Precision medicine represents a paradigm shift in healthcare, emphasizing individualized approaches to disease prevention, diagnosis, and treatment based on a patient’s genetic, proteomic, and immunologic profile. In the field of oncology, this paradigm has gained traction, particularly with the integration of immunotherapeutic modalities. Among the most promising advancements are therapeutic cancer vaccines, which harness the body’s immune system to fight tumors more effectively. This mini-review highlights recent developments in therapeutic vaccine engineering. It also discusses key barriers to clinical translation and summarizes findings from contemporary human clinical trials evaluating personalized cancer vaccines. In addition, it evaluates the growing potential of these therapies to redefine cancer treatment.

Amoebiasis, or amoebic dysentery, is a gastrointestinal disorder caused by the parasite Entamoeba histolytica. The disease is endemic in parts of Africa, Asia, North and South America, leading to several deaths annually. Reported adverse effects associated with the current first-line treatment for amoebiasis, coupled with the evolution of resistance to it, call for the need to search for plant-based alternatives. This study systematically reviews medicinal plants with activity against Entamoeba histolytica.

The PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines were followed to retrieve scholarly literature. The study reviewed 70 articles from 7 popular databases: Google Scholar, PubMed, ScienceDirect, Booksc.org, Emerald, Scopus, and MEDLINE, highlighting several plants with anti-amoebic properties.

The primary parts of the plant used in the treatment of Entamoeba histolytica were the leaves (61%), followed by rhizomes (13%), roots (8%), seeds (8%), stems (4%), and fruits (4%). The families Asteraceae (18%) and Zingiberaceae (18%) contain most plants that are effective against Entamoeba histolytica. These medicinal plants families are rich in phytochemicals such as terpenoids and flavonoids that have anti-entamoeba histolytica activity. Maceration is the most commonly used extraction method.

The results suggest that plants are a promising source of new agents to combat amoebiasis caused by Entamoeba histolytica. The most frequently used plant parts were leaves (61%), and the maceration method was the most common extraction technique due to its simplicity and cost-effectiveness. The majority of studies were limited to in vitro models, with only one plant (Adenophyllum aurantium) tested in vivo. Further research is needed to establish their mechanisms of action, toxicities, and clinical potential.

Acute-on-chronic liver failure (ACLF) is a life-threatening syndrome characterized by systemic inflammation and immune dysregulation, in which macrophages play a key role in organ injury. This study aimed to investigate the role and mechanism of pyruvate dehydrogenase kinase 4 (PDK4) in ACLF to identify therapeutic targets that modulate macrophage function and mitigate ACLF progression.

Single-cell RNA sequencing data from healthy and ACLF liver tissues were analyzed from the Sequence Read Archive database. Transcriptomic data of peripheral blood mononuclear cells from ACLF patients (GSE168048) were also examined. In vitro experiments assessed PDK4 expression and macrophage polarization, and conditioned-medium studies evaluated effects on LO2 hepatocytes. In vivo validation was performed in ACLF mouse models treated with a PDK4 inhibitor.

Single-cell analysis revealed a predominance of M1-polarized hepatic macrophages in ACLF with marked upregulation of PDK4. Peripheral blood mononuclear cell transcriptomics showed that higher PDK4 expression correlated with 28-day mortality. In vitro, PDK4 expression increased in M1 macrophages; PDK4 inhibition attenuated M1 polarization and reduced cytotoxic effects on LO2 cells. In vivo, pharmacologic inhibition of PDK4 suppressed M1 polarization in macrophages, alleviated liver inflammation, and reduced tissue injury. Mechanistically, PDK4 promoted M1 polarization via activation of signal transducer and activator of transcription 1 signaling.

PDK4 is a key pro-inflammatory regulator in ACLF by promoting M1 macrophage polarization. Targeting PDK4 may be a promising strategy to attenuate inflammation and improve clinical outcomes in ACLF.

Identifying patients at high risk for poor bowel preparation preceding a colonoscopy is critical to successful colorectal cancer screening. High-risk patients, such as those who are obese, diabetic, opioid users, or former smokers, often have comorbidity, medication, and sociodemographic factors that lead to suboptimal bowel preparation even when following protocol. Suboptimal preparation results in missed lesions, longer procedure times, and increased healthcare costs. Optimal visualization of the colon mucosa is achieved through effective bowel preparation. Polyethylene glycol (PEG) solutions are preferred for their safety, especially in patients with kidney or cardiac disease. Split-dose PEG regimens with a low-residue diet are recommended by the American Gastroenterological Association to promote cleansing and patient tolerance. Tailored regimens can be employed in high-risk patients, including those with chronic constipation, opioid dependence, or diabetes. Educational interventions, such as written and verbal instructions, patient navigators, and mobile device reminders, improve compliance. Medical strategies include split-dose PEG-electrolyte lavage solution with bisacodyl, additional purgatives for select patients, and avoidance of sodium phosphate in elderly or renally impaired individuals. Open-access colonoscopy services have expanded following the COVID-19 pandemic to manage backlogs and improve access. Improving education, simplifying regimens, and targeting interventions can reduce repeat procedures and enhance colorectal cancer detection. This narrative review summarizes patient-, medication-, and system-level risk factors for inadequate bowel preparation in high-risk populations and synthesizes practical, evidence-based strategies to optimize colonoscopy quality, including in open-access settings.

Sterol regulatory element-binding protein 1 (SREBP1), a key regulator of lipogenesis, is highly expressed in tumors, but the mechanisms sustaining its elevated levels remain unclear. The role of UFMylation, a posttranslational modification, in modulating SREBP1 stability and tumor progression has not been explored. This study aimed to investigate the role of UFMylation in the progression of liver cancer.

Liquid chromatography-tandem mass spectrometry was employed to investigate the interacting proteins of ubiquitin-fold modifier 1-specific ligase 1 (UFL1). Knockdown of UFL1 and DDRGK domain-containing protein 1 (DDRGK1) was performed to assess SREBP1 stability. In vitro and in vivo models of hepatocellular carcinoma (HCC) were used to evaluate tumor progression. Clinical correlations between UFL1/DDRGK1 and SREBP1 levels were analyzed in HCC patient samples.

SREBP1 undergoes UFMylation, which synergizes with ubiquitination to reduce its stability. Depletion of UFL1 or DDRGK1 increased SREBP1 stability, driving HCC progression. Clinically, UFL1 and DDRGK1 levels were reduced in HCC tissues and inversely correlated with SREBP1 expression. Fatostatin (an SREBP1 inhibitor) enhanced the therapeutic effect of Lenvatinib in HCC models with low UFL1 expression.

UFMylation is a critical posttranslational modification that destabilizes SREBP1, and its dysregulation contributes to HCC progression. Targeting the UFMylation-SREBP1 axis, particularly through Fatostatin and Lenvatinib combination therapy, represents a novel therapeutic strategy for HCC.

Dysphagia, a severe comorbidity of many neurological diseases, often lacks targeted therapies. Electrical stimulation of cranial nerves represents a novel therapeutic class. This critical review assessed the clinical effectiveness and safety of various approaches for electrical stimulation of the cranial nerves for treating dysphagia, categorized as implantable (directly targeting the nerve), minimally invasive (pharyngeal electrical stimulation), and non-invasive (transcutaneous). A critical literature review was conducted following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. The PubMed database was comprehensively searched, and studies were rigorously assessed for inclusion and exclusion criteria. The Newcastle–Ottawa Scale was used to assess the risk of bias. The analysis included 15 clinical studies: four assessing vagus nerve stimulation (including implantable and transcutaneous approaches) and eleven assessing pharyngeal electrical stimulation. Most evaluated studies, particularly for pharyngeal electrical stimulation and transcutaneous vagus nerve stimulation, demonstrated significant beneficial effects on validated dysphagia outcome measures. Importantly, no long-term severe adverse effects were reported across the evaluated stimulation approaches. Cumulative evidence indicates that vagus nerve stimulation and pharyngeal electrical stimulation approaches can effectively alleviate dysphagia symptoms. The different stimulation approaches appear to be complementary, with distinct profiles rendering them suitable for different therapeutic contexts (e.g., short-term hospital-based vs. long-term at-home treatment). Consequently, they represent distinct and valuable options for individualized dysphagia therapy.

Hepatic metastasis (HM) and lymph node metastasis in pancreatic ductal adenocarcinoma (PDAC) are associated with worse overall survival, largely due to the immunosuppressive microenvironment. However, the key immunosuppressive cells within this microenvironment remain inadequately defined. This study aimed to identify the cells contributing to HM and lymph node metastasis in PDAC and to investigate their regulatory mechanisms.

Single-cell RNA sequencing was used to profile the tumor microenvironment in HM, lymph node-negative, and lymph node-positive (LNP) PDAC tissues. Bioinformatic analyses revealed subtypes of immunosuppressive myeloid-derived suppressor cells (MDSCs). Immunofluorescence and flow cytometry were performed to detect the distribution and proportion of interleukin-1 receptor antagonist (IL1RA+) MDSCs. The immunosuppressive and pro-tumorigenic functions of IL1RA+ MDSCs were analyzed using enzyme-linked immunosorbent assay, quantitative reverse transcription polymerase chain reaction, Western blotting, and Transwell assays. Patient-derived xenograft mouse models were employed to validate the role of IL1RA+ MDSCs in vivo.

Polymorphonuclear-MDSCs were found to be recruited to metastatic PDAC tissues. Among these, IL1RA+ MDSCs were enriched in HM/LNP tissues and correlated with poorer prognosis. IL1RA+ MDSCs promoted M2 macrophage polarization and suppressed the activity of natural killer cells and cytotoxic T cells. Furthermore, IL1RA+ MDSCs accelerated PDAC migration and progression by upregulating epithelial–mesenchymal transition-related proteins in both in vitro and in vivo models.

IL1RA+ MDSCs represent a key immunosuppressive and pro-tumorigenic subtype in HM/LNP PDAC, providing a solid theoretical basis for prognostic prediction and the development of immunotherapeutic strategies targeting these cells in HM/LNP PDAC.