The development of brain metastasis is a major cause of significantly reduced survival in breast cancer patients. The initiation and progression of breast cancer brain metastasis (BCBM) involve multiple distinct molecular pathways and reprogramming of the tumor microenvironment (TME). This review systematically summarizes key mechanisms underlying BCBM, including epithelial-mesenchymal transition (EMT), extracellular matrix (ECM) remodeling, and the spatiotemporal dynamics of metabolic reprogramming regulated by critical signaling pathways during brain colonization. In particular, we highlight emerging mechanisms of breaching the specialized brain multifunctional barriers. Furthermore, this review provides an in-depth analysis of the cooperative immune-suppressive network within the BCBM TME, emphasizing the crosstalk among various immune cell components (such as T cells, B cells, macrophages, neutrophils, NK cells, MDSCs) and intracranial-specific cellular elements (including astrocytes, microglia, brain metastasis-associated fibroblasts). Through the complex interplay, these cells collectively facilitate immune evasion and metastatic outgrowth. Accordingly, we discuss the current clinical management of BCBM and potential future directions. Deeper mechanistic insights are expected to offer novel biomarkers and reveal new targets for developing precision therapeutic strategies against BCBM.

Common pancreatic diseases have caused significant economic and social burdens worldwide. The interstitial microenvironment is involved in and plays a crucial part in the occurrence and progression of pancreatic diseases. Innate lymphoid cells (ILCs), an innate population of immune cells which have only gradually entered our visual field in the last 10 years, play an important role in maintaining tissue homeostasis, regulating metabolism, and participating in regeneration and repair. Recent evidence indicates that ILCs in the pancreas, as well as in other tissues, are also key players in pancreatic disease and health. Herein, we examined the possible functions of different ILC subsets in common pancreatic diseases, including diabetes mellitus, pancreatitis and pancreatic cancer, and discussed the potential practical implications of the relevant findings for future further treatment of these pancreatic diseases.

The nervous system functions as a central regulatory network that maintains physiological homeostasis through the coordinated actions of the central and peripheral nervous systems. The emergence of cancer neuroscience has unveiled novel mechanisms underlying bidirectional regulation among the nervous system, tumor cells, and the immune system. This review focuses on pancreatic cancer, often referred to as the "king of cancers," a malignancy characterized by aggressive behavior, early perineural invasion, and dismal prognosis. We systematically analyze the interactions within the neuro-tumor-immune microenvironment. On one hand, the peripheral and central nervous systems promote neurotropic migration of cancer cells and the formation of a tumor immunosuppressive microenvironment through neurotransmitters, neurotrophic factors, and synaptic remodeling. On the other hand, cancer cells and the immune microenvironment reshape neural structures, exacerbating immune evasion and malignant progression. Furthermore, this review integrates fundamental mechanisms with translational and clinical research, and proposes neuroscience-guided precision therapeutic strategies, including the development of neural invasion-related biomarkers and the targeting of key nodes within neuro-tumor-immune interactions. Together, these approaches add a new dimension to overcoming therapeutic bottlenecks in pancreatic cancer and facilitate the translation of mechanistic insights into clinical applications.