Chordoma, a formidable and rare malignant bone tumor commonly originating along the axial skeleton, notably challenges clinicians and researchers due to its notoriously poor prognosis and resistance to standard therapeutic interventions. This neoplasm, thought to arise from remnants of the notochord, is characterized by intrinsic biological aggressiveness manifesting in frequent recurrences and invasive growth patterns. Traditional treatment strategies, including surgical resection complemented by radiotherapy, often encounter critical obstacles stemming from the tumor’s proximity to vital neurovascular structures, limiting the potential for complete excision and effective control.
In this daunting clinical landscape, the advent of immuno-oncology has heralded promising avenues, with the tumor immune microenvironment emerging as a pivotal determinant of tumor behavior and therapeutic response. However, despite this growing focus on immune-tumor interactions, the role of specific immune effector cells in chordoma pathophysiology has remained ambiguous. Among these, eosinophils—granulocytic leukocytes traditionally implicated in allergic responses and parasitic defenses—have attracted burgeoning interest for their multifaceted regulatory capabilities within the tumor milieu, particularly their secretion of a repertoire of cytokines and chemokines.
To address this knowledge void, a distinguished research consortium spearheaded by Professor Liu Pinan and Dr. Bo Wang from Capital Medical University, Beijing, undertook a comprehensive investigation into the immunological crosstalk between eosinophils and chordoma cells. Their groundbreaking work, recently published in the Chinese Neurosurgical Journal, delineates the antitumorigenic properties of eosinophils and unveils their mechanistic role in modulating tumor growth dynamics, offering a novel paradigm for therapeutic innovation.
The study meticulously examined clinical data from 142 histopathologically confirmed chordoma cases, stratifying patients based on the Ki-67 proliferation index—a robust proliferation marker conventionally employed to gauge tumor growth rates. Intriguingly, the analysis illuminated an inverse correlation between eosinophil abundance, measured both peripherally and within the tumor microenvironment, and Ki-67 indices. Patients exhibiting elevated Ki-67 levels, indicative of aggressive disease phenotypes, concurrently demonstrated marked eosinophil depletion, suggesting a suppressive nexus.
Professor Pinan contextualizes this finding, emphasizing that “the decrease in peripheral and tumor-infiltrating eosinophil counts alongside increased Ki-67 proliferation index—and notably, the further decline following tumor recurrence—underscores a close association between eosinophil presence and tumor proliferative behavior.” This observation implies that eosinophils may exert a modulatory influence capable of constraining tumor aggressiveness and recurrence.
To substantiate the clinical findings with functional evidence, the team conducted in vitro co-culture assays employing isolated human eosinophils alongside established chordoma cell lines. These experiments compellingly demonstrated that eosinophils directly inhibited chordoma cell proliferation, mediating this effect through the induction of apoptosis—programmed cell death critical for maintaining tissue homeostasis and preventing unrestrained tumor expansion. Quantitative analyses underscored a dose-dependent relationship, wherein increasing eosinophil concentrations corresponded with amplified tumor cell apoptosis.
Dr. Wang elaborates on the underlying mechanisms, stating, “Our data indicate eosinophil-mediated cytotoxicity hinges upon cytokine signaling, particularly through tumor necrosis factor alpha (TNF-α), a potent proinflammatory and apoptotic mediator.” Molecular interrogation of the co-culture milieu revealed elevated TNF-α levels, and neutralization of TNF-α attenuated the apoptotic cascade within chordoma cells, pinpointing this cytokine as a linchpin in the antitumor immune response orchestrated by eosinophils.
This compelling molecular insight enriches our understanding of the nuanced interplay between the immune system and chordoma, suggesting that eosinophils function not merely as bystanders but as active participants orchestrating inflammatory signals to curtail tumor expansion. Such revelations could recalibrate therapeutic strategies, positioning eosinophil activation or augmentation as a novel immunotherapeutic modality.
Collectively, these findings significantly advance the conceptual framework of chordoma immunobiology. They unmask a previously underappreciated immunosurveillance role of eosinophils, with potential translational implications for improving clinical outcomes. Given the paucity of effective treatments and the high recurrence rates associated with chordoma, leveraging the cytotoxic potential of eosinophils could redefine disease management paradigms.
Moreover, the work conducted by Professor Liu Pinan, whose expertise in complex neurosurgical interventions and tumor biology accentuates the clinical relevance of these discoveries, alongside Dr. Bo Wang’s extensive contributions to neuro-oncological research, fortifies the robustness and translational promise of this study. Their collaborative efforts epitomize the synergy between clinical acumen and molecular research necessary to tackle challenging neoplasms.
Future research endeavors building on these findings may explore avenues such as eosinophil-targeted therapies, cytokine modulation, or adoptive transfer of eosinophils engineered for enhanced cytotoxicity. Additionally, biomarkers reflective of eosinophil activity might emerge as prognostic tools, refining patient stratification and guiding personalized treatment approaches.
In conclusion, the revelation that human eosinophils exert pronounced antitumor effects against chordoma delineates a transformative leap in understanding tumor immunology relevant to this rare pathology. These insights advocate for the integration of immune modulation into the therapeutic arsenal against chordoma, holding promise to alter its clinical trajectory and improve patient prognoses substantially.
Subject of Research: People
Article Title: Human eosinophils exert antitumorigenic effects on chordoma
News Publication Date: 12-Dec-2025
Web References:
https://link.springer.com/article/10.1186/s41016-025-00414-6
http://dx.doi.org/10.1186/s41016-025-00414-6
References:
DOI: 10.1186/s41016-025-00414-6
Image Credits: Professor Liu Pinan and Dr. Bo Wang, Capital Medical University, Beijing, China
Keywords: Eosinophils, chordoma, tumor immune microenvironment, apoptosis, cytokines, tumor necrosis factor alpha, Ki-67 proliferation index, immunotherapy, tumor recurrence, granulocytes, immuno-oncology, neuro-oncology
Tags: challenges in chordoma treatmentchordoma research advancementscytokines and chemokines in tumorseosinophils and cancer researcheosinophils in chordomaimmune effector cells in cancerimmuno-oncology and chordomarare malignant bone tumorssurgical resection of chordomatherapeutic targets in bone tumorstumor biology and recurrencetumor immune microenvironment
