Abstract
Simple SummaryInflammatory breast cancer (IBC) is the most lethal and aggressive form of breast cancer; it is highly likely to spread to other sites in the body. There is an urgent need to establish novel treatment strategies to reduce IBC recurrence and metastasis. The aim of this work is to provide a comprehensive overview of signaling pathways in IBC, covering understanding of their function in IBC tumor cells and cells surrounding tumor, and clinical efforts to target these pathways for patients with IBC. The findings described in this work will help guide the development of effective therapies through preclinical and clinical research, eventually improving the treatment of patients with IBC.Inflammatory breast cancer (IBC), although rare, is the most aggressive type of breast cancer. Only 2–4% of breast cancer cases are classified as IBC, but—owing to its high rate of metastasis and poor prognosis—8% to 10% of breast cancer-related mortality occur in patients with IBC. Currently, IBC-specific targeted therapies are not available, and there is a critical need for novel therapies derived via understanding novel targets. In this review, we summarize the biological functions of critical signaling pathways in the progression of IBC and the preclinical and clinical studies of targeting these pathways in IBC. We also discuss studies of crosstalk between several signaling pathways and the IBC tumor microenvironment.
Highlights
Inflammatory breast cancer (IBC) is the most lethal type of breast cancer, with a high rate of metastasis [1,2,3,4]
They found a higher expression of phosphorylated epidermal growth factor receptor (EGFR) and more metastasis in tumors produced by the co-injection of SUM149 with mesenchymal stem cells compared with tumors grown from SUM149 cells only; the EGFR inhibitor erlotinib abrogated these effects [28]
Entinostat sensitized trastuzumab- or lapatinib-resistant HER2-overexpressing cells to single-agent treatment with trastuzumab or lapatinib [53]. These results suggest the potential of combining entinostat with HER2-targeted therapies to improve the treatment of patients with
Summary
Inflammatory breast cancer (IBC) is the most lethal type of breast cancer, with a high rate of metastasis [1,2,3,4]. Over the past two decades, researchers have identified some molecular changes of inflammatory mediators Janus kinase (JAK)/signal transducers and activators of transcription that play important roles in IBC. These include loss of WNT1-inducible-signaling pathway protein 3. Tumor transducers microenvironment (TME), which includes T (STAT) [17,18], nuclear factor kappa B (NF-κB) [19,20,21], and Cyclooxygenase-2 (COX-2) [20,22] as well cells, tumor-associated macrophages (TAMs), fibroblasts, mast cells, and mesenchymal stem cells as angiogenic factors [23,24] and translation initiation factor eIF4GI [25]; and enrichment of the cancer (MSCs), has been shown to play[26]. The co-injection of MSCs with IBC cells can drive IBC clinical phenotypes, patients to including neoadjuvant chemotherapy (NAC).
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