The following is a summary of “Modulation of the tumor microenvironment and mechanism of immunotherapy-based drug resistance in breast cancer,” published in the May 2024 issue of Oncology by Kundu et al.
Breast cancer stands as the most prevalent malignancy among women, with early-stage detection often leading to successful outcomes. However, managing metastatic breast cancer presents formidable challenges, frequently resisting standard therapies. Immunotherapy emerges as a cornerstone in the treatment of metastatic breast cancer, yet its efficacy is hampered by the development of resistance mechanisms. Central to this phenomenon is the tumor microenvironment (TME), orchestrating the response to immunotherapy. Notably, components within the TME, such as cancer-associated fibroblasts (CAFs), tumor-associated macrophages (TAMs), and myeloid-derived suppressor cells (MDSCs), play pivotal roles in driving immunotherapy resistance through their intricate modulation of the TME.
This review elucidates the critical involvement of stromal cells in shaping the breast tumor microenvironment, exploring the dynamic interplay between CAFs and TAMs, the impact of altered tumor metabolism on immunotherapy efficacy, and the latest advancements in high-throughput genomic screening and spatial omics techniques for identifying key tumor immune genes governing immunotherapy response. Furthermore, the review underscores therapeutic strategies aimed at surmounting immune resistance in breast cancer, encompassing approaches such as CAF reprogramming, TAM polarization modulation, manipulation of tumor metabolism, and targeted interventions addressing genomic alterations.
By delving into these multifaceted mechanisms and therapeutic avenues, this review endeavors to provide insights into overcoming immunotherapy resistance in breast cancer, thus paving the way toward enhanced treatment outcomes for affected individuals.
Source: molecular-cancer.biomedcentral.com/articles/10.1186/s12943-024-01990-4
