Triple-negative breast cancer (TNBC), an aggressive subtype lacking estrogen receptor (ER), progesterone receptor (PR), and HER2 expression, accounts for 10–20% of breast cancers and is characterized by high metastatic potential and poor survival outcomes. Despite advancements in chemotherapy, the 5-year survival rate for metastatic TNBC remains below 30%, underscoring the need for innovative therapeutic approaches. This review comprehensively examines recent breakthroughs in TNBC immunotherapy, focusing on immune checkpoint inhibitors (ICIs), combination strategies, and biomarker-driven therapy. Landmark trials such as KEYNOTE-355 and IMpassion130 have demonstrated that combining PD-1/PD-L1 inhibitors with chemotherapy improves survival in PD-L1-positive metastatic TNBC. Beyond monotherapy, combination therapies—including dual checkpoint inhibition, PARP inhibitors in BRCA-mutated tumors, and antibody-drug conjugates (ADCs) —show promise in overcoming resistance and enhancing antitumor immunity. Emerging targets further expand therapeutic possibilities, though their paradoxical roles as biomarkers and immunosuppressive mediators require precision-based approaches. Biomarkers like PD-L1, tumor-infiltrating lymphocytes (TILs), tumor mutational burden (TMB), and circulating tumor DNA (ctDNA) are critical for patient stratification and predicting immunotherapy response. Despite progress, challenges persist, including tumor heterogeneity, resistance mechanisms, and access to advanced therapies. Future directions emphasize next-generation ICIs, optimized combination regimens, and AI-driven biomarker integration to achieve durable, personalized treatments. This review underscores the potential of immunotherapy to redefine TNBC management while highlighting the imperative for continued innovation to address unmet clinical needs.

Introduction Oral cancer (OC), particularly squamous cell carcinoma and its variants such as verrucous carcinoma, represents a growing public health concern due to increasing global incidence. While tobacco and alcohol remain the main risk factors, attention has turned to the potential role of human papillomavirus (HPV), particularly with particular consideration on high-risk genotypes. Objective This systematic review evaluates current evidence on the association between HPV and OC. Methods A structured search was conducted in PubMed, Scopus, and Web of Science using keywords including “oral carcinoma,” “oral squamous cell carcinoma,” “oral verrucous carcinoma,” and “HPV.” Screening followed PRISMA guidelines, and 15 articles were selected. Additionally, a case series of patients treated at the Department of Interdisciplinary Medicine, University of Bari “Aldo Moro,” are presented to provide clinical context. Results. The evidence suggests a possible association between HPV infection, especially genotype 16, and a subset of oral squamous cell carcinomas. However, differences in detection techniques and study design contribute to variability in findings. Conclusion While HPV may play a role in oral carcinogenesis, further high-quality studies are required to clarify its impact. These findings may have implications for screening, prognosis, and prevention strategies, including HPV vaccination.

68Ga-Pentixafor PET/CT, a molecular imaging technique targeting the C-X-C chemokine receptor 4 (CXCR4), has emerged as a promising tool in the diagnosis and therapeutic evaluation of lung cancer. Lung cancer remains a leading cause of cancer-related mortality worldwide, and accurate imaging modalities are critical for early detection, staging, and treatment monitoring. Current imaging approaches face challenges in differentiating tumor subtypes and assessing tumor biology, which limits personalized treatment strategies. This review systematically summarizes the application of 68Ga-Pentixafor PET/CT across various histological subtypes of lung cancer, including non-small cell lung cancer (NSCLC), small cell lung cancer (SCLC), and rare lung cancer variants. We emphasize the correlation between PET imaging findings and immunohistochemical CXCR4 expression, highlighting the diagnostic value and unique imaging characteristics of this modality. Additionally, the potential role of 68Ga-Pentixafor PET/CT in guiding radioligand therapy is discussed, alongside its utility in tumor staging, therapeutic response assessment, and individualized treatment planning. By integrating recent clinical studies and systematic evaluations, this review aims to elucidate the advantages and limitations of 68Ga-Pentixafor PET/CT, providing theoretical insights and practical guidance for advancing precision medicine in lung cancer management.

Background Sexual health is a central component of wellbeing, identity, and intimate relationships, yet it remains insufficiently addressed in cancer care. Cancer treatments disrupt sexual functioning through interacting physical, hormonal, psychological, and relational mechanisms, leading to persistent and often under-recognized sexual dysfunction among survivors. Aim To synthesize current evidence on cancer-related sexual dysfunction, assessment strategies, and therapeutic interventions, with a focus on gender differences, tumor-site specificity, and implications for sexual medicine practice. Methods This narrative review integrates evidence from population-based studies, clinical guidelines, and systematic reviews addressing sexual dysfunction across cancer types. Gender-specific patterns and biopsychosocial mechanisms were examined to inform assessment and management within sexual medicine and survivorship care. Results Women commonly experience multidimensional and frequently “invisible” sexual difficulties, including reduced desire and arousal, orgasmic dysfunction, dyspareunia, vaginal atrophy, body image disturbance, and fertility-related distress. Men more often present with overt functional impairments, particularly erectile and ejaculatory dysfunction following prostate and other male cancer treatments. Existing assessment tools capture selected aspects of sexual function but often fail to reflect the full biopsychosocial complexity of post-cancer sexuality. Effective management requires integrated interventions combining medical and pharmacological therapies, physical rehabilitation, psychosexual and couples counseling, and structured communication models. Tailored, gender- and tumor-specific approaches embedded within multidisciplinary survivorship pathways are essential, including culturally competent care for sexual and gender minority patients. Conclusion Sexual dysfunction is a prevalent and clinically relevant consequence of cancer. Comprehensive assessment and personalized, multidisciplinary interventions are essential components of high-quality sexual medicine care for cancer survivors.

ObjectiveTo develop and validate a risk prediction model for Chemical cystitis in patients with non-muscle-invasive bladder cancer (NMIBC) undergoing intravesical instillation.MethodsThis study retrospectively enrolled 225 patients with NMIBC who received intravesical instillation between January 2024 and January 2026. Predictive variables, including demographic characteristics, oncological features, medical history, treatment-related factors, and procedural anatomy, were collected. Feature selection was performed using the Least Absolute Shrinkage and Selection Operator (LASSO) regression from 18 candidate variables. A multivariable logistic regression model was constructed based on the selected variables and visualized as a risk prediction nomogram. The model’s performance was evaluated and validated using the Area Under the Curve (AUC), calibration curves, and Decision Curve Analysis (DCA) to assess discrimination, calibration, and clinical utility.ResultsFive independent predictors were identified from the candidate variables through LASSO and multivariable logistic regression analysis: type of instillation agent, tumor multifocality, retention time of the agent, bladder capacity, and tumor grade. The predictive model demonstrated robust discriminative ability in both the training and validation cohorts, with AUC values of 0.840 and 0.868, respectively. Calibration curves showed high consistency between the predicted and observed risks, and DCA further confirmed the model’s positive net benefit in clinical decision-making.ConclusionWe successfully developed and validated a practical nomogram for the individualized prediction of Chemical cystitis risk in patients with NMIBC. This tool can assist clinicians in identifying high-risk patients prior to treatment, thereby enabling more targeted monitoring and preventive strategies. This study is limited by its single-center retrospective design, and external prospective validation is warranted.

BackgroundTo evaluate the impact of Body Mass Index (BMI) on survival and postoperative complications in older patients with esophageal squamous cell carcinoma (ESCC) following esophagectomy, we designed this study.Materials and methodsWe retrospectively analyzed 469 patients aged ≥70 years with thoracic ESCC who underwent esophagectomy at Sichuan Cancer Hospital (May 2016–August 2021). Patients were grouped by WHO BMI categories: underweight (<18.5 kg/m2), normal (18.5–24.9 kg/m2), and overweight/obese (≥25 kg/m2). Primary outcomes were overall survival (OS) and disease-free survival (DFS); secondary outcomes included Clavien-Dindo grade III–IV complications. Kaplan-Meier, Cox models, and restricted cubic splines (RCS) were used.ResultsMedian follow-up was 47.5 months; R0 resection was achieved in 96.4%. BMI distribution: 7.3% low, 76.8% normal, 16.0% high. Median OS was 44.9 months overall, with no significant OS or DFS differences among BMI groups. RCS demonstrated a significant U-shaped association between continuous BMI and survival: protective ranges were approximately 21.9–27.0 kg/m2 for OS (P non-linearity = 0.014) and 20.2–27.2 kg/m2 for DFS (P non-linearity = 0.033).ConclusionIn elderly ESCC patients after esophagectomy, BMI does not independently influence OS or DFS, though low BMI is associated with specific serious complications. Perioperative optimization—particularly nutritional support for underweight patients—remains essential.

The discovery of antibody-drug conjugates (ADCs) has revolutionized the therapeutic landscape of oncology patients, especially those suffering from breast cancer. Following the approval of the first ADC for solid tumors in breast cancer, numerous additional ADCs have also been launched in the therapeutic landscape of breast cancer and have become the new standard of care for all diverse subtypes. Sacituzumab tirumotecan (sac-TMT) (MK-2870/SKB264) is an innovative ADC targeting TROP2 and delivering a belotecan-derived topoisomerase I inhibitor payload. Several clinical trials of sac-TMT have demonstrated promising results including improved overall response and disease control rates as well as progression-free survival. The safety profile of sac-TMT seems easily manageable; adverse events include mainly grade 1/2 nausea and alopecia, while grade 3/4 neutropenia and leukopenia and grade 3/4 stomatitis have been also reported. However, no treatment-related deaths have been reported so far. Since sac-TMT offers an encouraging new option for diverse breast cancer populations with manageable toxicity profiles, this review aims to summarize the recent published data regarding its use in breast cancer.

Gastric cancer (GC) persists as a leading cause of global cancer morbidity and mortality, with its pathogenesis intricately linked to epigenetic dysregulation. Emerging research specifies the novelty of these mechanisms—including DNA methylation, histone modifications, non-coding RNAs (ncRNAs), and RNA modifications—in GC initiation, progression, and therapeutic resistance. This review systematically examines key epigenetic mechanisms in GC, dissect the therapeutic implications as diagnostic biomarkers and therapeutic targets. Key insights include (1) aberrant methylation of tumor suppressor genes (e.g., CDH1, RUNX3): in early carcinogenesis; (2) histone lactylation and acetylation modulating immune evasion (3) ncRNAs (e.g., miR-21, HOTAIR); as promising biomarkers; and (4) m6A RNA modification in chemotherapy resistance. We further discuss translational applications of epigenetic biomarkers in liquid biopsies and targeted therapies (e.g., DNMT/HDAC inhibitors). Integrating multi-omics and epigenetic editing technologies may advance precision medicine in GC.

Many drugs currently used in cancer chemotherapy exert their toxic action mainly by inhibiting ribosome biogenesis (RiBi). This is due to the fact that after inhibition of rRNA transcription ribosomal proteins, no longer used for ribosome building, bind to and neutralize the activity of the murine double minute 2 protein (MDM2, HMD2 in humans), thus hindering cell proliferation and possibly inducing apoptotic cell death. Here, we discuss the existing literature showing how RiBi rate and genomic alterations of ribosomal proteins (RP mutations/deletions) influence the degree of MDM2 inhibition after treatment with RiBi inhibitors in cancer cells. There is evidence that a high RiBi rate is associated with a high RPs release with strong inhibition of MDM2 activity and consequent induction of apoptotic cell death in response to RiBi inhibitors, whereas a low RiBi rate or RP mutations/deletions are associated with a degree of MDM2 inhibition insufficient to kill cancer cells. In the latter case, in cells with wild type p53, association with drugs which stabilize p53 with different mechanisms may overcome cancer cells resistance to RiBi inhibition, whereas in cancers lacking functional p53 addition of MDM2 inhibitors should be considered. From this, the necessity to evaluate the rate of ribosome biogenesis together with the presence of RP mutations/deletions in cancer tissues for predicting the sensitivity of cancer cells to RiBi inhibitors in order to choose more appropriate therapeutic protocols.

Pleural effusion, an atypical accumulation of fluid in the pleural space, has been identified as a potential indicator of several diseases, including lung cancer. The presence of biomarkers in malignant pleural effusion has been a subject of investigation; however, the expression of microRNAs has received limited attention. The objective of this study is to present a narrative review of the current scientific literature regarding the presence of microRNAs in malignant pleural effusion and their association as new biomarkers in the diagnosis of lung cancer. A comprehensive search was conducted using the databases: PubMed, ScienceDirect, and EBSCO to identify all original scientific articles published through 30 April 2025. The following terms were utilized in the search: "MicroRNA AND pleural effusion AND lung cancer", "microRNA AND pleural effusion AND lung adenocarcinoma", "microRNA AND pleural effusion AND lung squamous cell carcinoma", "miRNA AND pleural effusion", miRNA AND pleural effusion AND lung cancer", "miRNA AND pleural effusion AND lung adenocarcinoma", "miRNA AND pleural effusion AND lung squamous cell carcinoma". A total of 17 studies were identified that distinguished between 106 microRNAs. These studies demonstrated the most significant overexpression and downexpression in lung cancer patients compared to patients without malignancy. However, eight of these studies distinguished between 17 microRNAs expressions and exhibited elevated area under the curve values, sensitivity, and specificity for the involvement in several hallmarks of lung cancer. The regulatory mechanisms governing microRNAs in malignant pleural effusion are intricate and involve multiple genes that play pivotal roles in several cancer mechanisms. These mechanisms encompass but are not limited to, processes such as cell growth, migration, drug resistance, proliferation, apoptosis, invasion, angiogenesis, and apoptosis.