Incidence, risk factors, prevention and treatment of postmastectomy pain syndrome in breast cancer: A multicenter study.

BACKGROUND: Postmastectomy pain syndrome (PMPS) is a common postoperative condition after breast cancer surgery. PURPOSE: The aim of this study was to investigate the incidence rate and risk factors of PMPS, and to propose prevention and treatment methods. METHODS: The study included 1790 postoperative breast cancer patients from three hospitals from 2017 to 2021, of which 302 (13.0%) patients with PMPS were included in the study. RESULTS: Age, breast surgery type, axillary surgery type and radiotherapy are the risk factors of PMPS. Age, radiotherapy and chemotherapy affect the pain degree of PMPS during movement. CONCLUSIONS: For breast cancer patients with high risk factors, pain should be actively prevented during perioperative period. Oral pharmacological agents, multidisciplinary combination therapy, local anesthetics and regional anesthesia are the most common treatment of PMPS.

Estrogen-induced SDF-1α production promotes the progression of ER-negative breast cancer via the accumulation of MDSCs in the tumor microenvironment.

Estrogen plays a role in the processes of tumorigenesis, metastasis, and drug resistance in estrogen receptor (ER)-positive breast cancer (BC). Whether estrogen contributes to ER-negative BC is unclear. Here, we aimed to investigate whether estrogen could stimulate the secretion of stromal-derived factor-1 (SDF-1α) by cancer-associated fibroblasts (CAFs) to promote the progression of ER-negative BC. We transplanted ER-negative BC cells into ovariectomized mice, which was followed by continuous injection of estrogen, and found that estrogen promoted the tumorigenesis of BC. Furthermore, High levels of SDF-1α and tumor-infiltrating myeloid-derived suppressor cells (MDSCs) were detected in the estrogen treatment group. Estrogen stimulates secretion of SDF-1α by CAFs extracted from BC patients. Recombinant SDF-1α could recruit MDSCs isolated from bone marrow cells of mice. In addition, the co-culture of CAFs and MDSCs demonstrated that the recruitment of MDSCs was increased when CAFs were exposed to estrogen. Using AMD3100 to block the SDF-1α/CXCR4 axis or gemcitabine to delete MDSCs, we observed that both of these agents could neutralize the effect of estrogen on tumorigenesis. Together, these results suggest that estrogen may promote the progression of ER-negative BC by stimulating CAFs to secrete SDF-1α, which can recruit MDSCs to the tumor microenvironment to exert tumor-promoting effects.