About

Dr. Naziheh Assarzadegan is a board-certified anatomic and clinical pathologist with subspecialty expertise in gastrointestinal and liver pathology. She completed her GI/Liver pathology fellowship at Johns Hopkins Hospital and subsequently served as faculty at the University of Michigan, where she further developed her expertise in complex GI pathology. Currently, she is a faculty member at the University of Florida, serving as a GI and hepatobiliary pathologist. Her clinical work includes contributions to multidisciplinary care, particularly in liver transplant pathology, pediatric GI pathology, and high-volume diagnostic service. Dr. Assarzadegan maintains an active research portfolio focused on prognostic markers in colorectal and pancreatic cancer, colitis patterns, and molecular alterations in GI neoplasia. She has numerous publications in high-impact journals. In addition to her clinical and research activities, she is dedicated to medical education, providing daily teaching to residents and fellows, leading CME courses, and contributing to national pathology education through her editorial work with PathologyOutlines.

Research topics

• Medicine
• Pathology
• Internal medicine
• Biology
• Genetics
• Gerontology
• Gastroenterology
• Molecular biology

Selected publications

• Liver transplantation for valproic acid-induced acute liver failure in POLG mutation-related mitochondrial disease with cardiac and neurological involvement

  Journal of Liver Transplantation · 2026-03-25

  articleOpen access
  PublisherDOI

• Abstract 2261: Deciphering the role of macrophages in the development of pancreatic ductal adenocarcinoma.

  Cancer Research · 2026-04-03

  article

  Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive forms of cancer. Intraductal papillary mucinous neoplasms (IPMNs) are a well-documented precursor of invasive PDAC; however, the molecular and cellular alterations that drive malignant progression of IPMNs are poorly understood. Genetic alterations drive progression in only a minority of cases, highlighting the likelihood that the surrounding tumor microenvironment (TME) may play an important role. PDAC is characterized by an immunosuppressive TME with abundant macrophages, but the temporal accumulation of immunosuppressive macrophages in PDAC precursors and their role in the progression to invasive cancer has not been explored. A deeper understanding of the TME in IPMN and PDAC may reveal actionable mechanisms of progression, potentially identifying novel therapeutic targets or biomarkers of progression risk. To investigate the temporal recruitment, polarization state, and spatial localization of macrophages, we leveraged immunohistochemistry (IHC) and imaging mass cytometry (IMC) datasets of human IPMNs and adjacent PDAC. IHC from 24 patients showed significant upregulation of CD68+ macrophages in PDAC. IMC allows quantification of the densities and spatial distribution of distinct subtypes. IMC analysis of IPMN, transition zone, and PDAC regions from 12 patients identified heterogeneous changes in total macrophage count and proportions of macrophages subsets over the transition from IPMN to invasive PDAC. In addition, spatial transcriptomics was performed on a subset of samples from 4 patients to interrogate mechanisms of macrophage-epithelial crosstalk across the transition from IPMN to PDAC. In vitro culture of primary human macrophages and PDAC organoids further enables characterization of the functional impact of macrophage-epithelial crosstalk. Organoid-conditioned media treatment of macrophages demonstrates that the PDAC secretome is capable of polarizing macrophages toward an immunosuppressive phenotype with increased expression of IL-10 and CD163. This study provides a comprehensive molecular analysis of macrophages present in the TME of IPMN and PDAC, revealing heterogeneous patterns across patients. The results suggest a role for macrophages in malignant progression and pathways by which PDAC cells reprogram the macrophage population, offering new insights into the interaction between macrophages and neoplastic epithelial cells, which can be used to identify signaling dependencies that could serve as novel biomarkers of therapeutic targets. Citation Format: Maria F. Wissler, Jessie Kanacharoen, Daniel J. Salas-Escabillas, Shalini Datta, Naziheh Assarzadegan, Eugene Shenderov, Ashley Kiemen, Won Jin Ho, Laura DeLong Wood. Deciphering the role of macrophages in the development of pancreatic ductal adenocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 2261.

  PublisherDOI

• 287 Role of Peritoneal Fluids and Washes Cytology in Low-Grade Appendiceal Mucinous Neoplasms

  Laboratory Investigation · 2026-03-01

  article
  PublisherDOI

• Elevated T Cell Immunoreceptor with Ig and ITIM Domains (TIGIT) Expression and Immune Cell Dysfunction Characterize Complex Proteins Associated With SET1 (COMPASS)–Like Complex Gene–Mutated Pancreatic Ductal Adenocarcinoma (PDAC)

  Modern Pathology · 2026-02-02

  articleOpen access
  PublisherOA PDFDOI

• 1454 Characterizing Early Histologic Changes in Chronic Rejection Prior to Ductopenia in Liver Transplant Recipients

  Laboratory Investigation · 2025-03-01

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Tumor immune microenvironment alterations associated with progression in human intraductal papillary mucinous neoplasms

  Pancreatology · 2025-10-31 · 1 citations

  article
  PublisherDOI

• Revisiting the Role of <i>Epstein-Barr Virus</i> (EBV) in Gastric Cancer: A Case Study of EBV in Normal, Dysplastic, and Malignant Gastric Epithelium

  International Journal of Surgical Pathology · 2025-05-30

  articleSenior author

  (EBV) playing a key role in certain subtypes of the disease. However, the exact mechanisms by which EBV contributes to gastric carcinogenesis remain poorly understood. This case report presents a 78-year-old female patient with a history of chronic atrophic gastritis, intestinal metaplasia, and multiple hyperplastic gastric polyps, exhibiting both low- and high-grade dysplasia, who ultimately developed multifocal intramucosal adenocarcinoma and underwent subtotal gastrectomy. The gastrectomy specimen revealed numerous polyps of varying sizes throughout the gastric mucosa. Epstein-Barr encoding region in-situ hybridization testing demonstrated EBV expression not only within the neoplastic gastric epithelium but also in the nonneoplastic epithelium and gastric polyps, an unusual finding further confirmed by polymerase chain reaction testing for EBV DNA. While the role of EBV in some gastric carcinomas is well established, the detection of EBV in nonneoplastic gastric epithelium highlights the possibility that latent EBV infection may contribute to gastric carcinogenesis, particularly in the setting of chronic gastritis and intestinal metaplasia. This case report underscores the need for a deeper understanding of EBV's potential impact on cellular processes, including genome-wide hypermethylation, and calls for further research into the mechanisms underlying EBV-associated gastric carcinoma.

  PublisherDOI

• Deep immune profiling of intrahepatic cholangiocarcinoma with CODEX multiplexed imaging

  Hepatology Communications · 2025-02-19 · 9 citations

  articleOpen access

  BACKGROUND: Intrahepatic cholangiocarcinoma (iCCA) may be genomically subclassified by the presence of potentially actionable molecular aberrations, of which pathogenic alterations in isocitrate dehydrogenase (IDH)1 and fibroblast growth factor receptor (FGFR)2 are the most frequently observed. The impact of these molecular alterations on the tumor immune microenvironment remains incompletely understood. METHODS: We performed a high-parameter spatial immune phenotyping of iCCA samples with pathogenic FGFR2 or IDH1 alterations and FGFR2/IDH1 wild-type controls at the single-cell level using CO-Detection by indEXing. RESULTS: A total of 24 tumors were examined. Tumors with FGFR2 alterations were characterized by fewer CD8+ T cells and "M2-like" macrophages but higher levels of polymorphonuclear myeloid-derived suppressor cells as compared to FGFR2 wild-type tumors. Spatial relationships between polymorphonuclear myeloid-derived suppressor cells and multiple other cell types in the tumor microenvironment (including tumor cells, CD4+, and CD8+ T cells) were enriched in tumors with FGFR2 alterations. Tumors with IDH1 mutations had a trend toward more fibroblasts and were characterized by a closer proximity of tumor cells to CD4+ T cells, and between macrophages and multiple structural tumor microenvironment components as compared to other subtypes. CONCLUSIONS: iCCAs with pathogenic FGFR2 fusions/rearrangements and IDH1 mutations have distinct immunophenotypes. Tailoring immunotherapeutic approaches to specific molecular subsets could improve treatment outcomes across the divergent molecularly defined iCCA subtypes.

  PublisherDOI

• 598 Portal Hypertensive Colopathy: Clinicopathologic Features of a Relevant and Underrecognized Condition

  Laboratory Investigation · 2025-03-01

  articleOpen access
  PublisherOA PDFDOI

• An Atypical Presentation of a Typical Pancreatic Cyst

  Gastroenterology · 2025-09-18

  article
  PublisherDOI

Frequent coauthors

• Mareyuki Endo

  90 shared

• Purva Gopal

  The University of Texas Southwestern Medical Center

  70 shared

• Oyedele Adeyi

  University of Minnesota Medical Center

  61 shared

• Danielle Hutchings

  Cedars-Sinai Medical Center

  54 shared

• Ahmet Gürakar

  Johns Hopkins Medicine

  51 shared

• Cristine Charlesworth

  Mayo Clinic

  50 shared

• Andrew M. Cameron

  Johns Hopkins University

  50 shared

• Amit G. Singal

  50 shared