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. 2025 May 18;16(1):801.
doi: 10.1007/s12672-025-02654-5.

Exploring the causal relationship between immune factors and chondrosarcoma: a Mendelian randomization study

Taichuan Xu  1 , Wentao Xiao  1 , Wenjie Li  1 , Xianfa Xu  1 , Haiwen Zhang  1 , Xian Zhang  2
Affiliations

Exploring the causal relationship between immune factors and chondrosarcoma: a Mendelian randomization study

Taichuan Xu et al. Discov Oncol. .

Abstract

Background: Previous studies have investigated the potential role of immune factors in chondrosarcoma (CHS). However, the causal relationship is unknown.

Methods: A two-sample Mendelian randomization (MR) was used to explore potential correlations between 731 immunocyte phenotypes, 91 inflammatory proteins, and CHS. The data were derived from published summary statistics of genome-wide association studies. Inverse-variance weighted was employed as the primary method. Furthermore, a range of analytical methods, including MR-Egger, weighted mode, and weighted median was used to enhance the robustness of the results. A two-step MR was used to assess the mediating effects of inflammatory proteins. Subsequently, sensitivity and MR Steiger directionality tests were performed.

Results: MR analyses showed that 12 immunocyte phenotypes were positively correlated with CHS (P < 0.05, OR > 1), and 11 immunocyte phenotypes were negatively correlated with CHS (P < 0.05, OR < 1). Five inflammatory proteins were positively associated with CHS (P < 0.05, OR > 1). No heterogeneous or horizontal pleiotropy was found. The MR Steiger analysis found no statistically significant evidence of reverse causation. Mediation analysis did not identify any potential mediating effects.

Conclusion: Our study underscores the pivotal role of immune factors in CHS and offers insights that can inform future research.

Keywords: Chondrosarcoma; Immune trait; Inflammatory proteins; Mendelian randomization.

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Conflict of interest statement

Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
The workflow of this study
Fig. 2
Fig. 2
Forest plot of causal effects for immune traits on CHS. CHS, chondrosarcoma; IVW, inverse-variance weighted
Fig. 3
Fig. 3
Scatter plot of causal effects for immune traits on CHS. A CD38 on IgD- CD38dim on CHS, B IgD- CD38- %B cell on CHS, C CD38 on CD20- on CHS, D CD11c + CD62L- monocyte AC on CHS, E CD86 + myeloid DC %DC on CHS, F CD19 on PB/PC on CHS, G CM CD4 + %CD4 + on CHS, H CCR2 on monocyte on CHS, I Monocyte AC on CHS, J CD24 on IgD + CD24 + on CHS, K CD28- DN (CD4-CD8-) %T cell on CHS, L CD33dim HLA DR + CD11b + AC on CHS
Fig. 4
Fig. 4
Scatter plot of causal effects for immune traits on CHS. A HLA DR +  + monocyte AC on CHS, B IgD + %B cell on CHS, C Naive-mature B cell %B cell on CHS, D CD45 on Mo MDSC on CHS, E CD20 on IgD + CD38- naïve on CHS, F HLA DR on HLA DR + T cell on CHS, G Memory B cell %B cell on CHS, H CD20- CD38- %lymphocyte on CHS, I Sw mem %B cell on CHS, J CD11b on Gr MDSC on CHS, K CD80 on CD62L + myeloid DC on CHS
Fig. 5
Fig. 5
Forest plot of causal effects for inflammatory proteins on CHS
Fig. 6
Fig. 6
Scatter plot of causal effects for inflammatory proteins on CHS. A Monocyte chemoattractant protein-1 levels on CHS, B Leukemia inhibitory factor receptor levels on CHS, C Neurotrophin-3 levels on CHS, D Interleukin-24 levels on CHS, E C–C motif chemokine 23 levels on CHS
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