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Glioblastoma multiforme (GBM) is the most prevalent and aggressive primary brain tumor in adults, characterized by a poor prognosis and significant resistance to existing treatments. Despite progress in therapeutic strategies, the median overall survival remains approximately 15 months. A hallmark of GBM is its intricate molecular profile, driven by disruptions in multiple signaling pathways, including PI3K/AKT/mTOR, Wnt, NF-κB, and TGF-β, critical to tumor growth, invasion, and treatment resistance. This review examines the epidemiology, molecular mechanisms, and therapeutic prospects of targeting these pathways in GBM, highlighting recent insights into pathway interactions and discovering new therapeutic targets to improve patient outcomes.

Background Human Papillomavirus (HPV) is a prevalent STI (Sexually Transmitted Infection) that is estimated almost all sexually active Patients at some stage of their life will be infected by the virus. Although most HPV infections resolve spontaneously, some can result in health complications, such as genital warts and several types of cancer. This study analyzed the variety of HPV genotypes in females and males among the infected population. Methods Samples were obtained from the oral, vaginal, and genital sites of study participants and the samples underwent DNA extraction and subsequently amplified using Real-Time PCR. The recognition of high-risk (HR) and low-risk (LR) HPV genotypes was carried out using the HPV REALQUALITY RQ-Multi diagnostic kit and demographic information was analyzed alongside statistical virological data. Results Out of 936 samples, 324 cases (34.6%) were found to be positive for HPV, while 612 cases (65.4%) were negative. Of our participants, 70 samples of males (27.5%) and 254 samples of females (37.3%) were HPV-positive. Common genotypes included 16, 6, 11, and 18, while genotypes 59, 56, 31, 45, and 52 were also detected. Conclusion According to the findings of this study, a significant prevalence of HPV infection was seen in males and females, and the incidence of high-risk genotypes was more diverse in males. While the vaccine was effective in preventing some types of HPV, such as 16, 18, 6, and 11, there seems to be an increase in infections caused by other genotypes, and precautions should be taken to prevent future health problems.

Cancer is one of the leading causes of death worldwide, and the factors responsible for its progression need to be elucidated. Exosomes are structures with an average size of 100 nm that can transport proteins, lipids, and nucleic acids. This review focuses on the role of exosomes in cancer progression and therapy. We discuss how exosomes are able to modulate components of the tumor microenvironment and influence proliferation and migration rates of cancer cells. We also highlight that, depending on their cargo, exosomes can suppress or promote tumor cell progression and can enhance or reduce cancer cell response to radio- and chemo-therapies. In addition, we describe how exosomes can trigger chronic inflammation and lead to immune evasion and tumor progression by focusing on their ability to transfer non-coding RNAs between cells and modulate other molecular signaling pathways such as PTEN and PI3K/Akt in cancer. Subsequently, we discuss the use of exosomes as carriers of anti-tumor agents and genetic tools to control cancer progression. We then discuss the role of tumor-derived exosomes in carcinogenesis. Finally, we devote a section to the study of exosomes as diagnostic and prognostic tools in clinical courses that is important for the treatment of cancer patients. This review provides a comprehensive understanding of the role of exosomes in cancer therapy, focusing on their therapeutic value in cancer progression and remodeling of the tumor microenvironment. Graphical Abstract

Prostate cancer is a leading cause of death worldwide and new estimates revealed prostate cancer as the leading cause of death in men in 2021. Therefore, new strategies are pertinent in the treatment of this malignant disease. Macroautophagy/autophagy is a “self-degradation” mechanism capable of facilitating the turnover of long-lived and toxic macromolecules and organelles. Recently, attention has been drawn towards the role of autophagy in cancer and how its modulation provides effective cancer therapy. In the present review, we provide a mechanistic discussion of autophagy in prostate cancer. Autophagy can promote/inhibit proliferation and survival of prostate cancer cells. Besides, metastasis of prostate cancer cells is affected (via induction and inhibition) by autophagy. Autophagy can affect the response of prostate cancer cells to therapy such as chemotherapy and radiotherapy, given the close association between autophagy and apoptosis. Increasing evidence has demonstrated that upstream mediators such as AMPK, non-coding RNAs, KLF5, MTOR and others regulate autophagy in prostate cancer. Anti-tumor compounds, for instance phytochemicals, dually inhibit or induce autophagy in prostate cancer therapy. For improving prostate cancer therapy, nanotherapeutics such as chitosan nanoparticles have been developed. With respect to the context-dependent role of autophagy in prostate cancer, genetic tools such as siRNA and CRISPR-Cas9 can be utilized for targeting autophagic genes. Finally, these findings can be translated into preclinical and clinical studies to improve survival and prognosis of prostate cancer patients. Graphical abstract Highlights • Prostate cancer is among the leading causes of death in men where targeting autophagy is of importance in treatment; • Autophagy governs proliferation and metastasis capacity of prostate cancer cells; • Autophagy modulation is of interest in improving the therapeutic response of prostate cancer cells; • Molecular pathways, especially involving non-coding RNAs, regulate autophagy in prostate cancer; • Autophagy possesses both diagnostic and prognostic roles in prostate cancer, with promises for clinical application.

BackgroundHigh-risk human papillomavirus (HPV) infection, particularly HPV16 and HPV18, is the primary etiological factor in cervical cancer development. The oncogenic potential of these viruses stems from the action of viral E6 and E7 oncoproteins, which drive malignant transformation by degrading tumor suppressor proteins p53 and pRb, disrupting cell cycle regulation, and inducing genomic instability [1, 2]. These mechanistic insights underscore the critical need for sensitive, rapid, and reliable diagnostic tools suitable for point-of-care settings to enable early detection and intervention.MethodsWe designed, synthesized, and evaluated bimetallic nano mixture-based lateral flow assays (LFAs) employing Au–Cu, Ag–Cu, and Ag–Au nano mixtures for detection of HPV16 L1 and HPV18 L1 capsid proteins. Nanoparticles were characterized by dynamic light scattering (DLS), zeta potential analysis, scanning electron microscopy (SEM), Fourier transform infrared (FTIR) spectroscopy, UV–Vis spectroscopy, and X-ray photoelectron spectroscopy (XPS) before and after functionalization with CTAB and monoclonal antibodies. Analytical performance including linearity, limit of detection (LOD), limit of quantification (LOQ), accuracy, precision, specificity, and stability was systematically validated. Clinical evaluation was conducted using 100 cervical samples, with performance parameters calculated against PCR as reference standard. Additional experiments were performed to assess early infection detection capability, correlation with E6/E7 oncoprotein expression, and specificity in the presence of p53 and pRb tumor suppressor proteins.ResultsPhysicochemical characterization revealed successful antibody conjugation across all formulations, with predictable increases in hydrodynamic size (5–7 nm) and shifts toward less negative zeta potentials (−30 to −35 mV). Among monometallic systems, Au nanoparticles demonstrated the highest analytical sensitivity (LOD = 1 ng/mL), while Cu nanoparticles showed the poorest performance (LOD = 12 ng/mL). Remarkably, bimetallic nano mixtures dramatically outperformed monometallic counterparts, with Ag–Au nano mixtures achieving the lowest LOD (0.15 ng/mL), highest linearity (R2 = 0.998), and most rapid response time (10 min). Time-course experiments revealed that Ag–Au LFA detected infection as early as day 3 post-infection, 4 days before detection of integrated viral DNA. Among 20 PCR-positive clinical samples, 18 (90%) showed detectable E6/E7 oncoprotein expression, with strong correlations between LFA signal intensity and both E6 (r = 0.82) and E7 (r = 0.79) levels. No cross-reactivity was observed with p53, pRb, or E6/E7 oncoproteins. Clinical evaluation demonstrated that Ag–Au formulations achieved superior clinical performance (95% sensitivity, 91–92% specificity for both HPV targets), 96% positive predictive value (PPV), and 89–90% negative predictive value (NPV).ConclusionBimetallic nano mixture-based LFAs, particularly the Ag–Au formulation, represent a highly sensitive, specific, and rapid point-of-care diagnostic platform for HPV detection. By enabling early identification of high-risk HPV infection—the critical initiating event in cervical carcinogenesis driven by E6/E7-mediated disruption of p53 and pRb tumor suppressor pathways—this platform addresses a crucial need in cervical cancer prevention.

Background One of the most malignant tumors in men is prostate cancer that is still incurable due to its heterogenous and progressive natures. Genetic and epigenetic changes play significant roles in its development. The RNA molecules with more than 200 nucleotides in length are known as lncRNAs and these epigenetic factors do not encode protein. They regulate gene expression at transcriptional, post-transcriptional and epigenetic levels. LncRNAs play vital biological functions in cells and in pathological events, hence their expression undergoes dysregulation. Aim of review The role of epigenetic alterations in prostate cancer development are emphasized here. Therefore, lncRNAs were chosen for this purpose and their expression level and interaction with other signaling networks in prostate cancer progression were examined. Key scientific concepts of review The aberrant expression of lncRNAs in prostate cancer has been well-documented and progression rate of tumor cells are regulated via affecting STAT3, NF-κB, Wnt, PI3K/Akt and PTEN, among other molecular pathways. Furthermore, lncRNAs regulate radio-resistance and chemo-resistance features of prostate tumor cells. Overexpression of tumor-promoting lncRNAs such as HOXD-AS1 and CCAT1 can result in drug resistance. Besides, lncRNAs can induce immune evasion of prostate cancer via upregulating PD-1. Pharmacological compounds such as quercetin and curcumin have been applied for targeting lncRNAs. Furthermore, siRNA tool can reduce expression of lncRNAs thereby suppressing prostate cancer progression. Prognosis and diagnosis of prostate tumor at clinical course can be evaluated by lncRNAs. The expression level of exosomal lncRNAs such as lncRNA-p21 can be investigated in serum of prostate cancer patients as a reliable biomarker.

Messenger RNA (mRNA) vaccines offer an adaptable and scalable platform for cancer immunotherapy, requiring optimal design to elicit a robust and targeted immune response. Recent advancements in bioinformatics and artificial intelligence (AI) have significantly enhanced the design, prediction, and optimization of mRNA vaccines. This paper reviews technologies that streamline mRNA vaccine development, from genomic sequencing to lipid nanoparticle (LNP) formulation. We discuss how accurate predictions of neoantigen structures guide the design of mRNA sequences that effectively target immune and cancer cells. Furthermore, we examine AI-driven approaches that optimize mRNA-LNP formulations, enhancing delivery and stability. These technological innovations not only improve vaccine design but also enhance pharmacokinetics and pharmacodynamics, offering promising avenues for personalized cancer immunotherapy.

Curcumin (CUR) and piperine (PIP), as natural polyphenols, exhibit potent anti-cancer effects against many cancers, such as breast cancer. To enhance the efficiency of these drugs when used together and to impart magnetic properties to targeted drug delivery, CUR and PIP were loaded on magnetic iron nanoparticles (NPs) coated with silica (Fe3O4@SiO2). CUR-loaded Fe3O4@SiO2 NPs, PIP-loaded Fe3O4@SiO2 NPs, and CUR/PIP-loaded Fe3O4@SiO2 NPs were prepared using a co-participation approach followed by drug functionalization. The analysis of obtained NPs was done by Vibrating-Sample Magnetometer (VSM), Field Emission-Scanning Electron Microscopy (FE-SEM), Transmission Electron Microscopy (TEM), Energy Dispersive X-ray Spectroscopy (EDS), Element Mapping, Fourier Transform Infrared Spectrometer (FT-IR), and X-ray Powder Diffraction (XRD). Analysis confirmed successful loading of drugs on Fe3O4@SiO2 NPs and the presence of good magnetic properties of prepared NPs. According to the MTT assay, all drug-loaded NPs exhibited an anticancer effect on MCF-7 cells; however, the effect of Fe3O4@SiO2-CUR/PIP magnetic NPs was more pronounced than Fe3O4@SiO2-CUR and Fe3O4@SiO2-PIP applied alone, thus confirming the synergistic effect of the two drugs on NPs. Also, Flow Cytometry results showed the amount of cell apoptosis caused by the IC50 concentration and 48-hour treatment with Fe3O4@SiO2-CUR, Fe3O4@SiO2-PIP, and Fe3O4@SiO2-CUR/PIP were estimated to be 63.25%, 61.1%, 75.5% respectively. Furthermore, the Real-time PCR results confirmed the synergistic effect of Fe3O4@SiO2-CUR/PIP nanoparticles in the ratio of Fe3O4@SiO2-CUR and Fe3O4@SiO2-PIP in apoptosis induction.These findings offer a novel perspective for targeted cancer therapy using CUR and PIP.

Background The vaccine-mediated therapy is one interesting option to treat lung cancer. This research introduces a novel therapeutic vaccine based on nanoliposomes containing multi-epitopes of MAGE-A3, TGF-β2, and VEGF-A to enhance immune responses against lung cancer cells. Materials and methods A bioinformatics approach was used to select antigens and to design a peptide-based vaccine. Nanoliposomes containing the multi-epitope peptide were synthesized and characterized. In the next step, Balb/c mice were randomly distributed into 2 groups receiving the peptide vaccine with doses of 10 and 100 mg/ml. In week 4, we assessed the antibody titers and cytokine secretion. The vaccine’s effects on A549 lung cancer cells were evaluated using MTT and Annexin V/PI assays, while Real-time PCR measured the expression of the apoptosis-related genes, Bax and Bcl2 . Additionally, the vaccine’s efficacy was tested in a Humanized PDX model. Results Based on several bioinformatics analyses, such as Gene analysis by UALCAN, the protein-protein interactions by Zs Revelen, and the tumor purity by TIMER, we found that MAGE-A3, TGF-β2, and VEGF-A were good targets for vaccine design. The synthesized nanoliposomes exhibited a size range of 65–190 nm (mean size 110 nm) and a zeta potential of + 30 mV, with approximately 98% peptide loading. It was demonstrated the IgG antibodies against the merged peptide in both doses, even up to 10,000 times serum dilution. Also, the increased level of cytokines including, interleukin 4, interleukin 6, interleukin 10, tumor necrosis factor, and interferon-gamma has been shown in vaccinated mice. Our results showed that A549 cell viability decreased and apoptotic cells increased at both doses and exposure times. The real-time PCR analysis indicated a decrease in Bcl2 gene expression and an increase of Bax gene expression in lung cancer cells treated with serum of vaccinated mice. Importantly, the cancer volume significantly decreased in the immunized PDX models, from approximately 500 mm 3 to 50 mm 3 after 5 weeks. Conclusions This study suggests that nanoliposomal vaccines containing multi-epitope peptides may represent a promising therapeutic approach for lung cancer, eliciting robust immune and anti-tumor responses. Graphical Abstract Key points • Based on several bioinformatics analyses, we found that MAGE-A3, TGF-β2, and VEGF-A were good targets for vaccine design. • A549 cell viability decreased and apoptotic cells increased at both doses and exposure times. • The cancer volume significantly decreased in the immunized PDX models, from approximately 500 mm 3 to 50 mm 3 after 5 weeks.

This study aimed to investigate the activation of error-prone DNA repair pathway in response to Helicobacter pylori infection. Relative changes in the expression levels of genes involved in the non-homologous end-joining pathway (NHEJ) in H. pylori- infected (Cases) and non-infected patients (Controls) with chronic gastritis were measured. A significant increase in the relative expression level of TP53 , and significant decrease in the relative transcription of lncRNA LINP1 and XRCC5 were detected in the case group. The transcription of Lig4 and XRCC6 was increased in the case group, which was not statistically significant. The Spearman’s Correlation Coefficient analysis showed a significant positive-correlation between the transcriptional levels of LINP1 and XRCC4 / XRCC5/Lig4 , and between XRCC5 and TP53 / Lig4 both in the case and control groups. Moreover, a significant positive correlation between LinP1 and XRCC6 in the case, and a significant positive correlation between XRCC4 and Lig4 , and a negative correlation between TP53 and LinP1 / XRCC4 / XRCC5 in the control group was detected. Although a relative difference was detected in transcriptional levels of the NHEJ gene mediators, downregulation of LinP1 in H. pylori -infected patients proposed the activation of a negative feedback loop, which may interfere with the NHEJ activity at the early stages of gastritis.