Chemotherapy remodels lung adenocarcinoma’s tumor microenvironment by driving metabolic reprogramming and shifting immune cell functions to modulate tumor progression and immune responses.

Tissue-resident natural killer cells are important mediators of CD8 T responses in human cancers and these cells can be harnessed to increase immunity against pancreatic ductal adenocarcinoma.

In metastatic NSCLC patients, CHIP showed minimal impact on immunotherapy response but was more prevalent and associated with inflammatory pathways in myeloid cells, particularly in lung squamous cell carcinoma.

Structure-based designed chalcone and pyrazoline derivatives inhibited the ELF3-MED23 protein-protein interaction, leading to HER2 downregulation and retardation of tumor growth in HER2-positive gastric cancer.