James Poe

All Publications

• Biphasic, time-dependent neutrophil biology in glioblastoma revealed by <i>in vivo</i> survival and flow cytometry with single-cell transcriptomic corroboration Abikenari, M., Choi, J., Liu, J., Sjoholm, A., Nageeb, G., Poe, J., Hwa-Lin Bergsneider, B., Tran, A., Bakalov, D., Medikonda, R., Kim, L., Verma, R., Wu, C., Cho, K., Banu, M., Lim, M. AMER ASSOC CANCER RESEARCH. 2026

  View details for DOI 10.1158/1538-7445.AM2026-170

  View details for Web of Science ID 001734193700022

• Precision Immunotherapeutics for Glioblastoma: Current Approaches and Emerging Strategies in 2026. Cells Poe, J., Kim, C., Coleman, C., Nguyen, H., Velazhahan, V., Bergsneider, B., Sanker, V., Kim, S., Chen, Y., Abikenari, M., Choi, J., Lim, M. 2026; 15 (6)

  Abstract

  Glioblastoma (GBM) persists as one of the greatest challenges in the treatment of human cancer, despite extensive efforts to leverage the therapeutic potential of immunotherapy. While checkpoint blockade and other forms of immunotherapy have revolutionized the treatment of various cancers, their therapeutic efficacy in GBM has been hindered by the profound immunosuppressive environment, spatial heterogeneity, and dynamic immune metabolic challenges associated with the tumor microenvironment. In this review, we will synthesize recent advances and insights to develop a next-generation framework for GBM immunotherapy based on systems biology approaches to understanding the complex interplay between GBM and the immune system, as opposed to single-axis approaches to immune activation and modulation. We will discuss how the functional competence of the interferon system, myeloid antigen presentation status, T-cell clone status, spatial organization of the immune microenvironment, and resource competition between GBM and the immune system dictate therapeutic responsiveness. Furthermore, the current paper elucidates how recent advances in spatial transcriptomics, single-cell analysis, and high-parameter imaging enable us to understand how immune phenotype status varies across GBM regions and treatment status, and how this information can be used to develop predictive and pharmacodynamic biomarkers of therapeutic efficacy and failure. We will then discuss how these advances form the basis for rational combination approaches to GBM immunotherapy, which involve the integration of checkpoint blockade with metabolic reprogramming, myeloid modulation, and interferon system reactivation, and how artificial intelligence-based analytics and adaptive clinical trial design can guide the development of biomarker-based therapeutic selection approaches.

  View details for DOI 10.3390/cells15060561

  View details for PubMedID 41892350

  View details for PubMedCentralID PMC13025625

• Nexus of IDO1/Kynurenine Pathway to T-Cell Exhaustion: Hypoxia-Induced Tryptophan Metabolism in Glioblastoma. Metabolites Abikenari, M., Nageeb, G., Ha, J. H., Sjoholm, M. A., Liu, J., Bergsneider, B., Valenzuela, J., Poe, J., Bog Cho, K., Verma, R., Wu, C., Sanker, V., Medikonda, R., Kim, L. H., Choi, J., Banu, M. A., Lim, M. 2026; 16 (3)

  Abstract

  Glioblastoma (GBM) is a universally fatal cancer for which the standard of care has remained largely unchanged for the last 20 years. Recent work has demonstrated that most therapeutic trials for GBM fail due to complex mechanisms of immunosuppression mediated by both the innate and adaptive immune systems. Various metabolic alterations in the tumor microenvironment help maintain this local and systemic immunosuppression, of which the axis of hypoxia-driven tryptophan degradation has garnered substantial attention over the last decade. This paper synthesizes a much-needed elucidation of the immunometabolic reshaping of glioma, myeloid, endothelial, and lymphoid cell lineages induced by hypoxia. The current paper critically evaluates the role of IDO1/TDO2-mediated breakdown of tryptophan and the consequent accumulation of kynurenine, a metabolite that triggers GCN2- and AHR-mediated CD8+ T-cell exhaustion and supports regulatory T-cell differentiation and expansion. Furthermore, we propose a synthesis of mechanistic evidence that establishes a role for the Trp-GCN2-ATF4-VEGFA axis in hypoxia-induced immunosuppression, supporting that pro-tumoral metabolic dysregulation is directly linked to angiogenesis. In GBM, hypoxia and tryptophan-kynurenine pathway dysregulation operate as an integrated metabolic circuit that drives widespread immunosuppression. These mechanisms can be captured by a metabolic signature shared across nearly every cell type in the GBM microenvironment. Drawing on recent spatial transcriptomic, metabolomic, and pharmacologic studies, we outline how this metabolic axis shapes disease biology and how it can be targeted to restore effective antitumor immunity.

  View details for DOI 10.3390/metabo16030185

  View details for PubMedID 41893336

  View details for PubMedCentralID PMC13028454

• When Central Tolerance Fails: Thymic Malignancies at the Intersection of Cancer Immunity and Autoimmunity. Cancers Abikenari, M., Choi, J., Enayati, I., Tucker, A., Bhatnagar, K., Chen, Y., Himic, V., Liu, J., Nageeb, G., Poe, J., Ong, S. J., Sanker, V., Diehl, M., Szeifert, V., Terasaki, A., Prolo, L. M., Engleman, E., Okwan-Duodu, D. 2026; 18 (5)

  Abstract

  Thymic malignancies are rare cancers arising from thymic epithelial cells and are characterized by a highly diverse clinical phenotype, substantial histologic and morphologic heterogeneity, and frequent associations with autoimmune syndromes. Although the clinical, immunological, and cytoarchitectural changes associated with thymomas have been increasingly elucidated in the contemporary literature, very few studies have interrogated the direct role of tumor staging and histological grading in shaping autoimmunity burden and infection risk. In this narrative review, we synthesize contemporary clinical, immunological, and morphologic evidence linking thymic architecture and selection defects to the spectrum of paraneoplastic autoimmunity (MG, pure red cell aplasia, Good's syndrome) and to infectious vulnerability. We further appraise emerging therapeutic strategies, including immune checkpoint inhibition and adoptive cellular approaches, through a patient-stratified lens, emphasizing efficacy signals, immune-related adverse events, and practical considerations for selection and monitoring. We conclude by highlighting priorities for future investigation, including refining autoantibody signatures; mapping thymic microenvironments that drive tolerance failure, and prospectively evaluating stratified immunotherapeutic regimens that balance benefit with immune-mediated risk.

  View details for DOI 10.3390/cancers18050747

  View details for PubMedID 41827683