# Diagnostic value of cellular inflammatory markers in CNS tumor patients undergoing glucocorticoid therapy

**Authors:** Sofia Sklyar, Daria Sitovskaya, Nataliya Dryagina, Alexei Ulitin, Victor Olyushin, Stephanie E. Combs, Konstantin Samochernykh, Maxim Shevtsov

PMC · DOI: 10.3389/fonc.2026.1764339 · Frontiers in Oncology · 2026-02-18

## TL;DR

This study explores how cellular inflammatory markers can help diagnose CNS tumors, especially in patients taking glucocorticoids.

## Contribution

The study identifies specific inflammatory biomarkers that retain diagnostic value despite glucocorticoid therapy in CNS tumor patients.

## Key findings

- Glioblastoma patients had higher neutrophil and monocyte counts and elevated NLR and PIV compared to controls.
- LMR was a significant diagnostic marker in glioblastoma patients regardless of glucocorticoid use.
- Metastatic brain lesion patients showed increased diagnostic value in monocyte counts, PIV, and LMR.

## Abstract

While inflammation is recognized as a key driver of solid tumor progression, the diagnostic and pathophysiological relevance of cellular inflammatory biomarkers in central nervous system (CNS) neoplasms remains incompletely defined.

Clinical and hematological data were analyzed from 44 patients with glioblastoma, 32 with brain metastases, and 33 patients with meningioma who underwent primary surgical treatment between 2024 and 2025. A control group of healthy age-matched volunteers (n = 20) was included for comparison. The diagnostic performance of cellular inflammatory markers was evaluated across tumor entities, with additional stratification according to glucocorticosteroid exposure.

Patients with intracerebral tumors exhibited higher neutrophil and monocyte counts, as well as elevated neutrophil-to-lymphocyte ratio (NLR) and pan-immune inflammation value (PIV), along with a lower lymphocyte-to-monocyte ratio (LMR) compared to both the meningioma group and healthy volunteers (p<0.05). In glioblastoma patients, dexamethasone administration significantly affected neutrophil and monocyte counts, NLR and PIV (p<0.05). In the group with metastatic brain lesions, glucocorticoid therapy led to an increase in neutrophil count and NLR (p<0.05). The LMR level was not influenced by dexamethasone.

For patients with glioblastoma, the LMR serves as a diagnostically significant inflammatory biomarker independent of glucocorticoid administration. In patients with metastatic brain lesions, the most significant diagnostic value was demonstrated by monocyte counts, PIV and LMR.

## Linked entities

- **Chemicals:** dexamethasone (PubChem CID 5743)
- **Diseases:** glioblastoma (MONDO:0018177), meningioma (MONDO:0003057)

## Full-text entities

- **Genes:** CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, GFAP (glial fibrillary acidic protein) [NCBI Gene 2670] {aka ALXDRD}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IDH2 (isocitrate dehydrogenase (NADP(+)) 2) [NCBI Gene 3418] {aka D2HGA2, ICD-M, IDH, IDH-2, IDHM, IDP}, IDH1 (isocitrate dehydrogenase (NADP(+)) 1) [NCBI Gene 3417] {aka HEL-216, HEL-S-26, IDCD, IDH, IDP, IDPC}, CMPK1 (cytidine/uridine monophosphate kinase 1) [NCBI Gene 51727] {aka CK, CMK, CMPK, UMK, UMP-CMPK, UMPK}
- **Diseases:** lymphopenia (MESH:D008231), Tumor (MESH:D009369), lung cancer (MESH:D008175), CNS (MESH:D002493), edema (MESH:D004487), neuroinflammation (MESH:D000090862), metastatic disease (MESH:D000092182), NLR (MESH:D015467), melanoma (MESH:D008545), glioma (MESH:D005910), Inflammation (MESH:D007249), acute (MESH:D000208), seizures (MESH:D012640), status epilepticus (MESH:D013226), oral squamous cell carcinoma (MESH:D000077195), salivary gland carcinoma (MESH:D012468), non-small cell lung cancer (MESH:D002289), autoimmune disease (MESH:D001327), oncogenesis (MESH:D063646), CNS neoplasms (MESH:D016543), brain metastasis (MESH:D009362), intracerebral tumors (MESH:D002543), neutrophilia (MESH:C563010), urothelial carcinoma (MESH:D014523), brain (MESH:D001927), meningioma (MESH:D008579), immunodeficiency (MESH:D007153), neuro-oncological diseases (MESH:D000072716), brain metastases (MESH:D001932), infectious or inflammatory diseases (MESH:D003141), neurological deterioration (MESH:D009422), bladder cancer (MESH:D001749), Glioblastoma (MESH:D005909), renal cell carcinoma (MESH:D002292), Thrombocytosis (MESH:D013922), breast cancer (MESH:D001943), lymphomas (MESH:D008223), cutaneous melanoma (MESH:C562393), ovarian carcinoma (MESH:D010051), Gastrointestinal tract cancers (MESH:D005770)
- **Chemicals:** polymer (MESH:D011108), paraffin (MESH:D010232), ethanol (MESH:D000431), Dexamethasone (MESH:D003907), H&amp;E (MESH:D006371), PIV (-), hematoxylin (MESH:D006416), eosin (MESH:D004801), formalin (MESH:D005557), steroid (MESH:D013256)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12956639/full.md

## References

55 references — full list in the complete paper: https://tomesphere.com/paper/PMC12956639/full.md

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Source: https://tomesphere.com/paper/PMC12956639