Epidermal growth factor receptor activating mutations serve as core driver lesions of non-small cell lung cancer, while early EGFR inhibitors are restricted by T790M resistance and weak blood-brain barrier penetration. This review systematically sorts multi-layer pharmacological effects, clinical advantages and acquired resistance subtypes of third-generation targeted agent osimertinib based on domestic and global Phase III clinical data. Osimertinib forms stable covalent binding with mutant EGFR to block MAPK and PI3K/Akt oncogenic cascades, and exerts dual anti-tumor effects via direct tumor apoptosis induction and long-term remodeling of immunosuppressive microenvironment. Large clinical trials verify its prominent control efficacy for primary lesions and intracranial metastases, yet long-term monotherapy easily generates four categories of drug resistance represented by C797S mutation and MET amplification. This paper summarizes stratified combined intervention schemes matching different resistance phenotypes, which provide standardized theoretical references for dynamic individualized targeted treatment and novel EG inhibitor development. Novel liquid biopsy monitoring technology further optimizes the whole-process precision medication management of osimertinib in clinical practice.

As core subsets of extracellular vesicles, exosomes mediate intercellular signal communication and carry diverse biomolecules that faithfully reflect the phenotypic characteristics of parent cells. In oncology research, exosomes exert two opposing biological effects on tumor progression and clinical intervention. This paper systematically sorts the dual regulatory functions of exosomes and summarizes their translational prospects for tumor liquid biopsy and targeted drug delivery. Tumor-derived exosomes remodel local and distant tumor microenvironments, suppress anti-tumor immune responses, facilitate angiogenesis and epithelial-mesenchymal transition, and transmit drug-resistant traits to sensitive tumor cells. Meanwhile, exosomes with intact lipid bilayer structures can protect internal nucleic acids and proteins from enzymatic degradation, serving as stable non-invasive biomarkers for early tumor screening and efficacy monitoring. Genetically modified engineered exosomes can load chemotherapeutics, small interfering RNAs and immune regulators to achieve tumor-specific targeted delivery. This paper systematically elaborates the molecular mechanisms, clinical diagnostic value, therapeutic potential and translational bottlenecks of exosomes in precision oncology. Current evidence proves exosome-based liquid biopsy supports early tumor detection, primary lesion tracing and dynamic efficacy evaluation. However, standardized separation protocols, unified quality control standards and long-term safety evaluation systems have not been fully established, restricting large-scale clinical transformation. Follow-up interdisciplinary research needs to form unified technical specifications to promote the clinical application of exosome-based diagnosis and treatment integrated strategies.

With the rapid growth of the global aging population, the incidence of Alzheimer's disease (AD) has been increasing year by year. This progressive, irreversible and insidious neurodegenerative disease will lead to progressive cognitive deterioration, posing a major public health threat to seniors and bringing heavy burdens to families and society. However, its complex and multi-dimensional pathogenesis has not been fully clarified, and major bottlenecks still exist in early screening, accurate diagnosis, and radical treatment. This paper systematically reviews the progression of AD, categorizing it into three stages: the subjective cognitive decline, mild cognitive impairment and AD dementia and describes its progression from early latent symptoms to severe functional impairment in middle and late stages. Based on this, this article deeply analyzes the multiple and interrelated pathogenic mechanisms of AD from four dimensions: canonical amyloid-tau proteinopathy, cerebral metabolic dysfunction, cerebral white matter structural impairment and systemic inducing factors. The study summarizes current mainstream interventions, pointing out key dilemmas including delayed diagnosis, single-target therapeutic limitations, and comorbidity interference, and lack of curative drugs. Additionally, this paper reviews cutting-edge research fields: diabetes-associated pathological pathways, DTI imaging, AI-assisted diagnosis, gut-brain axis regulation, and new targeted treatments. The study shows that AD is a complex disease driven by multiple factors, systems and mechanisms, and a single intervention is difficult to overcome the current predicament. This paper offers a comprehensive theoretical reference for AD early warning, pathological mechanism research, precision diagnosis and treatment, and translational medical development.