Dynamic crosstalk within the tumor microenvironment of uterine cervical carcinoma: baseline network, iatrogenic alterations, and translational implications.

Abstract

Uterine cervical cancer is the fourth most frequent gynecological tumor worldwide. The tumor microenvironment of cervical cancer is the result of persistent high-risk human papillomavirus infection together with stromal activation of estrogen receptor alpha and the pro-angiogenic and pro-inflammatory activity of immune cells, mainly T-helper 17 cells and tumor-associated macrophages. Therapeutic management (e.g., immunotherapy, especially in advanced cases) may be influenced by the translational implications of tumoral stroma crosstalk and an abundance of tumor-infiltrating lymphocytes within the tumor microenvironment. The prognosis of cervical cancer is inversely correlated with microvessel density, making anti-angiogenic strategies with agents such as bevacizumab crucial for improving both progression-free survival and overall survival in patients with advanced and recurrent tumors.