Yasser Bustanji

The role of adipokines and inflammatory cytokines in the pathogenesis of epilepsy has been inconsistently described in the literature. Hence, the presence of distinguishing serum inflammatory markers for epilepsy, controlled epilepsy (CE), and uncontrolled epilepsy (UCE), including drug-resistant epilepsy (DRE) and non-drug-resistant epilepsy (NDRE), remains unclear. Therefore, the aim of this cross-sectional study was to characterize the serum levels of leptin, adiponectin, resistin, and an extended panel of inflammatory cytokines among the aforementioned groups of pediatric patients and in comparison with healthy controls (HCs). The study demonstrated that leptin and adiponectin levels were significantly higher in pediatric patients with epilepsy than in HCs, while resistin levels were significantly lower. The levels of adiponectin and resistin, but not leptin, were significantly higher in DRE than in CE. TNF-α levels were significantly higher in the DRE group than in the uncontrolled NDRE or CE groups. Binary logistic regression analysis showed that only resistin and TNF-α had significant predictive value for DRE compared with other epilepsy patients. Multiple linear regression analysis demonstrated that mannose-binding lectin (MBL), resistin, and body mass index (BMI) were the strongest predictors of leptin levels in pediatric epilepsy. Leptin levels, a shorter duration of time since the last seizure, and age were the strongest predictors of higher resistin levels. The presence of developmental delay and lower patient weight predicted higher adiponectin levels. These findings may aid in distinguishing patients with DRE, NDRE, and CE. Resistin and TNF-α might be potential new targets for disease-modifying, anti-inflammatory therapy in pediatric epilepsy, particularly for DRE.

Chemotherapy-induced cognitive impairment, widely known as chemobrain, has emerged as a pressing concern as cancer incidence and treatment success continue to rise worldwide. Patients frequently report persistent deficits in memory, attention, affective regulation, and executive function, which significantly diminish quality of life. While early explanations emphasized psychological causes, evidence now supports a biological basis involving oxidative stress, neuroinflammation, synaptic alterations, and blood-brain barrier disruption. Yet, the precise molecular mechanisms remain incompletely understood, in part due to methodological limitations of conventional neuroscience approaches. Recent advances in multi-omics technologies have opened new avenues to dissect the complexity of chemobrain at genomic, transcriptomic, proteomic, metabolomic, and lipidomic levels. Studies employing both untargeted discovery workflows and targeted validation strategies have revealed convergent disruptions in mitochondrial function, neurotransmitter pathways, and inflammatory signaling, despite differences across chemotherapeutic agents. Integrative analyses further highlight how these molecular perturbations align with behavioural deficits observed in preclinical and clinical settings. This review synthesizes current multi-omics evidence, emphasizing not only the shared downstream neurotoxic pathways across diverse chemotherapies but also the variability introduced by experimental design, tissue selection, and validation practices. Importantly, multi-omics profiling underscores the need for combination neuroprotective strategies, as chemotherapy-induced cognitive impairment arises from intertwined molecular insults rather than a single pathway. By consolidating mechanistic insights from multi-omics, this review aims to inform biomarker discovery, therapeutic innovation, and ultimately the development of precision strategies to mitigate the burden of chemobrain in cancer survivors.

Background and Aim: Cancer represents a major public health challenge in Jordan and remains one of the leading causes of morbidity and mortality. Over the past five decades, Jordan has developed a substantial body of cancer-related research spanning clinical, epidemiological, translational, and technological domains. However, the thematic evolution and intellectual structure of this research landscape have not been comprehensively characterized. This study aimed to map the thematic organization, temporal evolution, and citation impact of cancer research conducted in Jordan between 1974 and 2024. Materials and Methods: A thematic mapping study was performed using the Scopus database. Peer-reviewed English-language journal articles published between January 1974 and December 2024 and involving at least one Jordanian institutional affiliation were retrieved. After manual screening and removal of irrelevant records, eligible publications were exported and analyzed using VOSviewer version 1.6.20. Author-keyword co-occurrence analysis was conducted to identify major research themes. Temporal and normalized citation overlay visualizations were generated to evaluate thematic development and scholarly influence over time. A custom thesaurus file was applied to standardize keyword variations and improve clustering accuracy. Results: Of 5,073 retrieved records, 4,567 met the inclusion criteria. Analysis identified 33 high-frequency keywords grouped into five major thematic clusters. These included: (i) epidemiology, diagnostics, and computational approaches in major cancers; (ii) clinical management, prognosis, survival outcomes, and pediatric oncology; (iii) experimental therapeutics, cytotoxicity screening, apoptosis, molecular docking, and quantitative structure–activity relationship studies; (iv) palliative care and quality-of-life research; and (v) nanotechnology-based drug delivery and targeted therapeutics. Temporal overlay analysis demonstrated a progressive shift from predominantly clinical and epidemiological investigations toward translational, computational, and nanomedicine-oriented research. Citation analysis showed that established clinical themes maintained strong scholarly influence, whereas emerging areas such as machine learning, molecular modeling, and nanotechnology exhibited rapid growth and increasing scientific attention. The integration of experimental models, computational tools, and translational approaches highlighted the maturation of Jordan’s oncology research ecosystem. Conclusion: Cancer research in Jordan has evolved from a strong clinical and epidemiological foundation into an increasingly interdisciplinary and technology-driven field. The growing integration of artificial intelligence, molecular research, nanotechnology, and translational oncology reflects enhanced research capacity and alignment with global scientific priorities. These findings provide valuable evidence for future research planning, capacity building, policy development, and collaborative initiatives aimed at advancing cancer control and oncology innovation. Keywords: artificial intelligence, bibliometric analysis, cancer research, Jordan, nanomedicine, oncology, thematic mapping, translational research.

Non-coding RNAs (ncRNAs) have emerged as significant regulators in cancer biology, modulating gene expression via transcriptional, post-transcriptional, and epigenetic pathways. Their functions in apoptosis, autophagy, inflammation, and epithelial-mesenchymal transition (EMT) are essential to tumorigenesis, advancement, and metastasis. This study presents a bibliometric overview of global research trends, collaborative networks, and hotspots in cancer-related ncRNA research (2005–2024). Bibliometric mapping was integrated with a targeted literature review, employing prevalent author-keywords as anchors to identify theme clusters. These clusters underscore research hotspots, while the integrated literature synthesis contextualizes the most actively studied biological themes, correlating publication patterns with established knowledge. The Scopus database was employed for data collecting, providing extensive coverage of peer-reviewed literature. Bibliometric tools, such as VOSviewer and Biblioshiny, were utilized to examine keyword co-occurrences, define conceptual clusters, and show international cooperation. China published the most ncRNA-related cancer papers and had highest total number of citations, whereas the United States ranked second in both publishing output and total citations but had a higher citation rate per article. Overall, these findings show the distribution of research production and citation patterns among leading contributing countries, with variances in average citation rates due in part to disparities in publishing volume. A focused literature review, directed by the analyses of the retrieved author keywords, revealed that the main research domains center on the regulatory roles of ncRNAs in apoptosis, autophagy, metastasis, inflammation, and clinical applications. Emerging themes, such as their involvement in angiogenesis and immune evasion, underscore the dynamic and evolving nature of this field.Keywords:Lncrnas, Cancer Biology, Bibliometric Analysis, Apoptosis, Autophagy, Good Health and Well-Being

Colorectal cancer (CRC) remains a major global health burden, necessitating innovative therapeutic approaches with improved selectivity and reduced toxicity. DNA minor groove binders (MGBs) represent a promising class of agents that modulate DNA-associated processes without inducing permanent DNA damage. In this study, two previously reported distamycin-like DNA minor groove binders, MGB30 and MGB32, were investigated to elucidate their molecular mechanisms of action in HCT-116 human colorectal cancer cells. An integrated multiomics approach combining metabolomics and proteomics was employed using TIMS-QTOF-UHPLC-MS. Four biological replicates were used for each treatment condition. Following MGB30 treatment, 12 metabolites and 187 proteins were significantly dysregulated, whereas MGB32 treatment resulted in alterations of 41 metabolites and 409 proteins using a Student's t-test with q-value <0.05. Pathway enrichment analysis revealed that both compounds significantly disrupted purine metabolism, while MGB32 additionally affected beta-alanine metabolism, glutathione metabolism, and spermidine and spermine biosynthesis. Proteomic analysis further demonstrated deactivation of RNA processing, translation, and ribosome biogenesis, leading to impaired protein synthesis and reduced cancer cell proliferation. This study provides mechanistic insights into the downstream molecular effects of MGB30 and MGB32 that disrupt key mechanisms underlying tumor growth, offering new avenues for CRC treatment.

Background : Triple-negative breast cancer (TNBC) represents approximately 15% of breast cancer cases worldwide. This subtype is characterized by aggressive behavior, poor prognosis, and a high recurrence rate. The lack of estrogen receptor alpha (ERα) renders hormonal therapies ineffective, leaving chemotherapy as the mainstay of treatment. However, chemotherapy often causes severe side effects. This study investigates the cytotoxic activity of ononin against TNBC in vitro and evaluates its potential to enhance the chemosensitivity of doxorubicin (DOX) in MDA-MB-231 cells. Materials and methods : The effects of ononin and the ononin–DOX combination on cytotoxicity, migration, colony formation, and apoptosis were investigated. Results : Ononin exhibited a cytotoxic effect against MDA-MB-231 cells, with an IC ₅₀ of 50 µM, while DOX had an IC ₅₀ of 1.8 µM. The CompuSyn-calculated combination index (CI) values indicated synergistic interactions, ranging from 0.23 to 0.08 at a constant DOX concentration of 1.8 µM. Analysis of the dose-reduction index (DRI) revealed 6.98-, 16.22-, and 66.86-fold reductions in the effective doses of DOX at ED ₅₀ , ED ₇₅ , and ED ₉₅ , respectively, when combined with a 10-fold concentration of ononin. Combining 0.45 µM DOX with 6 µM ononin resulted in a significant decrease in colony formation compared with 0.45 µM DOX alone (p < 0.0001). Ononin also exhibited anti-migratory activity, and its combination with DOX further reduced cell migration compared with DOX alone after 72 hours (p < 0.05). However, ononin (25 µM) had no significant effect on caspase-3 gene expression. Conclusion : This study is the first to demonstrate that ononin alone inhibits viability, migration, and colony formation in MDA-MB-231 cells and synergistically enhances the cytotoxic activity of DOX. These findings suggest that ononin may serve as a promising adjuvant agent to improve DOX efficacy in TNBC therapy.

The journal retracts the article “Berberine Inhibited Growth and Migration of Human Colon Cancer Cell Lines by Increasing Phosphatase and Tensin and Inhibiting Aquaporins 1, 3 and 5 Expressions”

Prostate cancer (PCa) remains a major global health concern, ranking among the most prevalent cancer in men worldwide. Despite the availability of various therapeutic options, the clinical efficacy of current anti-PCa agents is often compromised by drug resistance and adverse effects. DNA minor groove binders offer a potential therapeutic alternative, owing to their selective mechanism of action and favorable safety profiles. In the present study, we utilized a multiomics strategy to investigate the molecular impact of novel compound MGB4. LNCaP cells were treated with doxorubicin, MGB4, or a combination of both, followed by LC-MS/MS-based untargeted proteomics and metabolomics analyses. One-way ANOVA (p-value <0.05) revealed 55 significantly dysregulated proteins and 57 altered metabolites across treatments. Our findings indicate that both MGB4 and doxorubicin impacted key cellular pathways, including inhibition of translation and alterations in sphingolipid and amino acid metabolism, while doxorubicin and the combination therapy also reduced spermine and spermidine metabolism. Notably, the combined treatment exhibited synergistic effects, significantly impacting purine metabolism and reducing metabolite levels more than individual therapies. This study provides key molecular insights into MGB4 and doxorubicin's mechanisms, supporting MGB4 as a potential prostate cancer drug candidate.

The hepatic protein Mannose-binding lectin (MBL) serves a pivotal role in the acute-phase immune response, potentially influencing the pathogenesis of type 2 diabetes (T2DM) and its associated complications, such as nephropathy and retinopathy. Recent evidence suggests that elevated plasma MBL levels may serve as a predictive marker for albuminuria in T2DM patients. Moreover, it is postulated that MBL ligands are present within the kidneys of diabetic individuals, thereby facilitating the deposition of MBL within the renal parenchyma or other target organs, thereby exacerbating pathological processes. This study aimed to assess serum MBL levels in T2DM patients and explore potential associations between MBL levels and the onset of diabetic complications. A cross-sectional investigation was conducted, encompassing 92 participants, comprising 71 individuals diagnosed with T2DM and 21 age- and sex-matched healthy counterparts. Among the T2DM cohort, patients were stratified into nephropathic and non-nephropathic subgroups based on the presence of nephropathy, as well as into subgroups with or without retinopathy based on retinopathy status. Serum MBL levels were quantified utilizing Enzyme-Linked Immunosorbent Assay (ELISA). The mean MBL levels were found to be significantly elevated in diabetic patients compared to healthy controls (1736 vs. 730.99 ng/mL, p-value = 0.011). Furthermore, MBL levels exhibited a statistically significant increase in individuals with microalbuminuria compared to normoalbuminuric T2DM patients (p-value = 0.019). Notably, a significant association was observed between heightened MBL levels in diabetic patients and the occurrence of retinopathy. The findings of this study support the hypothesis implicating MBL in the pathogenesis of T2DM and the initiation and progression of its associated complications, including nephropathy and retinopathy. Nevertheless, further investigation is warranted to delineate the precise underlying mechanisms governing the relationship between MBL and T2DM pathophysiology.