The gut microbiome has emerged as a key regulator of human health, influencing not only metabolism and immunity but also the development and treatment of cancer. Mounting evidence suggests that microbial dysbiosis contributes to oncogenesis by driving chronic inflammation, producing genotoxic metabolites, altering bile acid metabolism, and disrupting epithelial barrier integrity. At the same time, the gut microbiome significantly modulates the host response to oncotherapies including chemotherapy, radiotherapy, and especially immunotherapy, where microbial diversity and specific taxa determine treatment efficacy and toxicity. This review synthesizes current evidence on the role of the gut microbiome in both oncogenesis and oncotherapies, focusing on thirteen cancers with the strongest and most clinically relevant microbiome associations, colorectal cancer, gastric cancer, hepatocellular carcinoma, gallbladder cancer, esophageal cancer, pancreatic cancer, oral squamous cell carcinoma, cervical cancer, prostate cancer, breast cancer, lung cancer, brain cancer, and melanoma. These cancers were selected based on robust mechanistic data linking microbial alterations to tumor initiation, progression, and therapy modulation, as well as their global health burden and translational potential. In addition, we have provided mechanistic insights or clinical correlations between the microbiome and cancer outcomes. Across cancers, common microbial mechanisms included pro-inflammatory signaling (e.g., NF-κB and STAT3 pathways), DNA damage from bacterial toxins (e.g., colibactin, nitrosating species), and metabolite-driven tumor promotion (e.g., secondary bile acids, trimethylamine N-oxide). Conversely, beneficial commensals such as Faecalibacterium prausnitzii and Akkermansia muciniphila supported antitumor immunity and improved responses to immune checkpoint inhibitors. In conclusion, the gut microbiome functions as both a driver of malignancy and a modifiable determinant of therapeutic success. Integrating microbiome profiling and modulation strategies such as dietary interventions, probiotics, and fecal microbiota transplantation into oncology practice may pave the way for personalized and more effective cancer care.

Background and Objectives Antiseizure medications (ASMs) are often taken long term by patients with epilepsy yet may be associated with differing metabolic and cardiovascular risks, including hyperlipidemia and weight changes. This systematic review and meta-analysis evaluated the effects of individual ASMs on lipid profiles and weight changes in patients with epilepsy. This paper also provides detailed insights into safety profiles across different patient subgroups and the impact of treatment duration, which was previously underrepresented in individual studies that showed conflicting results. Methods PubMed, Scopus, and Cochrane Central databases were searched from inception until June 2024 for studies reporting lipid derangements after ≥ 3 months of ASM monotherapy in patients with epilepsy in comparison with healthy controls. Primary outcomes were total cholesterol (TC) and low-density lipoprotein cholesterol (LDL) levels. Secondary endpoints were high-density lipoprotein cholesterol, triglycerides, and body mass index (BMI). Mean difference (MD) and standardized mean difference (SMD) were computed using a random-effects model. Further subgroup analyses were performed for adult and pediatric populations, as well as for the duration of treatment, and sensitivity, when feasible. Results In total, 28 studies, totaling 2231 patients and 1582 healthy controls, were included in this meta-analysis. Significant TC and LDL alterations were observed soon after introducing carbamazepine {TC SMD 1.23 [95% confidence interval (CI) 0.93–1.54]; LDL SMD 1.00 [95% CI 0.70–1.30]} and oxcarbazepine [TC SMD 1.0 (95% CI 0.67–1.34)] in all patient subgroups, as well as phenytoin [TC 0.72 (95% CI 0.37–1.06); LDL SMD 0.41 (95% CI 0.03–0.79)] and valproate in long-term therapy in adult patients. Lamotrigine reduces LDL levels over time [MD − 5.15 (95% CI − 9.51 to − 0.80)] in adults. Levetiracetam has a neutral effect on lipid profile. BMI increases on valproate treatment in the pediatric population [MD 0.58 (95% CI 0.01–1.16)] and adults, commonly seen with long-term therapy [MD 2.73 (95% CI 1.77–3.69)]. Insufficient data existed to assess most other approved ASMs. Conclusions Individual ASMs may contribute to the overall metabolic and cardiovascular risk profile in patients with epilepsy. This systematic review and meta-analysis identified the need for TC and LDL monitoring in the early stages of treatment for patients taking carbamazepine or oxcarbazepine, as well as adults on phenytoin and long-term valproate therapy. Lamotrigine was associated with a reduction in LDL levels over time in adults, whereas levetiracetam had a neutral effect on the lipid profile. Furthermore, weight gain was commonly observed in both children and adults undergoing long-term treatment with valproate. Regularly ordering lipid tests could play an important role in evaluating and mitigating the metabolic risk of ASMs and should be implemented in clinical practice. International Prospective Register of Systematic Reviews (PROSPERO) Protocol CRD42024583306.

The use of anticoagulation for stroke prevention in embolic stroke of undetermined source (ESUS) is hypothesized to be beneficial over conventional antiplatelet use. However, randomized controlled trials (RCTs) have not found clear benefits, even when assessing cardioembolic enriching features. This study aimed to perform a meta-analysis exploring the efficacy and safety of direct oral anticoagulants (DOACs) following ESUS. PubMed, Scopus, and Cochrane Central were systematically searched for studies comparing DOACs versus aspirin after ESUS. The primary outcome was stroke recurrence, and the safety outcome was major bleeding. A random-effects model was used for the analyses. Statistical analysis was performed using Review Manager Web 8.0.0 (RevMan Web). 14,582 patients were included from 9 studies, of which 4 were RCTs. 7,341 (50.3 %) received DOACs as secondary prevention. For stroke recurrence, there was noted non-statistically significant trends towards benefit for DOACs (OR 0.93; 95 % CI 0.81-1.06; p = 0.29; I² = 34 %). No differences were found for major bleeding (HR 1.57; 95 % CI 0.86-2.86; p = 0.15; I² = 63 %). Among the atrial cardiomyopathy subgroup, no benefit was observed (OR 0.88; 95 % CI 0.50-1.55; p = 0.67; I² = 39 %). There is insufficient evidence to recommend the use of DOACs over aspirin following ESUS for the prevention of stroke recurrence. Nevertheless, the fears of increased bleed risks were also not seen. Further efforts should be directed towards identifying potential embolic sources and the population that benefit from OAC.