Recent studies suggest a role for the gut microbiota in the onset, progression, and prognosis of prostate cancer (PCa), one of the most common neoplasms in males. PCa screening relies on PSA testing, whose usefulness remains controversial due to its low specificity. This study was aimed at investigating the differences in the gut microbiota of PCa patients and healthy controls (HCs) and finding correlations between gut microbes and the clinical laboratory parameter assessed in the evaluation of PCa, to identify bacteria which could be used as diagnostic and prognostic biomarkers. Fecal samples collected from 18 PCa patients and 18 HCs were used to isolate bacterial DNA. 16S rRNA gene sequencing provided the gut microbial profiles of the enrolled subjects, whose functional impact was also predicted. A recursive partitioning tree method allowed us to identify a bacterial signature discriminating PCa from HC. A correlation analysis was performed between gut bacteria and the clinical laboratory parameters assessed in the evaluation of PCa. Differential bacterial patterns emerged between PCa patients and HCs, together with significant differences in beta-diversity, alpha-diversity, and richness. The functional prediction of the microbial profiles revealed several metabolic processes differentially regulated, including an enrichment in the Krebs cycle and in steroid hormone synthesis in PCa patients. A bacterial signature based on the abundance of Lactobacillus and Collinsella was found to discriminate between the two groups. Significant correlations were found between gut bacteria and the clinical laboratory parameters generally assessed in the evaluation of PCa. These results indicate that gut microbiota profiles may, in the future, represent potential biomarkers associated with prostate cancer risk or progression; however, further prospective studies and clinical validation are needed before considering their use as diagnostic or prognostic tools.

Pancreatic cancer (PC) remains one of the malignancies with the most unfavorable prognosis and limited treatment options. The lack of biomarkers for early diagnosis and the asymptomatic nature of the disease contribute to delays in diagnosis and high mortality rates. In recent years, the role of the human microbiota in cancer biology has become increasingly significant, and the oral microbiota in particular has been found to be involved in the pathogenesis and prognosis of several neoplasms. This review summarizes the current evidence relating the salivary microbiota to PC in three key areas: screening and diagnostic potential, pathophysiology and tumor progression, as well as presenting prognostic implications and potential influence on therapy. With regard to early diagnosis, it has been reported that patients with PC have reduced levels of Neisseria elongata (N. elongata) and Streptococcus mitis (S. mitis) and elevated levels of Granulicatella adiacens. Several studies have shown that bacteria present in the saliva can migrate from the oral cavity to pancreatic tissue via hematogenous or enteric routes, where they may actively contribute to tumor development and progression. In particular, it has been shown that Porphyromonas gingivalis (P. gingivalis) and Veillonella atypica (V. atypica) translocate from the mouth to pancreatic tumors, promoting carcinogenesis by inducing a pro-inflammatory tumor microenvironment. Furthermore, some studies have identified certain species associated with prognosis and response to PC treatment. Despite the encouraging results, differences in study methodology, the lack of standardized methods and the scarcity of longitudinal data currently hinder clinical application. Large-scale, multi-omics prospective studies are needed to clarify causality and validate their clinical utility. Overall, the salivary microbiota represents a promising and non-invasive tool for improving early diagnosis, understanding prognosis and enhancing the management of PC.

Cancer-associated thrombosis (CAT) is defined as venous or arterial thrombotic events occurring in patients with active malignancy or during anticancer treatment, most commonly presenting as venous thromboembolism and representing a leading cause of morbidity and mortality in oncology. Hormone-sensitive malignancies, including breast, ovarian, and endometrial cancers, are characterized by a complex interaction among tumor biology, endocrine signaling, inflammation, endothelial dysfunction, and coagulation activation. In these malignancies, venous thromboembolism (VTE) risk is influenced not only by intrinsic tumor-related mechanisms but also by patient-specific factors and anticancer therapies, particularly endocrine treatments, chemotherapy, targeted agents, and extensive surgical procedures. Breast cancer is generally associated with an intermediate thrombotic risk, although endocrine therapy—especially tamoxifen—significantly increases VTE incidence. Ovarian cancer represents one of the most thrombogenic solid tumors because of elevated tissue factor expression, inflammatory activation, advanced-stage presentation, and aggressive multimodal treatment strategies. Endometrial cancer exhibits a strong association with obesity, metabolic syndrome, prolonged estrogen exposure, and perioperative thrombotic complications. Emerging evidence highlights the role of immune-thrombosis, extracellular vesicles, inflammatory cytokines, and sex-specific coagulation pathways in cancer-associated hypercoagulability. Current guidelines increasingly support individualized thromboprophylaxis based on tumor biology, patient-specific risk factors, and bleeding risk assessment. This review summarizes the biological mechanisms linking hormones and thrombosis in breast and gynecologic cancers, discusses current evidence regarding VTE risk factors and treatment-related thrombotic complications, and explores modern approaches to biomarkers, risk stratification, and personalized thromboprophylaxis.