Medical gases were primarily used for respiratory therapy and anesthesia, which showed promising potential in the cancer therapy. Several physiological and pathological processes were affected by the key gases, such as oxygen, carbon dioxide, nitric oxide, hydrogen sulfide, and carbon monoxide. Oxygen targets shrinking the tumor via hyperbaric oxygen therapy, and once combined with radiation therapy it enhances its effect. Nitric oxide has both anti- and pro-tumor effects depending on its level; at high doses, it triggers cell death while at low doses it supports cancer growth. The same concept is applied to hydrogen sulfide which promotes cancer growth by enhancing mitochondrial bioenergetics and supporting angiogenesis at low concentrations, while at high concentrations it induces cancer cell death while sparing normal cells. Furthermore, carbon dioxide helps induce apoptosis and improve oxygenation for cancer treatments by increasing the release of oxygen from hemoglobin. Moreover, high-dose carbon monoxide gas therapy has demonstrated significant tumor reductions in vivo and is supported by nanomedicine and specialized medicines to boost its delivery to tumor cells and the availability of hydrogen peroxide. Despite the promising potentials of these gases, several challenges remain. Gas concentrations should be regulated to balance pro-tumor and anti-tumor effects for gases such as nitric oxide and hydrogen sulfide. Furthermore, effective delivery systems, such as nanoparticles, should be developed for targeted therapy.

Background: Pisa syndrome, also known as pleurothotonus, is a neurological condition characterized by more than ten degrees of constant lateral curvature of the spine when upright. In this way, the present manuscript aims to systematically review Pisa syndrome secondary to drugs. Methods: Two reviewers identified and assessed relevant reports in six databases without language restriction between January 1990 and June 2024. Results: The prevalence of Pisa syndrome varied from 0.037 to 9.3%. We found 109 articles containing 191 cases of drug-induced Pisa syndrome reported in the literature. The mean and median ages were 59.70 (SD = 19.02) and 67 (range = 12–98 years). The most prevalent sex was female, 56.91% (107/188). The most frequent medications associated with Pisa syndrome were acetylcholinesterase inhibitors in 87 individuals. Of 112 individuals in which the onset time from the medication to the movement disorder occurrence was reported, 59 took place within a month. In this way, a return to baseline was observed in 45.50% of the cases, and partial recovery was observed in 14.28%. Conclusion: We proposed new diagnostic criteria for Pisa syndrome based on previous findings in the literature. Moreover, multiple mechanisms are probably involved in balance control and the development of lateral trunk flexions.

Colorectal cancer (CRC) remains a global malignancy with over 1.9 million new cases annually. Emerging evidence implicates enterotoxigenic Bacteroides fragilis (ETBF) and its toxin (BFT) in activating STAT3 and promoting microsatellite instability (MSI), a novel microbial oncogenic axis. In analyses of more than 1200 CRC tumors, B. fragilis abundance correlated with a 2.14-fold higher MSI-high frequency and increased CpG island methylator phenotype. Mechanistically, BFT triggers E-cadherin cleavage, β-catenin activation, and IL-6/IL-17 up-regulation, fostering inflammation, oxidative stress, and mismatch-repair suppression. Animal models demonstrate a more than 60% rise in tumor burden following ETBF colonization, while human studies show B. fragilis present in about 80% of CRC tissues versus 50% of controls. These findings establish BFT-induced STAT3 signaling as a driver of genomic instability and tumor evolution. Targeting this pathway offers new prospects for biomarker development and precision therapy in colorectal cancer.

Emerging evidence suggests that bacterial extracellular vesicles (BEVs) and microbial-derived small RNAs (msRNAs) in human plasma represent a new class of circulating cancer biomarkers. Multi-cohort analyses of more than 1100 patients revealed 2.8- to 3.5-fold higher BEV levels in cancer cases versus controls, with microbial RNA cargo comprising up to 1.6% of total plasma RNA. Specific BEV-msRNA panels achieved area under the curve values of 0.87–0.94 for early-stage cancer detection, outperforming conventional CEA and CA19-9 markers. Functionally, BEV-associated msRNAs modulate tumor-related signaling by activating NF-κB and STAT3 pathways and suppressing TP53/PTEN expression, promoting cytokine release and oncogenic inflammation. BEVs also exhibit superior stability remaining detectable for more than 72 hours in circulation supporting their feasibility for clinical liquid biopsy. Collectively, circulating BEVs and msRNAs offer promising, mechanism-linked biomarkers for non-invasive cancer detection and precision monitoring.

Recent advances in microbiome research reveal that microbial metabolites directly regulate programmed death ligand-1 (PD-L1) expression and influence checkpoint immunotherapy outcomes. Multi-cohort analyses of over 1300 patients show that elevated short-chain fatty acids, indole derivatives, and secondary bile acids modulate PD-L1 and T-cell activity through histone deacetylase inhibition, STAT3 phosphorylation, and aryl hydrocarbon receptor signaling. High fecal butyrate correlates with a 2.4-fold higher response rate and 6.3-month improvement in progression-free survival during PD-1 blockade. Conversely, dysbiosis-associated metabolites, including lipopolysaccharide and succinate, induce PD-L1 hyperexpression and immune resistance. Metabolomic profiling now achieves AUCs of 0.82–0.89 in predicting immunotherapy response, outperforming tumor mutational burden and PD-L1 IHC. These findings establish microbial metabolites as active immunoregulatory mediators, offering new translational strategies for microbiome-informed immunotherapy personalization and biomarker integration in oncology.