 2021 · 55 citations

  • Biology
  • Immunology
  • Endocrinology

  In post-industrial settings, apolipoprotein E4 ( APOE4 ) is associated with increased cardiovascular and neurological disease risk. However, the majority of human evolutionary history occurred in environments with higher pathogenic diversity and low cardiovascular risk. We hypothesize that in high-pathogen and energy-limited contexts, the APOE4 allele confers benefits by reducing innate inflammation when uninfected, while maintaining higher lipid levels that buffer costs of immune activation during infection. Among Tsimane forager-farmers of Bolivia ( N = 1266, 50% female), APOE4 is associated with 30% lower C-reactive protein, and higher total cholesterol and oxidized LDL. Blood lipids were either not associated, or negatively associated with inflammatory biomarkers, except for associations of oxidized LDL and inflammation which were limited to obese adults. Further, APOE4 carriers maintain higher levels of total and LDL cholesterol at low body mass indices (BMIs). These results suggest that the relationship between APOE4 and lipids may be beneficial for pathogen-driven immune responses and unlikely to increase cardiovascular risk in an active subsistence population.

  DOI

• Transcriptional Landscape of Hepatocellular Carcinoma Reveals that Patient Ethnic-Origin Influences Patterns of Expression

  bioRxiv (Cold Spring Harbor Laboratory) · 2020

  Senior authorCorresponding
  • Political Science
  • Biology
  • Oncology

  Abstract The global incidence of hepatocellular carcinoma (HCC) has increased threefold in the last 30 years. In the United States, individuals with ancestry from Asia, Africa and Latin America have a significantly higher risk of developing HCC. However, the molecular mechanisms by which HCC disparities occur remain mostly understudied. Herein, we employed advanced bioinformatics analysis tools to identify genomic drivers that could explain the differences seen among HCC patients of distinct ethnicities (geographic origins). Data from TCGA and open-source software tools HiSTAT, StringTie, and Ballgown were used to map next-generation sequencing (NGS) reads from DNA and RNA, assemble transcripts, and quantify gene abundance. Differential genes/transcripts were mapped to known biomarkers and targets of systemic HCC therapeutics. Four overlapping transcripts were identified between each ethnicity group: FCN2, FCN3, COLEC10, and GDF2. However, we also found that multiple genes are expressed in an ethnicity-specific manner. Our models also revealed that both current and emerging biomarkers fail to capture heterogeneity between patients of different ethnicities. Finally, we have determined that first-line treatment, such as Sorafenib, may be better suited for Asian patients, while Lenvatinib may exhibit better efficacy for Caucasian patients. In conclusion, we have outlined that the pathways involved in early hepatocarcinogenesis may occur in an ethnicity-specific manner and that these distinct phenotypes should be taken into account for biomarker and therapeutic development.

  DOI

Frequent coauthors

• Meenakshi Devidas

  St. Jude Children's Research Hospital

  13 shared

• I‐Ming Chen

  National Taiwan University Hospital

  12 shared

• Jinghui Zhang

  10 shared

• Cheryl L. Willman

  St. Jude Children's Research Hospital

  10 shared

• Michael N. Edmonson

  10 shared

• Ying Hu

  National Cancer Institute

  10 shared

• Malcolm A. Smith

  10 shared

• Daniela S. Gerhard

  9 shared

Education

• Ph.D., Human Genetics

  University of Pittsburgh

  1985

• M.S., Human Genetics

  University of Pittsburgh

  1983

• B.A., Biology

  Indiana University

  1980

Similar researchers at Arizona State University

• Greg Asnerh-157
• Philip Christensenh-130
• Jianguo Wuh-119
• Carolyn Comptonh-118
• Osvaldo Salah-114