Abstract

Inflammatory breast cancer (IBC) is a rare and clinically more aggressive type of breast cancer. This type of breast cancer is called “inflammatory” because the breast often appears to be swollen, reddened, or “inflamed.” Some studies have demonstrated an association between familial history of breast cancer and IBC; however, additional studies are required to demonstrate this. IBC is classified as breast cancer at stage IIIB or IV. Some signaling pathways undoubtedly provide novel therapeutic targets for developing IBC inhibitors. By means of a cell line study, the loss has been identified of Wnt signaling pathway-induced protein 3 (WISP3/CCN6; LIBC [Lost in Inflammatory Breast Cancer]). Microarray analysis in IBC compared in noninflammatory tumors has demonstrated a signature of IBC that includes genes involved in IGF signaling, which we will discuss later in the section on microarrays and genomic signatures in IBC. Overexpression of epidermal growth factor receptors (ErbB) is very common in IBC. In another study, the expression and correlation was evaluated of the protein caveolin-1, which is a structural protein of the IBC-cell membrane caveolar microdomains (also described in breast cancer cell lines) and not in the cells of noninflammatory mammary cancer tumors. A protein that has demonstrated to possess tumor suppressor properties in breast cancer is E-cadherin; likewise, it has been demonstrated that it is found to be overexpressed in IBC, allowing the formation of lymphovascular emboli, which offers cytoprotector and resistance mechanisms to the chemotherapy of IBC cells. The genomic profile of IBC and of noninflammatory breast tumors stratified according to hormonal receptor state and HER2.

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