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Published on: December 3, 2020
Impact of Anatomical Localization on Systemic Inflammatory Markers and Immune Checkpoint CD47 in Desmoid Tumors
Sendag Yaslikaya1, Suheda Atas Ipek2, Ipek Balikci Cicek3
1Department of Medical Oncology, Giresun Training and Research Hospital, Giresun 28100, Turkey.
Abstract:
Background: Desmoid tumors (DT) are rare, locally aggressive neoplasms characterized by an unpredictable clinical course. Although anatomical localization has been associated with tumor behavior, its relationship with systemic inflammatory response remains insufficiently explored. This study aimed to evaluate the impact of tumor localization on systemic inflammatory markers and to investigate CD47 expression in DT. Methods: This retrospective cohort study included 127 patients diagnosed with DT between 2010 and 2023. Demographic, clinicopathological, and laboratory data were collected. Systemic inflammatory indices, including neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), prognostic nutritional index (PNI), HALP score, and pan-immune-inflammation value (PIV), were calculated. Tumor localization was categorized as trunk, extremity, or head and neck. CD47 expression was evaluated by immunohistochemistry. Results: Tumors were most frequently located in the trunk (50.4%), followed by extremities (40.9%) and head and neck region (8.7%). Significant differences in inflammatory markers were observed according to tumor localization. The head and neck group demonstrated lower neutrophil counts (p = 0.020), NLR (p = 0.009), PLR (p < 0.001), and PIV (p = 0.003), while showing higher PNI (p = 0.043) and HALP scores (p = 0.001) compared to trunk-localized tumors. Additionally, smaller tumors (<49 mm) were associated with lower NLR (p = 0.041) and neutrophil counts (p = 0.015). No detectable CD47 expression was observed in any tumor samples. Conclusions: Anatomical localization is closely associated with distinct systemic inflammatory profiles in patients with DT. These findings suggest that tumor location may influence host immune-inflammatory interactions and contribute to the biological heterogeneity of DT. The absence of CD47 expression indicates that alternative immune-related mechanisms may play a role in DT biology. Easily accessible inflammatory markers may provide valuable insights for risk stratification in clinical practice.
