Table 1 Major factors within the breast tumour microenvironment

Adipocytes

Adipocytes are a key source of metabolites, lipids and adipokines that can cause metabolic reprogramming of cancer cells, promoting proliferation, invasion, and resistance to therapy.

Cancer-associated fibroblasts (CAFs)

CAFs have a central role in regulating the tumour matrix. Heterogeneity of CAFs has been previously observed in BC, where subtypes have been shown to promote a cancer stem cell-like phenotype.

Myoepithelial cells

Epithelial cells that support luminal cells of the secretory mammary tissue. A loss of the intact myoepithelial ring surrounding BC cells shows a shift from non-invasive to invasive disease. However, myoepithelial cells have also been shown to drive suppression of BC.

Macrophages

Infiltration of macrophages into the adipose in obesity-associated BC leads to chronic inflammation and increased levels of pro-inflammatory macrophages. These macrophages form a ring around dying adipocytes called crown-like structures, which are associated with worse prognosis.

Extracellular matrix

The ECM has roles in cell adhesion, migration, and invasion. Matrix proteins such as fibrillar collagens, fibronectin and laminins are induced in breast cancer. Many of these ECM proteins play a role in breast tumour progression and metastasis. ECM remodelling enzymes become dysregulated in breast cancer, resulting in altered properties such as stiffness. In obesity, there is increased deposition of ECM and enhanced crosslinking of collagen fibres.