This article elucidates therapeutic approaches for KRAS G12C-mutant advanced non-small cell lung cancer, with focus on global advancements in inhibitor research. It also summarizes clinical evidence on the efficacy of targeted agents in monotherapy and combination therapies, analyzes their clinical advantages and challenges, and explores future directions for novel treatment modalities.

The cost economics of early-stage lung cancer treatments is a key focus in the field of lung cancer. The primary treatment modalities for early-stage lung cancer include radiotherapy and thoracic surgery, each offering distinct advantages in therapeutic outcomes and costs. To better understand the cost-effectiveness of radiotherapy versus thoracic surgery for early-stage lung cancer, this paper reviews the progress of recent research on economic evaluations of these two treatment approaches.

Tumor angiogenesis plays a crucial role in tumor proliferation, invasion and metastasis, representing one of the hallmarks of cancer. Cancer-associated fibroblasts (CAF), as the core component of tumor microenvironment, have a decisive impact on tumor angiogenesis. On the one hand, CAF can secrete various cytokines such as vascular endothelial growth factor and hepatocyte growth factor, which activate the related signaling pathways to promote angiogenesis; on the other hand, CAF-derived exosomes carry pro-angiogenic factors and specific microRNA that drive this process through multiple signaling cascades. In addition, CAF can also modify the extracellular matrix, create favorable conditions for angiogenesis, and interact with immune cells to promote angiogenesis by regulating macrophage polarization. Based on these mechanisms, anti-angiogenic therapy targeting CAF has become a new research hotspot, ProAgio protein, eicosapentaenoic acid and other formulations have shown potential therapeutic effects, and various biophysical therapies for CAF have also shown great potential, which are expected to bring new breakthroughs to tumor treatment in the future.

Tumor angiogenesis plays a crucial role in tumor proliferation, invasion and metastasis, representing one of the hallmarks of cancer. Cancer-associated fibroblasts (CAF), as the core component of tumor microenvironment, have a decisive impact on tumor angiogenesis. On the one hand, CAF can secrete various cytokines such as vascular endothelial growth factor and hepatocyte growth factor, which activate the related signaling pathways to promote angiogenesis; on the other hand, CAF-derived exosomes carry pro-angiogenic factors and specific microRNA that drive this process through multiple signaling cascades. In addition, CAF can also modify the extracellular matrix, create favorable conditions for angiogenesis, and interact with immune cells to promote angiogenesis by regulating macrophage polarization. Based on these mechanisms, anti-angiogenic therapy targeting CAF has become a new research hotspot, ProAgio protein, eicosapentaenoic acid and other formulations have shown potential therapeutic effects, and various biophysical therapies for CAF have also shown great potential, which are expected to bring new breakthroughs to tumor treatment in the future.

Approximately 50%of patients with non-small-cell lung cancer(NSCLC)are diagnosed at advanced stages and face a challenging prognosis despite the integration of targeted therapies,immun-otherapy,and systemic chemotherapy into current standard care.A key factor in this context is trophoblast cell-surface antigen 2(TROP2),which is widely expressed in NSCLC and strongly associated with poor patient outcomes.This article examines the latest developments in the application of datopotamab deruxtecan(Dato-DXd,DS-1062),a novel antibody-drug conjugate targeting TROP2,in the treatment of NSCLC.It provides a detailed assessment of Dato-DXd's technical design,evaluates its efficacy by using recent clinical trial data,and discusses its safety profile.

The ATP-binding cassette(ABC)transporter superfamily comprises membrane proteins that efflux various substrates across extra-and intracellular membranes.Among them,ABCB1,ABCG2,and ABCC1 are directly linked to tumor multidrug resistance(MDR).This review provides an overview of the current understanding on the novel mechanisms and functions of ABCB1,ABCG2,and ABCC1 transporters in tumor MDR,discusses the latest strategies to target these transporters,and explores further opportunities to overcome MDR.

Protein S-palmitoylation is a reversible post-translational modification of lipids that regulates protein localization, stability and protein-protein interactions. The thioesterification of palmitate to internal cysteine residues is catalyzed by palmitoyltransferase, while the removal of palmitate is mainly catalyzed by acyl-protein thioesterase. The S-palmitoylation of some tumor-related proteins is abnormally altered in tumor, which is closely related to the biological processes such as tumor cell proliferation, invasion, metastasis, drug resistance and immune response. Furtherly, exploring the characteristics of protein S-palmitoy-lation and its role in tumor progression could deliver new ideas in targeting protein S-palmitoylation for tumor therapy.

Bone is the main metastatic site of prostate cancer, and bone metastasis of prostate cancer seriously affects the prognosis and quality of life of patients. Exosomes are lipid bilayer vesicles secreted by cells, which play a significant role in intercellular communication. Exosomes can regulate the specific colonization of prostate cancer cells in bone tissue, reshape the pre-metastatic niche conducive to the survival of tumor cells, and modulate the immune microenvironment of bone. At the same time, exosomes can also regulate the differentiation and maturation of osteoblasts and osteoclasts, resulting in bone remodeling. Further understanding of the role of exosomes in bone metastasis of prostate cancer will help to develop new targets for delaying the progression of bone metastasis.

Lung cancer is one of the most common malignancies and has the highest number of deaths among all cancers. Despite continuous advances in medical strategies, the overall survival of lung cancer patients is still low, probably due to disease progression or drug resistance. Ferroptosis is an iron-dependent form of regulated cell death triggered by the lethal accumulation of lipid peroxides, and its dysregulation is implicated in cancer development. Preclinical evidence has shown that targeting the ferroptosis pathway could be a potential strategy for improving lung cancer treatment outcomes. In this review, we summarize the underlying mechanisms and regulatory networks of ferroptosis in lung cancer and highlight ferroptosis-targeting preclinical attempts to provide new insights for lung cancer treatment.

Lung cancer is the most fatal malignant tumor worldwide,with non-small cell lung cancer(NSCLC)being the predominant pathological subtype.The development of NSCLC is driven by mutations in the epidermal growth factor receptor(EGFR),and EGFR tyrosine kinase inhibitors(EGFR-TKIs)are employed as targeted therapies for first-line treatment of advanced NSCLC patients harboring EGFR mutations.However,varia-tions in molecular structures,concurrent mutations,and mechanisms of therapeutic resistance contribute to prog-nostic disparities among different EGFR subgroups.This review primarily summarizes the molecular structural basis and differential treatment responses associated with distinct types of EGFR mutations in NSCLC.