癌症预防的进展

抽象的

Lung Cancer Progression is not always Halted by Voluntary Exercise

Prakseema Baxla

Lung cancer remains a formidable global health challenge, characterized by diverse histological subtypes and varying clinical trajectories. This review comprehensively explores the intricate molecular and cellular mechanisms underlying the progression of lung cancer, encompassing non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). By dissecting the key drivers of tumor initiation, metastasis, and treatment resistance, this analysis sheds light on potential therapeutic targets and strategies for improved patient outcomes. The evolution of lung cancer involves a complex interplay of genetic alterations, epigenetic modifications, and dysregulated signaling pathways. Driver mutations, including alterations in EGFR, ALK, ROS1, and BRAF, delineate subgroups within NSCLC, driving tumor initiation and progression. Additionally, genomic instability, immune evasion, and angiogenic signaling contribute to the malignant phenotype.

Metastasis, a hallmark of advanced lung cancer, involves a cascade of events influenced by tumor microenvironment components, including immune cells, fibroblasts, and extracellular matrix elements. The elucidation of molecular mediators and signaling pathways governing metastatic dissemination provides opportunities for targeted intervention and the development of novel therapeutics. Furthermore, the emergence of treatment resistance poses a significant clinical challenge. Molecular mechanisms such as target gene amplification, activation of bypass pathways, and acquired mutations contribute to therapeutic resistance in both NSCLC and SCLC. Understanding these resistance mechanisms is imperative for the design of combination therapies and the development of next-generation treatment strategies.

Immunotherapy, particularly immune checkpoint inhibitors, has revolutionized the treatment landscape for lung cancer. However, patient selection and the identification of predictive biomarkers remain critical for optimizing immunotherapeutic outcomes. Additionally, the integration of targeted therapies, immunotherapies, and conventional treatments in a multimodal approach holds promise for overcoming resistance and improving long-term survival. In conclusion, this review provides a comprehensive overview of the molecular and cellular mechanisms driving lung cancer progression. By dissecting the intricacies of tumor initiation, metastasis, and treatment resistance, we gain valuable insights into potential therapeutic targets and strategies. The integration of personalized medicine approaches, including targeted therapies and immunotherapies, represents a promising avenue towards improved patient outcomes in lung cancer. Continued research efforts focused on unraveling the complexities of lung cancer progression will undoubtedly pave the way for more effective therapeutic interventions and ultimately lead to better prognosis for individuals affected by this devastating disease.