Chimeric antigen receptor (CAR)-T cell therapy faces significant challenges in treating solid tumors, including immune evasion, suppressive tumor microenvironments, and on-target/off-tumor toxicity, which limit its clinical efficacy. Although it has revolutionized treatment for hematological malignancies, these obstacles hinder its broader application in solid tumors. Nanotechnology offers innovative strategies to address these limitations through enhanced delivery, localization, and control. This review summarizes recent advances in nanotechnology-assisted CAR-T cell therapies for gynecologic cancers, with a particular focus on messenger RNA (mRNA)-based delivery systems, lipid nanoparticles, hydrogels, and external activation techniques such as photothermal and acoustogenetic modulation. The integration of nanotechnology, especially mRNA-based delivery systems, holds transformative potential for overcoming these barriers. mRNA enables transient, non-integrating expression of CARs, meaning the genetic modifications are temporary. This improves safety and allows flexible control over treatment intensity, while rational sequence optimization (e.g., codon usage, guanine-cytosine content, secondary structure) enhances mRNA stability and protein translation efficiency. Lipid nanoparticles, the leading delivery platform, can be engineered for cell-type specificity and tissue targeting through modulation of their components and surface functionalization. Recent innovations, including siloxane-modified lipid nanoparticles, injectable hydrogels, and photothermal or acoustogenetic activation strategies, enable precise spatiotemporal control of CAR-T cell function in vivo. In ovarian cancer, preclinical studies targeting nfP2X7 and employing multifunctional nanoparticles have demonstrated synergistic efficacy and tumor-specific delivery. This review highlights how nanotechnology platforms can be integrated with CAR-T cell therapies to enhance safety, precision, and therapeutic outcomes in ovarian cancer.

It is established that administration of the COVID-19 vaccine may be associated with an exaggerated immune response leading to enlargement of several lymph nodes. Although most cases are benign and self-limiting, some have been reported in the literature as B-cell or T-cell lymphomas, with no reported cases of chronic lymphocytic leukaemia (CLL). We report two cases of follicular lymphoma and CLL that occurred a few weeks after COVID-19 vaccination. Case 1 is a 48-year-old woman who noticed two significantly palpable masses, one in each axilla, 48 h after receiving the first dose of the Pfizer-BioNTech BNT162b2 vaccine for COVID-19. Seven days later, she noticed another mass on the right side of her neck, which was biopsied within 48 hours. Case 2 is a 75-year-old man who presented with localized swellings in the axilla and on the neck, noted 24 h after the first dose of the Moderna messenger RNA-1273 COVID-19 vaccine. Neither patient reported any constitutional or associated symptoms. Surgical biopsy of the axillary lymph node in case 1 revealed a non-Hodgkin lymphoma, confirmed via immunohistochemistry as CD20-positive B-cell follicular lymphoma. The patient also had multiple pre- and para-aortic lymph nodes. In case 2, complete blood count showed lymphocytosis (total white blood cell – 148 × 109/L; lymphocyte differential – 92%), while peripheral blood film showed lymphocytosis with a predominance of small, mature-looking lymphocytes, both suggesting CLL. Although requested, immunophenotyping and molecular testing were not performed due to patient-related challenges. Although a chance occurrence is possible, lymphoid malignancies should be considered a strong differential. The vaccination history of patients presenting with clinical manifestations suggestive of a lymphoid malignancy should be thoroughly investigated, while ruling out other possible differentials such as a benign, self-limiting inflammatory process.

Preclinical studies of the serotonin 2A (5-HT2A) antagonist deramciclane suggested an anxiolytic profile, which has not been unequivocally established in the clinic. The same receptor profile also indicated that the compound may exhibit antidepressant potential. However, evidence for these effects remains inconclusive. The present study examined the effect of the drug in two preclinical tests with predictive validity for antidepressant activity.

The antidepressant-like activity of deramciclane was assessed in male Sprague-Dawley rats by measuring immobility time in the forced swim test (doses: 1, 5 mg/kg) and ambulation scores in the bilateral olfactory bulbectomized (doses: 5, 10 mg/kg) rat model. In both tests, the clinically effective antidepressant imipramine served as the control condition.

In the forced swim test, there was a statistically significant effect of treatment on immobility time (F2,34 = 5.77; p < 0.01; analysis of variance), which was attributable to the effect of the 5 mg/kg dose (p < 0.01; Bonferroni post-hoc test). Deramciclane at 1 mg/kg was not significantly different from vehicle-treated animals. By contrast, neither dose of deramciclane (5 mg/kg or 10 mg/kg) reversed the hyperactivity of olfactory bulbectomized rats, whereas imipramine was active in both tests.

Deramciclane demonstrates contradictory evidence for antidepressant-like activity in two validated pharmacological tools that identify such potential. The agent is clearly active in the forced swim test but not in the bulbectomized rat model. Further evaluation of the antidepressant-like potential of deramciclane in pharmacological models with predictive validity is warranted, and a more detailed examination of the dose-response relationship may be informative.

A long-term high-fat diet (HFD) exerts lipotoxic effects on multiple organs, particularly the liver, leading to metabolic diseases. This study aimed to delineate the dynamic effects of HFD on lipid metabolism, elucidate the mechanisms underlying hepatic lipotoxicity, and investigate the protective effects of Ganoderma lucidum against lipotoxicity both in vitro and in vivo.

C57BL/6 mice were fed either a 45% or 60% HFD, followed by measurements of body composition, serum lipid profile, and liver pathology at four, eight, twelve, and sixteen weeks. Inflammatory responses, the unfolded protein response (UPR), and endoplasmic reticulum (ER)-phagy were examined in the livers of mice at 16 weeks. Male C57BL/6 mice were randomly assigned to four groups (n = 12 per group): normal diet, 45% HFD, and two HFD + Ganoderma lucidum water extract (GLE) groups (1 g/kg/d and 2 g/kg/d of crude drug, orally administered by gavage for eight weeks following a four-week HFD induction).

Body weight, body fat, serum lipids, and hepatic steatosis increased progressively, accompanied by impaired glucose tolerance and liver injury, as indicated by elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. HFD also induced activation of the STING and NF-κB signaling pathways, as well as the PERK and IRE1 branches of the UPR. Similarly, ER-phagy selective receptors, particularly FAM134B, which is primarily expressed in hepatocytes as shown by single-cell sequencing, were upregulated after 16 weeks of HFD feeding. Furthermore, GLE mitigated palmitic acid-induced lipotoxicity in primary hepatocytes, as evidenced by improved cell viability, reduced ALT, AST, and lactate dehydrogenase levels in the culture supernatant, and decreased transferase dUTP nick-end labeling-positive cell counts. In 45% HFD-fed mice, GLE reduced serum total cholesterol, low-density lipoprotein, and hepatic triglyceride levels.

HFD-induced lipotoxicity causes hepatic tissue injury and inflammatory responses, which may be alleviated by coordinated regulation of compensatory UPR and ER-phagy. Ganoderma lucidum shows promise as a dietary supplement for managing metabolic disorders.

5-methylcytosine RNA modification is a key regulator of neuroblastoma oncogenesis and differentiation. NSUN6, a 5-methylcytosine-specific messenger RNA methyltransferase, modulates messenger RNA methyltransferase activity and translation termination. Yet, its potential link to neuroblastoma risk has not been previously reported. The present study aimed to reveal the relationship between NSUN6 gene polymorphisms and the risk of neuroblastoma in children from Jiangsu province.

In this case-control study, we investigated three NSUN6 gene polymorphisms (rs3740102 A>C, rs12780826 T>A, and rs61842187 G>C) in 402 neuroblastoma cases and 473 controls, all of whom were children from Nanjing City, Jiangsu Province, China. DNA from these subjects was assessed using the TaqMan method. Multivariate logistic regression analysis was employed to examine the association between NSUN6 gene polymorphisms and neuroblastoma risk. Additionally, the Genotype-Tissue Expression database was utilized to elucidate the impact of these polymorphisms on NSUN6 and nearby gene expression. Kaplan-Meier analysis and the non-parametric test were conducted on the R2 platform to assess the relationship between gene expression, prognosis, and neuroblastoma risk.

Carriage of two to three protective genotypes (rs3740102 AA/AC, rs12780826 TT/TA, rs61842187 CC) was significantly associated with a lower risk of neuroblastoma (adjusted odds ratio = 0.41, 95% confidence interval = 0.23–0.73, P = 0.002), with consistent results across all subgroups. Expression quantitative trait locus analysis showed these single-nucleotide polymorphisms may upregulate the expression of NSUN6 and CACNB2. Furthermore, higher NSUN6 and CACNB2 expression was correlated with a potentially lower risk of neuroblastoma, improved overall survival (NSUN6: P = 2.54e-03; CACNB2: P = 6.35e-06) and event-free survival (NSUN6: P = 7.90e-04; CACNB2: P = 4.64e-06), as well as a lower likelihood of MYCN amplification.

NSUN6 rs3740102 AA/AC, rs12780826 TT/TA, and rs61842187 CC genotypes may be associated with a better prognosis of neuroblastoma. This association may be related to the potential upregulation of NSUN6 gene expression and a lower likelihood of MYCN amplification.

Antralization is considered a critical, reversible stage preceding gastric cancer. However, available biomarkers for identifying antralization are lacking. This study aimed to explore antralization-specific biomarkers in peripheral blood and gastric mucosa.

In this prospective cohort study, adult patients presenting with upper gastrointestinal symptoms were enrolled and categorized into antralization and non-antralization groups based on pathological examination of gastric mucosa. Helicobacter pylori (H. pylori) infection was detected using the 13C-urea breath test, rapid urease test, and/or H. pylori serological test. Blood samples and gastric biopsies were collected for biomarker analysis.

Of the 92 patients studied, 42 (45.7%) were diagnosed with H. pylori infection and 61 (66.3%) with antralization. The rate of H. pylori infection and the incidence of acid reflux were higher in the antralization group than in the non-antralization group (both P < 0.05). Patients with antralization had higher plasma lymphocyte counts and lower serum levels of lipopolysaccharide (both P < 0.05). The positive rates and intensity of trefoil factor-2 and mucin (MUC) 6 expression were higher, whereas the positive rate and intensity of MUC5AC expression were lower in the incisura and body mucosa with antralization compared with those without antralization (all P < 0.05). Additionally, the intensity of MUC5B expression was higher in the gastric body mucosa with antralization than in those without antralization (P < 0.05).

Increased lymphocyte counts and decreased lipopolysaccharide levels in the blood, along with increased expression of trefoil factor-2, MUC6, and MUC5B and decreased MUC5AC expression in the proximal gastric mucosa, appear to be antralization-specific.

Lactate exerts regulatory effects on both cellular homeostasis and disease progression, far beyond being a mere metabolic waste product. As lactate accumulates, the level of lactylation increases significantly. Lactylation, a novel type of post-translational modification, bridges metabolic reprogramming and epigenetic regulation in malignant tumors, including gynecological malignancies. Both lactate and lactylation play critical roles in the tumor microenvironment, ultimately promoting tumor proliferation, metastasis, and drug resistance. Therapies targeting lactate production and transport show considerable anticancer potential, particularly through the inhibition of lactate dehydrogenase and monocarboxylate transporters. These inhibitors can also act as immunotherapy potentiators, producing a synergistic therapeutic effect when combined with immunotherapy. This review emphasizes how lactate and lactylation drive the malignant progression of gynecological cancers and explores promising perspectives on potential therapeutic targets.

Craniopharyngioma (CP), although histologically benign, is a surgically challenging sellar-region tumor for which stereotactic irradiation is increasingly used as an alternative or adjuvant strategy. This review summarizes the role of stereotactic radiosurgery (SRS) in managing CP, with a focus on treatment outcomes, technical advances, and emerging strategies to support evidence-based clinical practice. Literature reports indicate that Gamma Knife radiosurgery achieves variable tumor control rates (36–100%), with optimal outcomes (79.6–91.4%) when marginal doses ≥12 Gy are delivered and patients receive adequate follow-up. Smaller tumors (<5 cm3) and those with higher solid components show particularly favorable outcomes. SRS demonstrates a favorable safety profile, with visual impairment occurring in approximately 4% of cases and endocrine dysfunction in 6%. Compared to conventional radiotherapy, SRS significantly reduces the risk of hypothalamic obesity in pediatric patients. The identification of BRAF mutations in papillary CPs has created novel opportunities for combining targeted therapies with SRS. Collectively, these advances underscore the role of SRS as an essential component of multidisciplinary CP management, particularly in the treatment of residual or recurrent lesions. It offers a more favorable toxicity profile and may improve quality of life outcomes compared to conventional radiotherapy. Further studies are needed to optimize patient selection, dosing strategies, and integration with novel systemic therapies.