VEGFA (rs1570360, rs699947, rs3025033, rs2146323, rs3024997) genotypes in patients with laryngeal squamous cell carcinoma

Abstract Background Laryngeal squamous cell carcinoma (LSCC) is a common and aggressive head and neck malignancy with poor prognosis due to late diagnosis and limited biomarkers. Angiogenesis, driven by vascular endothelial growth factor A (VEGFA), plays a key role in tumor growth and metastasis. Si...

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Main Authors: Agne Pasvenskaite, Alvita Vilkeviciute, Monika Duseikaite, Enrika Pileckaite, Greta Gedvilaite-Vaicechauskiene, Vykintas Liutkevicius, Rasa Liutkeviciene, Virgilijus Uloza
Format: Article
Language:English
Published: BMC 2025-07-01
Series:BMC Cancer
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Online Access:https://doi.org/10.1186/s12885-025-14536-8
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Summary:Abstract Background Laryngeal squamous cell carcinoma (LSCC) is a common and aggressive head and neck malignancy with poor prognosis due to late diagnosis and limited biomarkers. Angiogenesis, driven by vascular endothelial growth factor A (VEGFA), plays a key role in tumor growth and metastasis. Single nucleotide variants (SNVs) in the VEGFA gene have been linked to various cancers, but their role in LSCC remains unclear. Methods In this study, we investigated the association between VEGFA (rs1570360, rs699947, rs3025033, rs2146323, rs3024997) SNV and LSCC susceptibility in a large cohort of 297 LSCC patients and 390 age- and sex-matched control subjects. The DNA samples were obtained from peripheral blood leukocytes, which were purified using the DNA salting-out technique. Real-time polymerase chain reaction assessed SNVs. The data obtained were processed using the IBM SPSS Statistics 29.0 software. Using a detailed subgroup analysis based on tumor stage, size, metastasis, and differentiation grade, we assessed the potential links between VEGFA (rs1570360, rs699947, rs3025033, rs2146323, rs3024997) variants and LSCC development. Results Contrary to previous studies suggesting significant associations between VEGFA genetic variances with other squamous head and neck cell cancers, our study found no statistically significant differences in the distribution of these SNVs between LSCC patients and controls. Our findings suggest that VEGFA SNV may not be a key factor in LSCC susceptibility. However, the complexity of LSCC’s genetic underpinnings warrants further investigation with larger cohorts and additional genetic markers. Conclusions Our results contribute to the ongoing debate on the role of angiogenesis in LSCC and provide insights into the challenges of identifying reliable biomarkers for this malignancy.
ISSN:1471-2407