Search Results (1,730)

The potential impact of propofol on head and neck cancer (HNC) progression and clinical outcomes, in relation to both direct effects on tumor biology and indirect effects mediated by perioperative immune and inflammatory responses, remains controversial. Most mechanistic evidence currently available for HNC originates from studies of oral squamous cell carcinoma. Accordingly, mechanistic findings are interpreted primarily as OSCC-derived evidence and should not be generalized to all HNC subsites without further validation. To address this, we critically examined propofol’s potential role as a perioperative anesthetic modulator of tumor biology and host responses. Preclinical studies have demonstrated that propofol suppresses proliferation, induces apoptosis, inhibits angiogenesis, and enhances 5-fluorouracil chemosensitivity. Conversely, other studies report enhanced epithelial–mesenchymal transition, migration, and invasion through SNAI1 upregulation, highlighting the context-dependent nature of propofol-mediated effects. The generalizability of these molecular observations to other HNC subsites, including laryngeal, hypopharyngeal, and oropharyngeal cancers, remains unclear. Clinically, propofol-based total intravenous anesthesia has been associated with reduced postoperative pulmonary complications and improved perioperative recovery. However, currently available HNC-specific studies have not demonstrated a consistent improvement in overall or recurrence-free survival. These discrepancies likely reflect tumor heterogeneity, variations in experimental design, perioperative confounding factors, and differences in host immune and inflammatory responses. This narrative review was based on literature identified through PubMed, Scopus, and Google Scholar, and integrates current mechanistic, immunological, and clinical evidence regarding propofol exposure during cancer surgery. Current evidence supports the perioperative benefits of propofol-based anesthesia; however, its long-term oncologic significance in HNC remains inconclusive and warrants further prospective, mechanism-driven, and biomarker-guided investigations. Full article

Background/Objectives: Cutaneous squamous cell carcinomas (cSCC) of the head and neck district are among the most common non melanocytic malignant skin carcinomas. The proposal to differentiate, within the N stage, parotid metastases from lateral cervical metastases, originates from the different prognostic value of the metastatic region involved. Methods: We retrospectively evaluated 61 patients, surgically treated for parotid metastases from cSCC between January 2002 and June 2023, in four Departments of Surgery, to assess the geographic distribution of parotid metastases and to describe their recurrence patterns, to evaluate the prognostic value of the number of affected lateral cervical lymph nodes (LN) and the number of positive intra-glandular lymph nodes (IGLN) and to identify the main prognostic histopathological factors. Results: Our results did not show significant differences between participating centers in the distribution of parotid metastases, nor in their recurrence rates. However, our results highlight how adjuvant radiotherapy is deeply associated with the Overall Survival (OS), improving survival rates in patients with advanced-stage neoplasms (Odds Ratio 5.0), although causality cannot be inferred because of the retrospective study design. Moreover, a statistically significant correlation was found between the major inflammatory biomarkers and the OS. The presence of IGLN was identified as one of the main factors associated with recurrence and poor prognosis in patients with cSCC and in particular, in patients with N3b nodal stage. Conclusions: our findings suggest that both LN and IGLN could be used to propose an additional staging stratification for the N parameter, thereby guiding the treatment strategy and postoperative follow-up for patients with parotid metastases from cSCC of the head and neck district. Full article

Immune checkpoint inhibitors (ICIs) have improved clinical outcomes in recurrent or metastatic head and neck squamous cell carcinoma (HNSCC), including oral squamous cell carcinoma (OSCC). However, many patients eventually develop resistance to systemic therapy, highlighting the need for novel strategies that can restore or sustain antitumor immunity. Near-infrared photoimmunotherapy (PIT) has emerged as a tumor-selective locoregional treatment that not only induces targeted tumor cell death but also promotes antitumor immune activation through immunogenic cell death. This narrative review summarizes current evidence regarding PIT for recurrent oral cancer and explores the immunological rationale for sequential ICI–PIT–ICI therapy (ICI–PIT–ICI sequence). Within this framework, PIT-induced tumor antigen release and inflammatory activation may reinitiate elements of the cancer-immunity cycle, whereas continued PD-1 blockade may help sustain newly activated tumor-reactive T-cell responses. To illustrate this concept, we present two cases of recurrent oral cancer treated with the ICI–PIT–ICI sequence. Both patients achieved durable clinical and radiological complete responses following PIT and subsequent nivolumab continuation. Longitudinal analyses of peripheral immune surrogate markers demonstrated a biphasic temporal pattern characterized by transient increases in inflammatory markers, including neutrophil-to-lymphocyte ratio, C-reactive protein, platelet-to-lymphocyte ratio, and systemic immune-inflammation index, followed by recovery trends in absolute lymphocyte count and lymphocyte-to-monocyte ratio during continued PD-1 blockade. These observations support the biological plausibility of PIT as an immune-modulating intervention with potential immune-reprogramming effects. Although hypothesis-generating, the ICI–PIT–ICI sequence may represent a promising strategy integrating locoregional tumor destruction with systemic immune modulation in recurrent oral cancer. Further prospective studies incorporating peripheral and tissue-based immune profiling are warranted. Full article

Head and neck squamous cell carcinoma (HNSCC) is characterized by marked intratumoral heterogeneity and complex tumor–immune–stromal interactions, which shape therapeutic response and clinical outcome. Despite extensive transcriptomic efforts, bulk RNA sequencing has faced significant limitations, often failing to generate robust prognostic or predictive biomarkers, highlighting the need for approaches capable of resolving the cellular and spatial complexity of the tumor ecosystem. Single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) have refined our understanding of HNSCC biology by enabling high-resolution mapping of malignant, stem-like, immune, and stromal compartments. Three major spatial domains have been defined in HNSCC: tumor core (TC), tumor invasion front (TIF), and leading edge (LE). Each ecosystem exhibits distinct cellular programs that promote immune evasion, tumor dissemination, and therapy resistance, particularly in high-risk clinical settings. In this Review, we integrate recent single-cell and spatial studies and propose a translational framework linking ecosystem architecture with clinical stratification across resectable locally advanced (r-LAD), unresectable locally advanced (u-LAD), and recurrent/metastatic (R/M) disease. We further discuss how spatially resolved transcriptomic approaches may support biomarker discovery and hypothesis generation for risk stratification and trial design, while emphasizing that clinical implementation remains limited by cohort size, methodological heterogeneity, and the need for large-scale prospective validation. Finally, we outline key methodological and translational challenges that must be addressed before these technologies can reliably inform precision oncology and decision-making in HNSCC. Full article

Background/Objectives: Temporal muscle thickness (TMT) has been proposed as a practical surrogate marker for skeletal muscle mass, whereas the geriatric nutritional risk index (GNRI) reflects nutritional status. However, the independent and combined prognostic value of TMT and GNRI in surgically treated head and neck squamous cell carcinoma (HNSCC) remains unclear. Methods: We retrospectively analyzed 214 patients with HNSCC who underwent curative-intent surgery. Disease-free survival (DFS) and overall survival (OS) were evaluated using Cox proportional hazards models. In the primary analyses, TMT and GNRI were entered simultaneously as continuous variables and adjusted for age, sex, clinical stage, and postoperative adjuvant treatment. For clinical interpretability, Kaplan–Meier analyses were additionally performed using a composite TMT–GNRI score. Results: In the multivariable analyses, higher TMT was independently associated with longer DFS (hazard ratio [HR] 0.83 per 1 mm increase, 95% confidence interval [CI] 0.72–0.96, p = 0.014) and OS (HR 0.73, 95% CI 0.60–0.89, p = 0.002). GNRI was significantly associated with DFS and OS in the univariate analyses; after simultaneous adjustment for TMT and clinical covariates, it remained independently associated with OS (HR 0.98 per 1-point increase, 95% CI 0.96–0.99, p = 0.015) and showed a borderline association with DFS (HR 0.984, 95% CI 0.966–1.001, p = 0.068). Kaplan–Meier analyses using the composite TMT–GNRI score demonstrated clear risk stratification, with the poorest outcomes observed in patients with concomitantly low TMT and low GNRI. Conclusions: In surgically treated HNSCC, preoperative TMT was independently associated with both DFS and OS. GNRI may provide additional prognostic information, particularly for OS. Full article

Background: Head and neck squamous cell carcinomas (HNSCCs) are highly immunosuppressive, and tumor-associated macrophages constitute a major component of HNSCC tumor microenvironments. Here, we investigate the effects of circulating small extracellular vesicles (sEVs) from HNSCC patients on primary macrophages, to elucidate systemic sEV-mediated immune regulation in HNSCC patients. Methods: sEVs were isolated from plasma by size-exclusion chromatography. Internalization of PKH26-labeled sEVs was demonstrated, and mass spectrometry analysis was performed on HNSCC sEVs and sEV-treated macrophages. NF-κB activation was investigated by Western blot and p65 translocation assay. Downstream, mRNA and protein levels of cytokines and chemotaxis of T cells were investigated. Results: Proteomic analysis revealed time-dependent modulation of the macrophage proteome and NF-κB signaling pathway, which was confirmed by Western blot and p65 translocation assay. sEVs from HNSCC patients negative for human papillomavirus type 16 (HPV) differentially modulated NF-κB signaling and sEV uptake mechanisms compared with sEVs from HPV-positive patients and healthy donors. Conclusions: Circulating sEVs derived from HNSCC patient plasma modulate macrophage proteomic profiles and NF-κB signaling. HPV16 status was associated with differential sEV-mediated macrophage regulation, suggesting a potential role of sEVs in systemic immune modulation in HNSCC. Full article

Background/Objectives: Data on the value of tumor debulking surgery are scarce. We aimed to examine whether tumor debulking surgery followed by non-surgical treatment (cases) improves survival compared to non-surgical treatment alone (controls) in patients with head and neck cancer (HNC). Methods: We performed a systematic review of studies published in the databases PubMed, Scopus and Cochrane Central Register of Controlled Trials up to 10 December 2024. Studies evaluating tumor debulking surgery followed by non-surgical treatment and reporting survival (local recurrence, disease-free survival or overall survival) in subjects with HNC were included; case reports were excluded. We assessed the quality of observational studies with the Newcastle–Ottawa Scale. Results: Among 11 retrospective small studies, three case–control studies (one of high quality, i.e., 7/9, and two of moderate quality, i.e., 6/9 and 5/9) suggested longer survival in 72 cases with predominantly squamous cell carcinoma (SCC) than in 40 controls with predominantly SCC. However, these survival benefits cannot be attributed solely to tumor debulking surgery, as confounding by indication is the most likely explanation. In supraglottic laryngeal SCC, one study reported a local recurrence-free survival rate and overall survival of 80% and 88%, respectively, in 25 cases compared with 86% and 77%, respectively, in 24 controls. In sarcomas, local recurrence-free survival was 25%, 65% and 100% for unknown resection margins, wide local excision and radical excision, respectively. Conclusions: The heterogeneous data indicate the need for higher-quality research. It would be interesting to investigate whether an attempt to surgically debulk paranasal sinus tumors while preserving adjacent vital organs (e.g., the orbit and/or brain) should be incorporated into the treatment strategy for patients with extended paranasal sinus squamous cell carcinoma. Tumor debulking surgery did not improve survival in supraglottic laryngeal SCC or head and neck soft tissue sarcomas. Full article

Background/Objectives: Perineural invasion (PNI) and lymphovascular invasion (LVI) are adverse histopathological features in head and neck squamous cell carcinoma (HNSCC). Their relationship with clinical and pathological T categories remains clinically relevant, particularly in surgically treated cohorts. This exploratory retrospective study evaluated the frequency of PNI and LVI according to clinical and pathological T stage in primary HNSCC staged according to the AJCC/UICC 8th edition. Methods: We analyzed 170 consecutive surgically treated patients with primary HNSCC. PNI and LVI were recorded from histopathology reports of resection specimens. Results: PNI status was available in 124 cases and was positive in 61 (49.2%); LVI status was available in 126 cases and was positive in 62 (49.2%). PNI frequency increased with advancing clinical T stage (12.5% in cT1, 54.3% in cT2, 70.0% in cT3, and 69.2% in cT4) and pathological T stage (14.3% in pT1, 51.5% in pT2, 71.9% in pT3, and 66.7% in pT4). LVI also increased with higher clinical T stage (28.1%, 53.2%, 57.1%, and 61.5%) and pathological T stage (25.7%, 50.0%, 54.6%, and 75.0%). Tongue tumors showed descriptively high crude proportions of PNI and LVI, but these subgroup findings were based on small numbers and were not adjusted for T stage, depth of invasion, or other confounders. Conclusions: In this single-center cohort, PNI and LVI were more frequent in higher T categories. These findings should be interpreted as descriptive and hypothesis-generating, because no recurrence, survival, or treatment-outcome analyses were available and the adjusted models were exploratory. Full article

Despite advances in multimodal treatment, head and neck squamous cell carcinoma (HNSCC) remains a major clinical problem owing to its high recurrence rate and frequent development of treatment resistance. Abnormal histone modifications, particularly lysine methylation regulated by methyltransferases (KMTs) and demethylases (KDMs), have emerged as key drivers of HNSCC initiation, progression, and cellular plasticity. This review aims to comprehensively evaluate the role of selected KMTs and KDMs in HNSCC biology, with a focus on their contribution to resistance to immunotherapy, radiotherapy, and cytotoxic chemotherapy. We summarize and critically analyze preclinical and clinical studies investigating histone methylation dynamics in HNSCC, with particular emphasis on enzymes such as KMT2C/D, EZH2, NSD1/NSD2, SMYD3, G9a/EHMT2, LSD1, KDM2A/B, KDM3, KDM4, KDM5, KDM6, KDM7, and KDM8. Attention is given particularly to pharmacological approaches targeting these proteins: we discuss small-molecule inhibitors of EZH2, LSD1, KDM4/5/6, and other KMT/KDMs that are currently in preclinical development or in early clinical trials, and we highlight completed and ongoing studies testing EZH1/2 inhibitors and epigenetic combinations in patients with recurrent and metastatic HNSCC. The deregulation of specific KMTs and KDMs reshapes histone methylation at key residues, thereby controlling cell cycle progression, epithelial–mesenchymal transition (EMT), stem cell phenotypes, DNA damage responses, and multiple interactions with the immune system in HNSCC. Targeting disrupted histone methylation pathways may partially reverse the epigenetic reprogramming of HNSCC cells and represents a promising strategy to improve treatment efficacy in patients with advanced disease. We also summarize the preclinical evidence and the currently limited clinical data on targeting histone methylation dynamics in HNSCC and discuss their therapeutic implications. Full article

Background/Objectives: Oral squamous cell carcinoma (OSCC) remains clinically heterogeneous, and prognosis is not always fully explained by conventional clinicopathological parameters. Systemic inflammation and tumor metabolic alterations may provide complementary information on tumor biology. This study aimed to assess associations between preoperative inflammatory markers, isotope ratio mass spectrometry (IRMS)-derived tumor signatures, clinicopathological features, and survival outcomes in OSCC. Methods: This exploratory retrospective secondary analysis included 50 consecutive patients with surgically treated, histologically confirmed OSCC. Preoperative blood-based markers, including neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic immune-inflammation index (SII), white blood cell count, lymphocyte count, and C-reactive protein, were retrieved from routine laboratory tests. Matched tumor, surgical margin, and healthy oral mucosa samples were analyzed by IRMS for δ¹³C, δ¹⁵N, carbon and nitrogen content, and [N]/[C] ratio. Associations with clinicopathological variables, nodal status, overall survival (OS), and disease-free survival (DFS) were evaluated using non-parametric tests, Spearman correlations, and Cox regression models. Results: Tumor tissue showed a consistent isotope and elemental phenotype compared with healthy mucosa, including higher nitrogen content, lower carbon content, increased [N]/[C] ratio, lower δ¹⁵N, and less negative δ¹³C values. NLR, PLR, SII, and CRP were not robustly associated with standard clinicopathological features after correction for multiple testing. Correlations between inflammatory and isotope-derived parameters were modest. Higher NLR was associated with worse OS and DFS and remained significant after adjustment for pathologic nodal status. Less negative tumor δ¹³C showed a potential adverse prognostic signal. Conclusions: Systemic inflammatory markers and IRMS-derived tumor signatures appear to reflect partly distinct biological domains in OSCC. NLR may provide accessible prognostic information, while tumor δ¹³C warrants further validation as a metabolic biomarker. Full article

Unc-51-like kinase 3 (ULK3) is a key member of the ULK serine/threonine kinase family. Aberrant ULK3 expression has been increasingly linked to tumorigenesis and malignant progression in multiple cancer types. However, the precise role of ULK3 in tumor initiation and progression remains incompletely understood. Leveraging integrated multi-omics data from The Cancer Genome Atlas (TCGA), the Genotype-Tissue Expression (GTEx) project, and the Clinical Proteomic Tumor Analysis Consortium (CPTAC), we systematically characterized the expression of ULK3 at both the transcript and protein levels across 33 cancer types. We also evaluated genomic alterations, prognostic significance, alternative splicing, pathway enrichment, tumor stemness, immune infiltration, and immunotherapy-related biomarkers. In parallel, we investigated the function of ULK3 in prostate cancer PC-3 cells using cellular localization analysis, wound-healing assays, and MTT assays. We further applied Connectivity Map (CMap) screening and molecular docking to identify candidate ULK3 activators. ULK3 was significantly upregulated in 13 cancer types, including Bladder Urothelial Carcinoma, Breast Invasive Carcinoma, and Lung Adenocarcinoma. In contrast, ULK3 was downregulated in Cholangiocarcinoma and Head and Neck Squamous Cell Carcinoma. High ULK3 expression was associated with poor overall survival in Adrenocortical Carcinoma, Kidney Renal Clear Cell Carcinoma, and Skin Cutaneous Melanoma. Copy number amplification contributed to ULK3 overexpression. A recurrent A206V missense mutation was detected in the protein kinase (Pkinase) domain. Genes co-expressed with ULK3 were enriched in RNA splicing, methylation, oxidative phosphorylation, and energy metabolism. ULK3 expression showed positive correlations with tumor stemness indices and m1A/m5C/m6A RNA modification regulators. From an immunological perspective, high ULK3 expression was associated with lower Immune Score, increased M2 macrophage infiltration, and co-expression of PD-L1, CTLA4, and LAG3 in most cancers. ULK3 expression was also correlated with Tumor Mutational Burden in Kidney Renal Clear Cell Carcinoma and Rectum Adenocarcinoma. In addition, ULK3 expression was associated with Microsatellite Instability in Brain Lower Grade Glioma, Lung Adenocarcinoma, and Uterine Corpus Endometrial Carcinoma. ULK3 overexpression promoted proliferation and migration in PC-3 cells. Cephaeline was screened as a putative ULK3 activator. Overall, ULK3 expression and amplification were associated with poor clinical outcomes, tumor stemness, immunosuppression, and RNA dysregulation. These findings highlight the potential value of ULK3 as a pan-cancer diagnostic and prognostic biomarker and as a predictor of immunotherapy response, particularly in prostate cancer. Full article

Background: Head and neck squamous cell carcinoma (HNSCC) remains a highly aggressive malignancy with poor clinical outcomes. Although poly(ADP-ribose) polymerase (PARP) inhibitors have shown promising activity in tumors with homologous recombination deficiency, their efficacy in BRCA wild-type HNSCC remains limited. Reactive oxygen species (ROS)-induced DNA damage may increase cellular dependence on DNA repair pathways and thereby enhance sensitivity to PARP inhibition. This study investigated whether ROS-mediated DNA damage could sensitize BRCA wild-type HNSCC cells to the PARP inhibitor olaparib. Methods: BRCA wild-type HSC-3 and SCC-25 HNSCC cell lines were exposed to H₂O₂ to induce oxidative stress. Intracellular ROS levels were quantified using DCFDA assays, DNA double-strand breaks were evaluated by γ-H2AX ELISA, PARP activity was assessed by ELISA, and cell viability was determined using MTT assays. Expression levels of DNA repair genes (PARP1, PARP2, BRCA1, BRCA2, RAD51, and MLH1), checkpoint kinases (ATM, ATR, and CHK1), the homologous recombination regulator FANCD2, and redox defense genes (NQO1, GPX4, and SLC7A11) were analyzed by qRT-PCR. Therapeutic selectivity was assessed using HGF-1 normal human gingival fibroblasts as a normal cell control. Apoptosis was measured through caspase-3/7 activity assays, and drug interactions were evaluated using the Chou–Talalay method. Results: H₂O₂ treatment increased intracellular ROS levels in both cell lines, accompanied by significant induction of DNA damage as demonstrated by elevated γ-H2AX levels. ROS induction markedly enhanced olaparib sensitivity, significantly reducing IC₅₀ values in both HSC-3 and SCC-25 cells. Combined H₂O₂ and olaparib treatment produced strong synergistic cytotoxicity, suppressed DNA repair, checkpoint kinase, and redox defense gene expression, and increased caspase-3/7 activity compared with control cells. Importantly, the combination demonstrated selective cytotoxicity toward cancer cells, with normal HGF-1 cells retaining significantly higher viability. Conclusions: ROS-induced DNA damage significantly enhances the anti-tumor activity of olaparib in BRCA wild-type HNSCC cells through a functional synthetic lethal-like interaction involving the simultaneous collapse of DNA repair capacity, checkpoint activation, and oxidative stress buffering, culminating in apoptosis induction. These findings support the rationale for combining ROS-generating therapies with PARP inhibitors in HNSCC treatment. Full article

Oral squamous-cell carcinoma (OSCC) is a prevalent malignancy of the head and neck region. A delay in the diagnosis of OSCC often results in a high metastatic tendency, which is the main reason for the high patient mortality. Dynamic monitoring and management of the onset and progression of OSCC are critical for improving patient survival rates. Liquid biopsy technology—characterized by its non-invasive nature, procedural convenience, and capacity for longitudinal monitoring—is a promising adjunct to histopathological examination for the early diagnosis of OSCC. Epigenetic alterations, characterized by reversibility and long-term stability in physiological fluids, are critical enablers of liquid biopsy and its clinical utility. Advances in detection technologies, including quantitative polymerase chain reaction (qPCR), digital droplet PCR (ddPCR), next-generation sequencing (NGS), and electrochemical biosensors, have significantly facilitated the research and clinical translation of epigenetic biomarkers in oral liquid biopsies. However, translating epigenetic biomarkers from research discovery to clinical practice for OSCC remains hindered by several critical challenges: the scarcity of large-scale, rigorously designed cohort studies, limited multicenter validation, inconsistent preprocessing protocols, and a lack of harmonized analytical platforms. Finally, we propose a conceptual framework to outline potential clinical application models for these biomarkers. Full article

Background: Comparative oncology uses naturally occurring cancers in companion animals to study tumor biology and therapeutic responses relevant to human cancer. Spontaneous feline tumors are increasingly recognized as useful comparative models because they arise in immunocompetent hosts, develop under shared environmental exposures, and can reproduce selected clinical, histopathologic, molecular, and therapeutic features of human malignancies. Methods: This review compares feline oral squamous cell carcinoma (FOSCC) with human head and neck squamous cell carcinoma (HNSCC), and feline mammary carcinoma (FMC) with human breast cancer, emphasizing shared pathologic, molecular, tumor microenvironment, and therapeutic features. Results: Recent immunohistochemical, genomic, transcriptomic, and biomarker studies have identified shared features between feline and human cancers. FOSCC resembles human HNSCC through aggressive local invasion, histologic features, therapeutic resistance, and recurrent alterations of TP53, MYC, and PTEN. FMC shows strong overlap with aggressive human triple-negative breast cancer, including reduced hormone receptor expression, recurrent TP53, PIK3CA, and CXCL12/CXCR4 signaling alterations, and tumor microenvironment features involving immune-checkpoint, inflammatory, and angiogenic pathways. FOSCC clinical trials and emerging clinical investigations into FMC treatments further support the use of cats for translational therapy evaluation. Conclusions: FOSCC and FMC are promising comparative oncology models for human HNSCC and aggressive breast cancer, respectively. Future multicenter studies incorporating standardized tumor classification and grading, predefined stratification criteria, and clinically meaningful endpoints will be essential to strengthen their translational value. Full article

Objective: We aimed to investigate the effects of traditional acupuncture combined with auricular acupressure on quality of life in patients with head and neck squamous cell carcinoma undergoing radiotherapy. Study Design: This is a two-arm, parallel, randomized clinical trial with blinded outcome assessment. The study population comprised 107 patients (55 without intervention and 52 with intervention). Data were collected at Dilson Godinho Hospital in Brazil from March 2017 to June 2018, and all patients provided informed consent and were registered under the UTN U1111-1204-8410/RBR-10v5gcdk. Patients in the intervention group received traditional and auricular acupressure in weekly sessions during their radiotherapy treatment, and patients in the control group received no acupuncture. In addition, quality-of-life assessment data were collected using the WHOQOL-BREF instrument. Results: Analysis of the scores obtained in the WHOQOL-BREF before and after radiotherapy demonstrated that the use of traditional and auricular acupressure had a positive impact on physical, psychological, social, environmental, and overall quality of life. Conclusions: Our findings suggest benefits and provide a context for patients and physicians to decide if acupuncture is a desirable treatment option. However, further studies are required to understand the therapy’s effectiveness better. Full article