Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin condition characterized by intense pruritus and a significant impact on a patient’s quality of life. Despite advancements in understanding AD pathophysiology, there remains a critical need for innovative therapeutic options to better manage this debilitating disease. This review focuses on the evolving landscape of biological therapies for AD, offering insights into their role, mechanisms of action, and potential to revolutionize patient care. In this review, we explore the underlying immunological mechanisms of AD, particularly the role of cytokines and immune pathways implicated in the disease, and how targeted biological therapies modulate these pathways. Current FDA- and EMA-approved biologics, such as Dupilumab, are also discussed in terms of their mechanisms of action, efficacy, and safety. Additionally, we compare their effectiveness, highlighting the benefits and limitations observed in clinical practice. Emerging biological therapies currently under development offer new hope, with innovative targets like IL-13, IL-31, and thymic stromal lymphopoietin (TSLP) representing promising avenues for intervention. We also delve into personalized medicine, emphasizing the importance of biomarkers for predicting treatment response and stratifying AD patients to optimize therapeutic outcomes. Moreover, the synergistic potential of combining biologics with traditional therapies is reviewed, along with a discussion of the challenges involved, including safety, long-term efficacy, and patient adherence. We address the future direction of AD treatment, including microbiome-targeting biologics and the development of next-generation immune modulators. We highlight a new era of targeted treatment possibilities for this complex condition.

Amelanotic melanoma (AM) is a subtype of hypomelanotic or completely amelanotic melanoma. AM is a rare subtype of melanoma that exhibits a higher recurrence rate and aggressiveness as well as worse surveillance than typical melanoma. AM shows a dysregulation of melanin production, cell cycle control, and apoptosis pathways. Knowing these pathways has an application in medicine due to targeted therapies based on the inhibiting elements of the abovementioned pathways. Therefore, we summarized and discussed AM biochemical and molecular induction pathways and personalized medicine approaches, clinical management, and future directions due to the fact that AM is relatively rare. AM is commonly misdiagnosed. Hence, the role of biomarkers is becoming significant. Nonetheless, there is a shortage of biomarkers specific to AM. BRAF, NRAS, and c-KIT genes are the main targets of therapy. However, the role of BRAF and KIT in AM varied among studies. BRAF inhibitors combined with MAK inhibitors demonstrate better results. Immune checkpoint inhibitors targeting CTLA-4 combined with a programmed death receptor 1 (PD-1) show better outcomes than separately. Fecal microbiota transplantation may overcome resistance to immune checkpoint therapy of AM. Immune-modulatory vaccines against indoleamine 2,3-dioxygenase (IDO) and PD ligand (PD-L1) combined with nivolumab may be efficient in melanoma treatment.

Background: Human Papillomavirus (HPV) is a predominant and clinically significant virus affecting individuals of all ages, including children and adolescents. Despite its well-documented role in adult health, particularly in cervical cancer, HPV’s impact on younger populations still remains underexplored. Methods: This review investigates the epidemiology, clinical manifestations, transmission pathways, and historical context of HPV in children and adolescents. Results: The study demonstrates a significant prevalence of HPV DNA within paediatric populations, with diverse clinical manifestations such as verruca vulgaris, anogenital warts, and Juvenile Recurrent Respiratory Papillomatosis, alongside substantiating vertical transmission from mother to infant. We also highlight ground-breaking research milestones, including improvements in genetic studies, the development of HPV vaccines, and ongoing investigations into infection dynamics, and long-term health outcomes. Conclusions: By synthesising existing knowledge, this review aims to enhance clinical decision-making, improve management strategies, and pave the way for future research in HPV-related paediatric diseases.

The liver is one of the most common sites for metastasis, which involves the spread from primary tumors to surrounding organs and tissues in the human body. There are a few steps in cancer expansion: invasion, inflammatory processes allowing the hepatic niche to be created, adhesions to ECM, neovascularization, and secretion of enzymes. The spread of tumor cells depends on the microenvironment created by the contribution of many biomolecules, including proteolytic enzymes, cytokines, growth factors, and cell adhesion molecules that enable tumor cells to interact with the microenvironment. Moreover, the microenvironment plays a significant role in tumor growth and expansion. The secreted enzymes help cancer cells facilitate newly formed hepatic niches and promote migration and invasion. Our study discusses pharmacological methods used to prevent liver metastasis by targeting the tumor microenvironment and cancer cell colonization in the liver. We examine randomized studies focusing on median survival duration and median overall survival in patients administered placebo compared with those treated with bevacizumab, ramucirumab, regorafenib, and ziv-aflibercept in addition to current chemotherapy. We also include research on mice and their responses to these medications, which may suppress metastasis progression. Finally, we discuss the significance of non-pharmacological methods, including surgical procedures, radiotherapy, cryotherapy, radiofrequency ablation (RFA), and transarterial embolization (TAE). In conclusion, the given methods can successfully prevent metastases to the liver and prolong the median survival duration and median overall survival in patients suffering from cancer.

Ototoxicity represents a clinically significant complication of anticancer therapy in pediatric patients. Cytotoxic agents used in oncology, particularly platinum-based chemotherapy, may induce damage to the auditory and vestibular systems, resulting in hearing loss, tinnitus, and balance disturbances. Even mild hearing impairment during childhood may negatively affect speech perception, language development, communication abilities, and subsequent educational and psychosocial functioning. This narrative review aims to synthesize current evidence on treatment-related ototoxicity in children, with particular focus on commonly implicated therapies, clinical consequences, diagnostic approaches, and potential preventive strategies. A focused literature search was conducted in PubMed for publications from 2019 to 2025 addressing ototoxicity associated with pediatric anticancer treatment and audiological monitoring methods. The analysis indicates that platinum-based compounds, especially cisplatin and carboplatin, remain the primary agents associated with ototoxicity, with reported incidence ranging from approximately 20–70% for cisplatin and 10–30% for carboplatin. Additional risk factors include young age, baseline hearing status, renal function, and exposure to other ototoxic agents such as aminoglycoside antibiotics. Early detection relies on comprehensive audiological monitoring combining behavioral and objective methods, including pure-tone audiometry, extended high-frequency audiometry, otoacoustic emissions, and auditory brainstem response testing. Standardized grading systems such as ASHA, Brock, Chang, and SIOP Boston criteria play a key role in identifying and classifying ototoxic changes. Emerging research focuses on improved monitoring protocols, biomarker identification, and the development of otoprotective strategies, including sodium thiosulfate and experimental molecular therapies. Implementing systematic hearing monitoring and preventive strategies is essential to reduce long-term auditory complications and improve quality of life in pediatric cancer survivors.

Brain tumors represent a major clinical challenge due to their complex biology, inherent resistance to conventional therapies and the limited delivery of anticancer agents across the blood–brain barrier. Natural phytochemicals such as curcumin, resveratrol and berberine have gained increasing attention for their multi-targeted anticancer properties, including induction of apoptosis, inhibition of proliferation, suppression of mitochondrial and BCL-2-family signaling and modulation of the tumor microenvironment. This comprehensive review critically examines current evidence on the use of curcumin, resveratrol and berberine in the context of brain tumor treatment, with an emphasis on gliomas’ mechanisms of action, pharmacokinetic limitations, and potential for integration into novel delivery platforms. We discuss how these compounds interact with key pathways in brain tumors—including BCL-2 inhibition, PI3K/AKT/mTOR signaling and epigenetic regulation—and the emerging strategies to overcome glioma-specific obstacles such as blood–brain barrier permeability and microenvironmental hypoxia. Furthermore, the review explores innovative formulations and carrier systems that enhance brain uptake and bioavailability of these agents, bridging the gap between preclinical promise and clinical translation. By identifying current gaps and proposing future research directions, this article aims to provide a roadmap for harnessing curcumin, resveratrol and berberine as adjuvant or combinatorial treatments in brain tumor therapy, focusing particularly on glioma treatment. The adoption of such phytochemicals may open new avenues for improved outcomes in patients with highly refractory brain malignancies.