Abstract
ObjectiveThe promotion of neovascularisation is a crucial aspect of carcinogenesis. The study evaluates the microvascular density (MVD) and expression of hypoxia-induced factor (HIF-1α) in hypertrophic vocal fold (VF) lesions of different histopathological states including non-dysplastic, low-grade, high-grade dysplasia and invasive glottic cancer.Materials and methodsHistological specimens collected from patients diagnosed and treated in a single centre with different histological grades were immunohistochemically stained with CD31, CD34 and HIF-1α. Of the total number of 77 analysed VF specimens, 20 were non-dysplastic, 20 had low-grade dysplasia, 17 high-grade dysplasia and 20 were invasive cancers.ResultsThe highest mean value for MVD evaluated with expression of CD31 (MVD CD31) was 21.23 ± 14.46 and identified in the low-grade dysplasia group. The average MVD CD31 was 13.74 ± 5.56 and 20.11 ± 9.28 in the high-grade dysplasia and invasive cancer group, respectively. The highest MVD evaluated with CD34 (MVD CD34) was revealed for invasive cancer 35.64 ± 17.21. The MVD CD34 was higher for low-grade than in high-grade dysplasia (25.87 ± 12.30 vs 24.65 ± 15.92, respectively). The expression of HIF-1α was strong or very strong in 60% of non-dysplastic lesions, 100% of low-grade dysplasia cases, 53% of high-grade dysplasia cases and 50% of invasive cancer cases. The comparison of MVD CD31 with MVD CD34 revealed a strong positive correlation (ρ value 0.727). The comparison of both MVD CD31 and MVD CD34 with HIF-1α resulted in no linear relationship (ρ value of 0.143 and 0.165, respectively).ConclusionThe stage of low-grade dysplasia in intraepithelial vocal fold lesions is related to significant advancement of angiogenesis together with the highest hypoxia level.
Highlights
The model of the genetic changes responsible for progression of hypertrophic laryngeal lesions to dysplastic and invasive cancer is still incomplete and lacking [1]
European Archives of Oto-Rhino-Laryngology (2019) 276:1117–1125 growth factors including vascular endothelial growth factor (VEGF), transforming growth factor (TGF) and various cytokines secreted by the altered cells [3]
The groups with nondysplastic lesions, low-grade dysplasia and invasive cancer consisted of 20 patients each
Summary
The model of the genetic changes responsible for progression of hypertrophic laryngeal lesions to dysplastic and invasive cancer is still incomplete and lacking [1]. The architectural and cytological disorder found within epithelial cells can be histopathologically classified as squamous hyperplasia, dysplasia or invasion This pathology is controlled by a multistep process of genetic changes, which influence the potential for cellular multiplication at this level, and inevitably alter the surrounding microenvironment indirectly, providing for the most optimal conditions for tumour expansion [2]. Our study was designed to investigate the relation of microvascular density and hypoxia in premalignant and malignant vocal fold lesions and enable for a better understanding of the mechanisms involved in the carcinogenesis of the laryngeal epithelium This can be further utilised in the future development of more targeted and individualized therapies, during the course of early treatment and prevention, where changes to intervention can influence patient outcomes
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