Inflammation is produced by eicosanoids and cytokines, which are released by injured or infected cells. Eicosanoids include prostaglandins that produce fever and the dilation of blood vessels associated with inflammation, and leukotrienes that attract certain white blood cells (leukocytes). Common cytokines include interleukins that are responsible for communication between white blood cells; chemokines that promote chemotaxis; and interferons that have anti-viral effects, such as shutting down protein synthesis in the host cell. Growth factors and cytotoxic factors may also be released. These cytokines and other chemicals recruit immune cells to the site of infection and promote healing of any damaged tissue following the removal of pathogens. The pattern-recognition receptors called inflammasomes are multiprotein complexes (consisting of an NLR, the adaptor protein ASC, and the effector molecule pro-caspase-1) that form in response to cytosolic PAMPs and DAMPs, whose function is to generate active forms of the inflammatory cytokines IL-1β and IL-18. Humoral defenses
The complement system is a biochemical cascade that attacks the surfaces of foreign cells. It contains over 20 different proteins and is named for its ability to "complement" the killing of pathogens by antibodies. Complement is the major humoral component of the innate immune response. Many species have complement systems, including non-mammals like plants, fish, and some invertebrates. In humans, this response is activated by complement binding to antibodies that have attached to these microbes or the binding of complement proteins to carbohydrates on the surfaces of microbes. This recognition signal triggers a rapid killing response.
This biplasia can be arranged in two growth patterns: pericanalicular (stromal proliferation around epithelial structures) and intracanalicular (stromal proliferation compressing the epithelial structures into clefts). These tumors characteristically display hypovascular stroma compared to malignant neoplasms. Furthermore, the epithelial proliferation appears in a single terminal ductal unit and describes duct-like spaces surrounded by a fibroblastic stroma. The basement membrane is intact. Molecular pathology
Up to 66% of fibroadenomas harbor mutations in the exon (exon 2) of the mediator complex subunit 12 (MED12) gene. In particular, these mutations are restricted to the stromal component. Diagnosis
A fibroadenoma is usually diagnosed through clinical examination, ultrasound or mammography, and often a biopsy sample of the lump. Suspicious findings on imaging may result in a person needing a biopsy in order to gain a definitive diagnosis. There are three types of biopsies: Fine-needle aspiration, core-needle biopsy and surgical biopsy. The method of biopsy depends on the appearance, size and location of the breast mass. Treatment
Fibroadenomas can be expected to shrink naturally and so, most are simply monitored. Monitoring fibroadenomas involves regular check-ups to make sure that the breast mass is not growing and is not potentially cancerous. Check-ups involve physical examinations performed every 3–6 months and optional diagnostic imaging performed every 6–12 months for 1–2 years. Generally, surgery is only recommended if the fibroadenoma gets larger or causes increased symptoms. They are removed with a small margin of normal breast tissue if the preoperative clinical investigations are suggestive of the necessity of this procedure.