Exploring the Link between Inflammatory Biomarkers and Head and Neck Cancer: Understanding the Impact of Smoking as a Cancer-Predisposing Factor

Abstract

Head and neck cancer (HNC) is associated with significant morbidity globally, with smoking recognized as a key risk factor. This study investigates the interplay between smoking and inflammatory biomarkers in HNC development. The study involved 50 HNC patients, divided into smoking and non-smoking groups, and a control group of 30 healthy individuals. Serum levels of 48 cytokines, chemokines, growth factors, and other inflammatory markers were meticulously assessed. Significant differences in the levels of an extensive panel of inflammatory markers were observed between the patient groups and healthy controls. Elevated macrophage colony-stimulating factor (M-CSF) in both HNC groups implicated increased activity in pathways known for immunomodulation, proliferation, and angiogenesis during HNC cancerogenesis. In contrast, non-smokers with HNC demonstrated higher levels of interleukin 10 (IL-10) and interleukin 15 (IL-15), suggesting a more robust immune response. Platelet-derived growth factor BB (PDGF-BB) levels were particularly high in smokers with HNC. Smoking seems to alter the levels of crucial biomarkers in HNC, potentially affecting disease progression and responses to treatment. The data indicate that smokers may experience a more aggressive cancer phenotype, while non-smokers maintain a profile suggestive of a more active and effective immune response against HNC.

Keywords: biomarkers; cytokines; head and neck cancer; inflammation; risk factors; smoking.

Figure 1

Correlations in the head and neck cancer (HNC) smoking group. Average number of cigarettes smoked per day vs. (A) body mass (r = 0. 469; p = 0. 018); (B) CTACK (r = −0. 407; p = 0.044); (C) M-CSF (r = −0.450; p = 0.024); and (D) MIP-1β (r = 0.413; p = 0.040). Abbreviations used: CTACK: cutaneous T-cell-attracting chemokine; M-CSF: macrophage colony-stimulating factor; MIP-1β: macrophage inflammatory protein 1 beta. p < 0.05 was considered statistically significant.

Figure 2

Effects of cigarette smoking on the levels of M-CSF, IL-10, IL-15, and PDGF-BB in the course of head and neck cancer. The main sources of cytokines and the signaling pathways activated by them are included. Abbreviations used: IL-10: interleukin 10; IL-15: interleukin 15; JAK-STAT: Janus kinase-signal transducer and activator of transcription pathway; M-CSF: macrophage colony-stimulating factor; MAPK/ERK: mitogen-activated protein kinase/extracellular signal-regulated kinase pathway; NK cells: natural killer cells; PDGF-BB: platelet-derived growth factor BB; PI3K/Akt/mTOR: phosphoinositide 3-kinase/Protein kinase B/mammalian target of rapamycin. Symbols used: ↑: higher; ↓: lower.