Breast cancer remains a leading cause of cancer-related mortality worldwide, with treatment resistance and tumor heterogeneity posing major clinical challenges. MicroRNAs (miRNAs), small non-coding RNAs regulating gene expression, have emerged as key players in breast cancer biology, influencing tumor initiation, progression, and therapy resistance. This narrative review synthesizes recent evidence on the involvement of miRNAs in breast cancer subtypes and their impact on treatment response. Notably, miR-155, miR-503, and miR-21 have shown potential as non-invasive biomarkers and modulators of pathways such as PI3K-Akt, MAPK, and TNF signaling. Additionally, exosomal miRNAs may reflect chemoresistance profiles and predict pathological response to neoadjuvant therapy. Emerging data also support the use of specific miRNAs to sensitize tumors to radiotherapy or modulate immune checkpoints like PD-L1 in triple-negative breast cancer. However, challenges persist regarding standardization, sample types, and study heterogeneity. Further translational research is needed to validate miRNA signatures and their utility in guiding personalized treatment. By highlighting mechanistic insights and potential clinical applications, this review aims to contribute to the ongoing efforts of integrating miRNAs into precision oncology for breast cancer.

Background/Objectives: The diversity of the oral microbiota exerts its effects in maintaining dental and overall health. The unique genetic profile of each individual influences the composition of the oral microbiota, determining susceptibility to certain diseases. The aim is to observe its role by highlighting the pathogenic mechanisms involved in oral dysbiosis and identify genetic determinism’s influence in maintaining balance. Methods: This study was designed as a narrative review of the oral microbiota, utilizing some of the principles and guidelines of systematic review to increase methodological rigor. We examined 121 articles such as reviews, meta-analyses, editorials, and observational studies, which met the inclusion and exclusion criteria. The inclusion criteria for studies were as follows: (1) studies that evaluated the impact of the microbiota in oral or/and systemic diseases; (2) studies that observed pathogenic mechanisms in the oral microbiota; (3) studies that evaluated the interaction of the microbiota with the immune system (4); studies that evaluated genetic implications in the microbiota. Results: Host genes regulate inflammatory and immunological reactions that play a role in microbiological balance. This explains the increased resistance of some to diseases, including gingivitis or periodontitis. Also, the implications of oral dysbiosis are reflected not only locally, but also generally, being associated with various systemic conditions. Conclusions: Understanding the pathogenic mechanisms and genetic determinants involved in oral dysbiosis may help create individualized therapies for preventing and managing oral and systemic disorders. A healthy lifestyle and adequate oral hygiene can facilitate a diverse and balanced microbiome, crucial for overall health.

Background/Objectives: Inflammatory bowel disease (IBD) and Parkinson’s disease (PD) are chronic disorders affecting different organs, and evidence has proposed a bidirectional link between them. Fecal calprotectin, which reflects intestinal inflammation and gut barrier injury, is augmented in different neurodegenerative diseases, including PD. In this study, we aimed to investigate whether fecal calprotectin levels in PD increase independently of gastrointestinal inflammation and aging. Methods: Fecal calprotectin values were compared in two groups (PD and IBD) of 30 patients each, taking into consideration variables such as endoscopic aspects and age. Analyses of fecal calprotectin levels in PD patients show an increase with advancing age, which was not observed in the IBD cohort. Results: Most PD patients had fecal calprotectin values exceeding 200 μg/g (mean value 366.25 μg/g), and their levels were comparable to those of patients with inflammatory bowel disease (Ulcerative Colitis, Crohn’s Disease, mean value 537.70 μg/g). In the PD cohort, a weak positive association between calprotectin levels and inflammatory signs was observed, and in the IBD cohort, higher calprotectin levels were strongly associated with more severe endoscopic modifications. Conclusions: This weak but positive correlation with intestinal inflammation in PD patients suggests the involvement of complex mechanisms, other than those related to inflammaging or gut barrier injuries.

This review systematically examines the oral complications associated with conventional and novel anti-cancer therapies. It highlights that while molecularly targeted agents including monoclonal antibodies targeting the vascular endothelial growth factor and its receptor, the epidermal growth factor receptor, tyrosine kinase inhibitors, and immune checkpoint inhibitors tend to exhibit a lower overall toxicity profile compared to traditional cytotoxic chemotherapeutics, they are nonetheless linked to significant oral adverse events. These complications encompass inflammatory mucosal reactions known as mucositis, salivary gland dysfunction leading to a sensation of dryness in the mouth, taste alterations referred to as dysgeusia, and, critically, medication-related osteonecrosis of the jaw. In particular, bone-modifying agents such as bisphosphonates and denosumab disrupt bone remodeling and the formation of new blood vessels, thereby increasing the susceptibility to osteonecrosis of the jaw, especially following invasive dental procedures. The review delineates the multifactorial pathogenesis underlying these toxicities, which involves direct cell toxicity, impaired wound healing, and secondary infections. Furthermore, it emphasizes the importance of pre-treatment dental evaluation and preventive strategies including patient education, prophylactic dental care, and the integration of adjunctive therapies such as laser therapy and autologous platelet concentrates to mitigate these adverse effects. The analysis advocates for interdisciplinary collaboration between oncologists and dental professionals to optimize management protocols, enhance treatment adherence, and ultimately improve the quality of life for oncology patients undergoing anti-cancer therapy.

Background: Advanced-stage ovarian cancer presents a significant therapeutic challenge, with primary cytoreductive surgery (PCS) followed by chemotherapy and neoadjuvant chemotherapy (NACT) with interval debulking surgery (IDS) as the two main treatment modalities. This study aims to compare the clinical outcomes, surgical complexity, and survival rates between these approaches and to assess the impact of molecular markers such as BRCA and HRD status. Methods: This retrospective, single-center observational study included 100 patients diagnosed with stage III-IV high-grade serous ovarian cancer. The patients were divided into two cohorts based on their treatment strategy: PCS followed by adjuvant chemotherapy or NACT followed by IDS. Clinical outcomes, recurrence-free survival (RFS), progression-free survival (PFS), and overall survival (OS) were analyzed, along with the impact of genetic biomarkers. Results: No statistically significant differences were observed in OS and PFS between the two treatment approaches. Patients who underwent NACT followed by IDS had lower surgical complexity scores and reduced perioperative morbidity. The HRD-positive patients exhibited improved responses to PARP inhibitors, reinforcing the significance of molecular profiling in therapeutic decision-making. The KELIM scores demonstrated prognostic relevance, particularly in the patients receiving neoadjuvant chemotherapy. Conclusion: Both PCS and NACT-IDS are viable treatment options for advanced ovarian cancer, with similar survival outcomes. The choice between strategies should be tailored based on patient-specific factors, including tumor burden, performance status, and molecular profile. The integration of biomarkers such as BRCA mutations and HRD status into clinical practice can further refine treatment selection and improve personalized management strategies.