Cervical Squamous Cell Carcinoma and Endocervical Adenocarcinoma (CESC) is a highly prevalent female malignancy. As the epigenomic characteristics of immune cells and cancer cells can serve as predictive indicators for the response to cancer immunotherapy, analysis of epigenetically modified genes (EpiGenes) could contribute to CESC treatment.

Human metapneumovirus (HMPV) is a respiratory virus that presents symptoms similar to those of the common cold or influenza, including cough, nasal congestion, sore throat, fever, wheezing, and shortness of breath. The primary mode of transmission is through respiratory droplets from an infected person's cough or sneeze, as well as through contact with contaminated surfaces. HMPV was first recognized in 2001 and poses a significant public health concern, particularly affecting vulnerable groups like children, the elderly, and those with weakened immune systems. Its impact is notably severe in children under five years, contributing to rates of infant mortality. The main goal of the review article is to improve public health by gathering vital information on the human metapneumovirus (HMPV) and how it affects respiratory illnesses. It seeks to advance knowledge of these illnesses and methods of response.

5-alpha reductase deficiency is an inherited autosomal recessive disorder that can present with severe masculinization defects and ambiguous genitalia. Up to more than 100 mutations have been reported, but phenotype and genotype associations have not been directly evidenced. Testosterone-to-dihydrotestosterone (T/DHT) ratio is a clinically diagnostic test, and the cut-off value is expected to be higher than 10.

Background: The battle against cancer has gained the interest of various researchers, scientists, pharmacologists, and pharmaceutical intervenors in China. Cancer is a leading cause of death worldwide, and the exploration of Traditional Chinese medicine plays an active role in modern medicine and patients with tumors.

Method: The literature search was done in PubMed, Web of Science, Scopus, PubChem, Google Scholar, SCI, and various online data sources. The review summarizes the pharmacology and applications of TCM as an adjuvant cancer therapeutic.

Results: More than 75% of cancer cases are treated using herbal remedies and alternative therapies like TCM in China. Researchers have focused on Western medicines for inhibiting cancer cell growth, apoptosis, and metastasis, with applications of TCM medicines in cancer patients. Furthermore, the complementary and alternative therapies used for cancer patients in China are helpful for cancer-fatigue patients with a combination of chemotherapy and radiotherapy.

Discussion: TCM is a promising strategy for researchers and provides a solid foundation for formulating future hypotheses for studies on TCM-based cancer therapy with fewer side effects and improving patient health.

Conclusion: TCM anticancer progress regulates immune responses and the role of natural killer cells, T and B cells, innate immunity, macrophages, and CD4+ lymphocytes. Additionally, chemopreventive measures in TCM nanotherapeutics shed light on underlying cancer mechanisms and cancer-suppressing genes, promoting the survival of cancer-affected patients in China. Further, it provides newer insights into the therapeutic effects of traditional Chinese medicine in controlling cancer cell growth, cancer stem cells, DNA methylation, apoptosis, and improving patient compliance, promoting health.

There is an urgent and ongoing need to develop effective therapeutic strategies for lung cancer. CCR2 is considered a valid target for lung cancer treatment. However, singletarget- oriented monotherapy frequently fails to yield satisfactory results, and multi-target therapy has become the current trend. IL-21 exerts anti-tumor effects across various cancers, including lung cancer. Whether the combination of CCR2-targeted therapy and IL-21 exerts a stronger anti-tumor effect remains to be verified.

Epithelial Ovarian Cancer (EOC) is a highly aggressive gynecological malignancy with a high mortality rate primarily due to late-stage diagnosis and metastatic dissemination. Regulatory T cells (Tregs) have emerged as critical mediators of immune evasion, yet the role of Foxp3⁺ Tregs in modulating Tumor-Associated Macrophage (TAM) polarization and the underlying molecular mechanisms in EOC remains unclear.

One of the most significant issues facing the world today is antibiotic resistance, which makes it increasingly difficult to treat bacterial infections. Regular antibiotics no longer work against many bacteria, affecting millions of people. A novel approach known as CRISPR-phage therapy may be beneficial. This technique introduces a technology called CRISPR into resistant bacteria using bacteriophages. The genes that cause bacteria to become resistant to antibiotics can be identified and cut using CRISPR. This enables antibiotics to function by inhibiting the bacteria. This approach is highly precise, unlike conventional antibiotics, so it doesn't damage our bodies' beneficial bacteria. Preliminary studies and limited clinical trials suggest that this technique can effectively target drug-resistant bacteria such as Klebsiella pneumoniae and Methicillinresistant Staphylococcus aureus (MRSA). However, challenges in phage engineering, host delivery, and the growing threat of bacterial CRISPR resistance demand urgent and strategic innovation. Our perspective underscores that without proactive resolution of these hurdles, the current hopefulness could disappear. Looking ahead, integrating next-generation Cas effectors, non-DSB editors, and resistance monitoring frameworks could transform CRISPR-phage systems from an experimental novelty into a clinical mainstay. This shift will require not only scientific ingenuity but also coordinated advances in regulatory, translational, and manufacturing efforts.

Alzheimer's Disease (AD) is a progressive neurodegenerative disorder with a complex genetic basis involving both rare mutations and common variants. This review provides a comprehensive synthesis of established and emerging genetic risk factors implicated in AD pathogenesis. Mendelian forms are strongly associated with mutations in APP, PSEN1, and PSEN2, whereas the APOE ε4 allele remains the most robust genetic risk factor for late-onset AD. Recent Genome- Wide Association Studies (GWAS) have uncovered additional susceptibility loci, including TREM2, CLU, ABCA7, and SORL1, which reflect diverse biological pathways such as amyloid metabolism, lipid regulation, and immune response. The review also highlights the roles of epigenetic mechanisms such as DNA methylation and histone modifications, as well as geneenvironment interactions in modulating disease risk and progression. Although substantial progress has been made in identifying genetic contributors, translating these findings into clinical applications remains challenging. This article underscores the need for integrative, multi-omic approaches and population-diverse studies to enhance risk prediction and enable personalized interventions for prevention and therapy in AD.

Exosomes represent the smallest size among extracellular vesicles, which also include apoptotic bodies and microvesicles. Exosomes are natural nanocarriers that play a key role in intracellular communication, consisting of a hydrophobic lipid bilayer membrane and a hydrophilic core. The membrane compositions of exosomes are similar to those of the parent cells from which they are generated. Normally, the exosome membrane contains diacylglycerol, ceramide, cholesterol, and various surface proteins, including tetraspanins and Lamb2. Almost all cell types secrete exosomes into body fluids through exocytosis, including stem cells, epithelial cells, endothelial cells, immune cells, tumor cells, neurons, mast cells, oligodendrocytes, reticulocytes, macrophages, platelets, and astrocytes. Every cell type expresses a distinct type of exosomes carrying various bioactive molecules. Exosomes are major transporters of bioactive cargo, including enzymes, receptors, growth and transcription factors, nucleic acids, lipids, and other metabolites, which strongly affect the physiology of recipient cells. Exosomes are not only potent drug and gene delivery nanocarriers, but also have potential for disease diagnosis, tissue regeneration, and immunomodulation. Exosomes are present in various body fluids, including plasma, serum, saliva, milk, nasal secretions, urine, amniotic fluid, semen, and cerebrospinal fluid, among others. Stem cell-made exosomes are potential natural therapeutics, which is due to their rejuvenating cargo and ability to cross biological barriers. However, natural exosomes' inefficient cargo transfer and short lifespan in the bloodstream have hindered their progress in therapeutic interventions. Genetic engineering of the parent cell allows for loading specific therapeutic cargo into the lumen of newly generated exosomes and/or displaying certain homing peptides or ligands at their surface, leading to extension of their lifespan and precise delivery to specific organs or tissues. This minireview explores the creation of designer exosomes through parent cell engineering and their utilization for guiding the delivery of tailored therapeutic cargo to specific organs while evading the host's innate immune response.

Pancreatic Cancer (PC) is recognized as a highly aggressive malignancy and is anticipated to become the second leading cause of cancer-associated deaths across the United States by 2030. Owing to its late-stage diagnosis and the substantial risk of metastasis, current therapeutic strategies exhibit limited efficacy, resulting in a five-year survival rate below 10%. Consequently, identifying reliable biomarkers and therapeutic approaches remains imperative for enhancing treatment effectiveness.

Identifying potential biomarkers for the detection, diagnosis, and monitoring of cervical cancer (CC) constitutes a key area for future research.

Gene therapy has revolutionized the therapeutic landscape for hemophilia A and B, offering the prospect for persistent endogenous production of coagulation factors VIII and IX. Recent advances in adeno-associated virus (AAV)-mediated gene transfer, particularly the approvals of valoctocogene roxaparvovec (Roctavian) and etranacogene dezaparvovec (Hemgenix), mark significant milestones in hemophilia care. This mini-review synthesizes emerging clinical data from phase I-III trials published between 2022 and 2025, emphasizing efficacy, durability, and immunogenicity profiles of leading AAV-based therapies. Innovations in vector design, such as liverspecific promoters, codon-optimized constructs, and novel capsids (e.g., AAVhu37, AAVrh10, AAV-Spark100), have improved transgene expression and expanded eligibility. Despite notable success, challenges persist, including immune-mediated transaminitis, declining factor activity over time, particularly in hemophilia A, and limitations posed by preexisting neutralizing antibodies. Additionally, CRISPR-Cas9 and non-viral delivery systems are emerging as complementary strategies, potentially enhancing therapeutic precision and overcoming AAV-related barriers. The review also addresses the critical need for equitable access and scalable production models to ensure global availability of gene therapies. With ongoing innovation and multidisciplinary collaboration, gene therapy is poised to transition from experimental intervention to mainstream curative care in hemophilia and other hematologic diseases.

PAK1, a serine-threonine kinase, acts as an effector of Rac, Ras, and CDC42, which are pivotal in oncogenic signaling pathways. Its involvement spans critical cellular processes like cell cycle regulation, angiogenesis, and metastasis. PAK1 also influences therapeutic resistance mechanisms in various cancers. Serving as a linchpin in diverse signaling pathways pivotal to cancer progression, PAK1 positions itself as a promising therapeutic target. The comprehensive understanding of PAK1's roles in cancer biology underscores its potential for targeted interventions and offers prospects for improved cancer diagnostics and treatment strategies.

The fusion of nanotechnology with gene editing promises a revolutionary strategy in combating cancer, providing the possibility of precise and focused treatments. This review examines the synergistic integration of these two potent technologies, specifically emphasising their combined effectiveness in oncological therapies. Nanotechnology offers a flexible framework for administering gene-editing tools, improving their accuracy, and reducing unintended side effects, all of which are significant obstacles in existing cancer treatments. Nanoparticles can improve the effectiveness of therapies, lower the risk of systemic toxicity, and allow the simultaneous manipulation of many genetic pathways involved in cancer growth by delivering CRISPR-Cas9 and other gene-editing systems directly to tumour sites. We conduct a thorough analysis of recent progress in this burgeoning field, emphasising significant advancements in the design of nanoparticles and gene-editing techniques that propel the development of next-generation cancer medicines. In addition, we address the present obstacles and constraints, such as the effectiveness of delivery, apprehensions over safety, and regulatory obstacles, while suggesting potential areas of future research to surmount these barriers. This study thoroughly examines the promise of nano-precision gene editing as a transformative approach to cancer treatment by incorporating findings from recent clinical trials and case studies. By highlighting recent clinical advancements and emerging innovations, this review underscores the potential of nano-precision gene editing as a groundbreaking approach in next-generation cancer therapy.

The discovery of the gene as the primary unit of inheritance marked the beginning of intensive research into targeted genome modifications for treating rare genetic diseases. Despite conventional approaches such as continuous factor replacement or novel non-factor therapies, the need for a one-time infusion and long-term sustenance of clotting factors is evident. This review focuses on gene therapies discovered to treat patients with hemophilia. This narrative review seeks to highlight the current potential of gene therapies for hemophilia, elucidate their mode of action, and assess their long-term effectiveness and clinical significance.

Lung cancer, specifically non-small cell lung cancer (NSCLC), is a leading cause of cancer-related mortality worldwide. TP53, a crucial tumor suppressor gene, is often mutated in various cancers, including lung cancer. This study focuses on the differences in transcriptomic profiles between TP53-mutated (TP53+) and TP53-wildtype (TP53-) NSCLC tumor samples, aiming to develop a gene signature that can predict overall survival and immune response, particularly in the context of immunotherapy. It aims to identify differentially expressed genes (DEGs) associated with TP53 status in non-small cell lung cancer and develop a gene signature that can predict overall survival and immune response.

Diabetic Nephropathy (DN) is a leading cause of chronic kidney disease and end-stage renal failure, highlighting the need for improved diagnostic and therapeutic strategies. This review examines the emerging roles of exosomal microRNAs (miRNAs) and epigenetic modifications in disease, with a focus on their diagnostic and therapeutic potential.

Crohn's disease (CD), a chronic inflammatory disorder of the gastrointestinal tract, presents significant challenges in clinical medicine due to its multifactorial etiology and varied therapeutic responses. This review examines the diverse causes of CD, including genetic predispositions identified through genome-wide association studies (GWAS), which involve scanning the genome for single-nucleotide polymorphisms associated with CD risk, as well as environmental triggers, such as diet and alterations in the microbiome. Biomarkers, such as fecal calprotectin and Creactive protein (CRP), as well as genetic markers like NOD2 mutations, provide critical tools for diagnosis and treatment stratification. Advances in computational methodologies, including multiomics analyses and machine learning, have enhanced our understanding of CD pathophysiology and therapeutic outcomes. Traditional treatments, including immunomodulators and biologics, such as anti-TNF agents, have laid the groundwork for novel cytokine-targeted therapies, such as IL-12/23 inhibitors (e.g., ustekinumab) and integrin inhibitors (e.g., vedolizumab), which aim to improve mucosal healing and reduce relapse rates. However, integrating personalized medicine into clinical practice remains challenging due to the heterogeneity of CD and limitations in biomarker validation. The integration of predictive biomarkers with computational tools enables clinicians to tailor therapy at the individual level, improving remission rates, minimizing adverse effects, and enhancing long-term disease control. These personalized strategies show promise in shifting CD management toward a more effective, patient-specific model of care. This review underscores the potential of personalized therapeutic strategies, leveraging molecular and computational insights, to optimize disease management and improve patient outcomes in CD.

Hereditary forms of diabetes, including Maturity-Onset Diabetes of the Young (MODY) and Neonatal Diabetes Mellitus (NDM), are rare monogenic disorders caused by mutations in genes involved in pancreatic development, beta-cell function, and insulin secretion. Unlike the polygenic nature of type 1 and type 2 diabetes, these forms provide a unique model for precision medicine.

Cerebral Cavernous Malformations (CCMs) are vascular anomalies in the central nervous system that arise from both genetic and non-genetic factors, and can cause hemorrhage, seizures, and neurological deficits. Approximately 80% of CCMs are sporadic, while 20% are Familial (FCCMs), an autosomal dominant, monogenic disorder characterized by multiple lesions and severe clinical manifestations. Over the past three decades, linkage analyses have identified KRIT1/CCM1, MGC4607/CCM2, and PDCD10/CCM3 as major pathogenic genes in FCCMs. However, existing surgical and pharmacological treatments have not adequately prevented disease progression, underscoring the need for more effective strategies. Recent advancements in gene editing tools and delivery systems have transformed gene therapy from a laboratory concept to a clinical reality, offering renewed hope for FCCM patients. Given the multifactorial nature, complexity, and neurological comorbidities of FCCMs, exploring non-surgical gene therapies provides a promising approach for addressing these cerebrovascular lesions. This review summarizes the latest progress in gene editing for FCCMs and examines its therapeutic potential, while acknowledging both the promising benefits and the remaining uncertainties in this evolving field.