About

Amiko Uchida, MD, is an Assistant Professor in Medicine, Gastroenterology at the University of Utah. She is a member of the Round Lab, which is part of the Department of Pathology, Microbiology, and Immunology. Her role involves research in the field of gastroenterology, contributing to the lab's focus on microbiology and immunology within pathology. Specific details about her research focus, background, or key contributions are not provided on the page.

Research topics

• Medicine
• Immunology
• Internal medicine
• Cell biology
• Biology
• Genetics
• Cancer research

Selected publications

• 910 DISTINCT AND SHARED TRANSCRIPTIONAL PATHWAYS IN EOSINOPHILIC GASTRITIS: INVESTIGATIONS INTO ANTRAL, BODY, AND HISTOLOGICALLY UNAFFECTED REGIONS, WITH COMPARISON TO ISOLATED AND CONCURRENT EOSINOPHILIC ESOPHAGITIS

  Gastroenterology · 2026-05-01

  article
  PublisherDOI

• Sa1112 EOSINOPHILIC ESOPHAGITIS AS A COMPLICATION OF IMMUNE CHECKPOINT INHIBITORS

  Gastrointestinal Endoscopy · 2026-05-01

  articleSenior author
  PublisherDOI

• Mo1151 RELATIVE RISK OF COMORBID AUTONOMIC DYSFUNCTION AND EOSINOPHILIC ESOPHAGITIS IN THE UTAH POPULATION DATABASE

  Gastroenterology · 2026-05-01

  article
  PublisherDOI

• Colibactin-associated mutations in the human colon appear to reflect anatomy and early exposure, not oncogenesis

  medRxiv · 2026-04-15

  articleOpen access

  Abstract Colorectal cancer (CRC) is the second leading cause of cancer death globally and the number one cause of cancer death in people under 50 years old. The reasons for the rise of early-onset CRC are unknown, and while anatomically distinct subtypes of CRC have substantial clinical and molecular associations, the etiology of region-specific disease, such as early-onset CRC’s enrichment in the distal colon, remains unclear. Understanding regional mutagenesis may identify risk factors for this public health concern and CRC more broadly. To evaluate mutational dynamics across the premalignant colon, we performed whole-genome sequencing of 125 individual colon crypts taken from six standardized regions biopsied during colonoscopy, collected from 11 donors without polyps and 10 with polyps. We observed mutation spectra and accumulation rates consistent with previous whole-organ studies, with greater subclonal mutation capture enabled by experimental design. T>[A,C,G] mutations, which are associated with colibactin genotoxicity from pks+ Escherichia coli , were significantly enriched in the rectum of donors with and without polyps (adjusted p-values < 0.01). Moreover, when comparing findings to crypts from individuals with CRC and sequenced CRC tumors, we observed consistent enrichment of the colibactin-associated mutational signature “ID18” in the rectum in both normal colon crypts and CRC tumors, without significant difference in colibactin-specific single nucleotide variant or insertion-deletion burden in crypts across the three clinical groups (i.e., no polyp, polyp, and CRC). These findings argue against a causal or prognostic role for colibactin in CRC, instead indicating that the proposed association with early-onset disease reflects anatomic specificity rather than cancer-specific clinical relevance.

  PublisherDOI

• Mo1151 RELATIVE RISK OF COMORBID AUTONOMIC DYSFUNCTION AND EOSINOPHILIC ESOPHAGITIS IN THE UTAH POPULATION DATABASE

  Gastrointestinal Endoscopy · 2026-05-01

  article
  PublisherDOI

• Unmet Needs in Eosinophilic Esophagitis: Do We Still Have Some?

  Inflammatory Intestinal Diseases · 2026-02-19

  articleOpen access1st authorCorresponding

  Background: Since the late 1990s, eosinophilic esophagitis (EoE) became a known disease characterized by eosinophilic infiltration into the esophagus accompanied by esophageal symptoms. Over the past 2 decades, there has been an exponential increase in the understanding of the epidemiology and pathogenesis of disease leading to new therapies. Despite this, we still have significant knowledge gaps in our clinical care. Summary: Despite a plethora of knowledge gained about EoE over the last 3 decades, medical care of EoE continues to struggle with uncertainties. Presently, we lack available methods to predict who is at risk of complications or who will be refractory to therapy. There is only a paucity of data about how to maintain long-term control of inflammation, and we have yet to develop clinically applicable biomarkers to predict clinical phenotypes (i.e., those who will recur while on therapy). This review focuses on a few of the common limitations in current care of EoE: (1) diagnosis, (2) accurate food antigen testing, (3) prediction of clinically relevant phenotypes, (4) maintenance and surveillance strategies, (5) optimal disease endpoints, and (6) need for less invasive monitoring. Key Messages: Despite rapid increase in our comprehension of EoE, patients continue to have unmet needs. However, with the continued rapidity of investigation, many of these current deficiencies are being addressed and will likely be resolved in the future.

  PublisherOA PDFDOI

• 911 BIDIRECTIONAL ASSOCIATION OF EOSINOPHILIC ESOPHAGITIS AND IRRITABLE BOWEL SYNDROME IN A SWEDISH NATIONWIDE COHORT STUDY

  Gastrointestinal Endoscopy · 2026-05-01

  article
  PublisherDOI

• 454 INCREASING INCIDENCE AND PREVALENCE OF EOSINOPHILIC ESOPHAGITIS IN SWEDEN: A NATIONWIDE POPULATION-BASED STUDY FROM 2005 TO 2021

  Gastrointestinal Endoscopy · 2026-05-01

  article
  PublisherDOI

• Mo1149 EOSINOPHILIC ESOPHAGITIS AND AUTOIMMUNE THYROID DISEASE: A POPULATION-BASED MATCHED COHORT STUDY

  Gastroenterology · 2026-05-01

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  PublisherDOI

• Response to: An Overview of Predictive Biomarkers and Detection Approaches for Immunotherapy Response in GI Malignancies

  Journal of Gastroenterology and Hepatology · 2026-01-15

  articleSenior authorCorresponding

  We were very interested to read the article titled “An Overview of Predictive Biomarkers and Detection Approaches for Immunotherapy Response in GI Malignancies” by Xinyu Chai and collaborators in the March 2025 issue of the Journal of Gastroenterology and Hepatology [1]. Gastrointestinal (GI) malignancies are rapidly increasing, particularly in younger age groups, prompting the need for better detection and therapies [2]. Thus, Chai et al. provide a detailed and evidence-based review of immunotherapies and GI cancers to discuss immune checkpoint inhibitors and biomarkers that contribute to cancer detection and prognostication, and optimization of therapeutic outcomes. This article emphasizes the urgent need for an improved understanding of disease mechanisms underlying prognostic biomarkers of GI malignancies, as well as for more effective detection strategies and treatments to address the rising incidence and mortality burden of GI cancers. The authors highlight many advances that will aid in these processes including checkpoint inhibitor immunotherapy, artificial intelligence-driven models, next-generation sequencing, and multiplex immunohistochemistry. In addition to the incorporation of these fascinating approaches, we would like to acknowledge that generating relevant large-scale, longitudinal biobanks will be critical to advancing our understanding of GI malignancies, biomarkers, and immunotherapy responses. Human biobanks function as centralized repositories for the acquisition, processing, storage, and distribution of high-quality biospecimens [3]. More specifically, biorepositories should collect biospecimens from patients with and without GI malignancies, incorporating human microbiota-relevant samples (e.g. saliva, tissue, and stool) along with environmental health data. The field is increasingly appreciating the importance of environmental factors such as the microbiota, diet, exposures in early life or pollutants later in life as critical determinants of cancer development, behavior, and response to therapies. As pointed out by the authors, checkpoint immunotherapy efficacy is modulated by several factors including tumor genomic factors and the patient's microbiome, and clinical trials dissecting mechanisms and efficacy are well underway [4, 5]. Furthermore, organizations such as the United States National Institute of Health (NIH) have begun shifting funding priorities toward research grounded in human biology. On July 7, 2025, the NIH announced that it will no longer solicit research proposals for projects that rely exclusively on animal models [6]. Researchers in the United States who previously focused on basic science and translational research centered on animal methods will now need to incorporate direct human relevance to remain competitive for federal funding. In this context, biobanks can provide a practical and scalable resource. Biobanks play a significant role in translational research by enabling large-scale genomic, proteomic, and population-level epidemiologic studies that require diverse and well-annotated human samples. Among cancer-related research in the United States, biobank samples contribute to over 40% of data for research papers and “play a crucial role in all aspects of healthcare” [7]. As Chai et al. suggest, advancing the study of GI cancers will require research infrastructure capable of capturing the complexity of human disease on multiple levels. Biobanks provide a critical foundation for this work by enabling access to diverse, clinically linked biospecimens that are essential for mechanistic studies, early-detection research, and improved treatment efficacy. Biobanks and biorepositories can prove to be useful in addressing the needs of ongoing GI cancer biomarker studies. As the field moves toward more human-based science, expanding biobank capacity and utilization will be critical for generating the kinds of insights needed to address the rising burden of GI cancers. EY has no conflicts to disclose. AMU is a medical advisor and consultant for Sanofi-Regeneron, Areteia, AstraZeneca, Uniquity, and Takeda. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.

  PublisherDOI

Frequent coauthors

• John J. Garber

  40 shared

• Jonas F. Ludvigsson

  Karolinska Institutet

  31 shared

• José Ordovás-Montañés

  Broad Institute

  30 shared

• Alex K. Shalek

  Ragon Institute of MGH, MIT and Harvard

  27 shared

• Benjamin A. Doran

  University of Chicago

  24 shared

• Michael Dougan

  19 shared

• Paul Kelly

  Queen Mary University of London

  18 shared

• Conner Kummerlowe

  Massachusetts Institute of Technology

  18 shared

Labs

• Round LabPI

Education

• M.D.

  University of Utah

• Other, Internal Medicine

  University of Washington

• Other, Gastroenterology

  Massachusetts General Hospital