Laryngeal cancer is a relatively uncommon malignancy with predisposing genetic factors that remain unclear. Single-nucleotide polymorphisms (SNPs) in genes involved in innate immune signaling may contribute to the development and progression of laryngeal carcinoma. This study aimed to evaluate the association of TLR4 (rs7037225, rs11536889, rs7037117) and MYD88 (rs7744, rs6853) polymorphisms with the risk of laryngeal squamous cell carcinoma (LSCC), as well as its clinical and pathological characteristics and survival. A retrospective case–control study involving 172 LSCC patients and 220 healthy controls was conducted. Genotyping was performed using real-time PCR from venous blood samples. MYD88 rs7744 was significantly associated with tumor size and lymph node involvement. Survival analysis showed a significant association between rs7744 and recurrence-free survival (RFS), with the AG and GG genotypes linked to poorer outcomes. Conversely, carriers of the TLR4 rs7037225 CT genotype showed significantly improved RFS, with p ranging from 0.024 to 0.037 across models. Considering the significant roles of TLR4 and MYD88 in Toll-like receptor signaling, these findings may reflect the involvement of innate immune pathways in LSCC progression. In summary, MYD88 rs7744 was associated with clinicopathological features and RFS, while TLR4 rs7037225 appeared to have a potential protective effect on survival.

Introduction: Radiotherapy is a vital therapeutic option in the treatment of breast cancer nowadays. However, a major obstacle to the full effectiveness of radiation therapy is still the radioresistance of cancer cells. Various studies have proven sulforaphane's (SFN) beneficial effects against cancer and its possible utilization as a radiosensitizer in radiotherapy. This study aimed to investigate whether SFN has a radiosensitizing effect on breast cancer cells.Material and methods: The anticancer efficiency of SFN and radiosensitizing effect in MCF-7 and MDA-MB-231 cell lines were assessed by the MTT assay. Using a flow cytometric assay, the apoptosis level and changes in the cell cycle were measured. RT-qPCR and Western blot analysis were used to determine BCL-2 and BCL-XL genes expresion and proteins level.Results: According to our results, SFN reduced the viability of cells, and combining SFN with radiation therapy (IR) caused much greater anticancer effects on cells. SFN+IR was shown to enhance the number of cells in the G2/M phase and the percentage of cells going through apoptosis. SFN reduced the expression of apoptosis-relative genes BCL-2 and BCL-XL. Consistent with this data, Western blot analysis revealed that BCL-2 and BCL-XL protein levels were decreased in tested cells. As a result of the combination treatment, the downregulation of the BCL-2 protein was observed only in MDA-MB-231 cells.Conclusions: These results indicate that SFN acts as a radiosensitizer by enhancing apoptotic cell death and reducing anti-apoptotic genes in breast cancer cells.

This study investigated the antiproliferative effects of luteolin (LUT) and its potential to modify the response of breast cancer (BC) cells to ionizing radiation (IR). LUT effects alone or with IR were evaluated in MCF-7 and MDA-MB-231 cells using clonogenic and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. Apoptosis and cell cycle distribution were assessed by flow cytometry, while reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting were used to determine apoptosis-related gene and protein expression. LUT reduced the clonogenic survival and metabolic activity in both BC cell lines. In MCF-7 cells, combined LUT and IR treatment produced a greater reduction in metabolic activity and clonogenic survival than either treatment alone, whereas no comparable effect was observed in MDA-MB-231 cells. LUT induced apoptosis in both cell lines. Cell cycle analysis indicated G2/M phase accumulation, reaching statistical significance in MDA-MB-231 cells. In MCF-7 cells, LUT decreased BCL2 and MCL1 gene expression, with a further reduction following combined LUT and IR treatment. Consistently, BCL-2 protein levels were reduced in MCF-7 cells. In MDA-MB-231 cells, LUT modulated the expression of selected anti-apoptotic genes. Overall, these findings demonstrate cell line-dependent effects of LUT and suggest that its ability to modify the response to IR may depend on the molecular characteristics of BC cells.