Abstract:

Pituitary adenoma （PA） is a common primary brain tumor， and its tumor microenvironment （TME） plays a critical role in the occurence and development and treatment response of tumor. The TME consists of various cellular components， including regulatory T lymphocytes （Tregs）， cytotoxic T lymphocytes （CTLs）， B lymphocytes， macrophages， and stromal cells. Tregs promote immune escape and tumor progression by secreting inhibitory cytokines， while CTLs exhibit dual roles， either killing tumor cells or， under certain conditions， facilitating tumor growth. B lymphocytes show limited infiltration in PA， but their presence is associated with tumor progression and prognosis. The macrophages predominantly exhibit the M2 phenotype， promoting immune evasion and metastasis through the secretion of inhibitory cytokines， pro-angiogenic factors， and matrix metalloproteinase. Stromal components， including the extracellular matrix （ECM） and cancer-associated fibroblasts （CAFs）， remodel the TME and influence tumor growth and invasion. In recent years， immunomodulatory therapies and anti-angiogenic therapies targeting the TME have achieved some progress.The immune checkpoint inhibitors have demonstrated certain efficacy in aggressive pituitary tumors， while anti-angiogenic drugs restrict tumor growth by inhibiting vascular endothelial growth factor （VEGF）. However， current therapeutic strategies still require further optimization to improve efficacy and life quality of the patients. This review summarized the cellular components of TME in PA and their mechanisms， highlighted the advances in immunotherapy and anti-angiogenic therapy， and explored future optimization strategies， aiming to provide the insights for precision treatment of PA.

Key words: Pituitary adenoma, Tumor microenvironment, Immune checkpoint inhibitor, Anti-angiogenic therapy, Regulatory T lymphocyte, Macrophage