RESUMO
Melanoma, a highly aggressive skin cancer, is characterized by rapid progression and high mortality. Recent advances in molecular pathogenesis have shed light on genetic and epigenetic changes that drive melanoma development. This review provides an overview of these developments, focusing on molecular mechanisms in melanoma genesis. It highlights how mutations, particularly in the BRAF, NRAS, c-KIT, and GNAQ/GNA11 genes, affect critical signaling pathways. The evolution of diagnostic techniques, such as genomics, transcriptomics, liquid biopsies, and molecular biomarkers for early detection and prognosis, is also discussed. The therapeutic landscape has transformed with targeted therapies and immunotherapies, improving patient outcomes. This paper examines the efficacy, challenges, and prospects of these treatments, including recent clinical trials and emerging strategies. The potential of novel treatment strategies, including neoantigen vaccines, adoptive cell transfer, microbiome interactions, and nanoparticle-based combination therapy, is explored. These advances emphasize the challenges of therapy resistance and the importance of personalized medicine. This review underlines the necessity for evidence-based therapy selection in managing the increasing global incidence of melanoma.
Assuntos
Melanoma , Neoplasias Cutâneas , Humanos , Melanoma/patologia , Neoplasias Cutâneas/patologia , Mutação , Transdução de Sinais , Proteínas de Ligação ao GTP/metabolismoRESUMO
Acne vulgaris is a common dermatological condition that can present across different ages but predominantly affects adolescents and young adults. Characterized by various lesion types, the pathogenesis of acne is complex, involving genetic, hormonal, microbial, and inflammatory factors. This review comprehensively addresses current and emerging acne management strategies, emphasizing both topical and systemic treatments, procedural therapies, and dietary modifications. Key topical agents include retinoids, benzoyl peroxide, antibiotics, and other specialized compounds. Systemic options like antibiotics, hormonal therapies, and retinoids offer significant therapeutic benefits, particularly for moderate to severe cases. Procedural treatments such as laser devices, photodynamic therapy, chemical peels, and intralesional injections present viable alternatives for reducing acne symptoms and scarring. Emerging therapies focus on novel biologics, bacteriophages, probiotics, and peptides, providing promising future options. This review underscores the importance of personalized approaches to treatment due to the multifaceted nature of acne, highlighting the potential of innovative therapies for improving patient outcomes.
Assuntos
Acne Vulgar , Acne Vulgar/terapia , Humanos , Antibacterianos/uso terapêutico , Fármacos Dermatológicos/uso terapêutico , Retinoides/uso terapêutico , Fotoquimioterapia/métodosRESUMO
In order to determine whether CO poisoning was the definitive cause of death, the concentration of carboxyhemoglobin (COHb) in spleen specimens was analyzed using a gas chromatography-thermal conductivity detector. 125 cases of forensic autopsy reports containing COHb analysis requests were analyzed and subdivided into two groups, improbable and highly probable of CO intoxication. In the first group which consists of 100 cases, the results of COHb analysis were negative, and the circumstances of death, as well as the postmortem findings could not validate the exposure to CO. In the second group which consists of 25 cases, the results of COHb were positive, and both postmortem findings and circumstances of death confirmed the exposure to CO. In the cases of indoors and vehicle fires or those including the use of briquettes, COHb levels reached 43.1-97.5â¯%, whereas in individuals without any feature of CO poisoning had COHb level high as 29.8â¯%. However, certain cases without any connection to fire nor CO exposure also contained significant amount of CO based on post-mortem analysis. This study focuses on cases without any relationship to fire or CO and proves that COHb levels below 30â¯% may be considered as a contributing factor to but not exclusively as the cause of death.