The Role of Inflammation in Inflammatory Breast Cancer

Abstract

Inflammatory breast cancer (IBC) is the most aggressive form of breast cancer. Despite extensive study, whether inflammation contributes to the tumorigenicity or aggressiveness of IBC remains largely unknown. In this chapter, we will review the potential role played by inflammation in IBC based on the results of in vitro, in vivo, and patient studies. Current evidence suggests that several major inflammatory signaling pathways are constitutively active in IBC and breast cancer. Among them, the NF-κB, COX-2, and JAK/STAT signaling systems seem to play a major role in the tumorigenesis of IBC. Inflammatory molecules such as interleukin-6, tumor necrosis factor alpha (TNF-α), and gamma interferon have been shown to contribute to malignant transformation in preclinical studies of IBC, while transforming growth factor-β, interleukins 8 and 1β, as well as TNF-α appear to play a role in proliferation, survival, epithelial-mesenchymal transition, invasion, and metastasis. In this chapter, we also describe work thus far involving inhibitors of inflammation in the development of prevention and treatment strategies for IBC.

A multi-targeted approach to suppress tumor-promoting inflammation

“…Possible associations have also been found between inflammatory diseases, such as esophagitis and Barrett's metaplasia, and esophageal cancer [12] and between chronic pancreatitis and pancreatic cancer [13]. Emerging studies have established a crucial role of chronic, unresolved inflammation in the promotion and progression of breast cancer, including the most aggressive type known as inflammatory breast cancer [14, 15]. The ovarian epithelial inflammation is linked to ovarian cancer [16].…”

Steamed root of Rehmannia glutinosa Libosch (Plantaginaceae) alleviates methotrexate-induced intestinal mucositis in rats

“…Generally, TNF-α has suppressive action on cancer cells and angiogenesis when locally applied at a higher dose (Van Horssen et al, 2006). A high level of TNF-α following cancer chemotherapy, however, is known to cause tissue damage, leucopenia, sickness behavior, and malignant transformation and progression as well as increased bone resorption (Fouad et al, 2014;Ganz et al, 2013;King et al, 2012;Myers, 2008;Palin et al, 2009;Sethi et al, 2008). Thus, it is vital to suppress the production of TNF-α during cancer chemotherapy (Logan et al, 2007(Logan et al, , 2008Zidi et al, 2010).…”

Genomic and Immunological Tumor Profiling Identifies Targetable Pathways and Extensive CD8+/PDL1+ Immune Infiltration in Inflammatory Breast Cancer Tumors

“…Inflammatory breast cancer (IBC) is the most aggressive and lethal form of primary breast cancer (1,2). IBC is a clinically and pathologically unique subtype of breast cancer that accounts for up to 5% of breast cancer.…”

“…1,5), but the exact function of the immune response remains elusive. Immune cells and inflammatory signaling may promote IBC tumor cell proliferation, angiogenesis, and metastasis (1).…”

“…1,5), but the exact function of the immune response remains elusive. Immune cells and inflammatory signaling may promote IBC tumor cell proliferation, angiogenesis, and metastasis (1). On the other hand, the presence of cytotoxic tumor-associated lymphocytes has also been associated with a more favorable breast cancer prognosis (6).…”