Scheme 1

The influence of inflammation on the receptors of breast cancer cells. Tumor cells are recognized by the antigen presenting cells (APC) and the immune response is triggered. I. CD8 cells are activated by Th1. As a result of their interaction the inflammatory mediators are freed. They stimulate the accumulation of Hsp90 in a cell. Hsp90 stimulates several functions: 1) the stabilization of HER2/neu receptors; 2) the maturation and reparation of such proteins as VEGF, p53, HIV-1A, MMP2; 3) the blocking of APAF-1, which inhibit the function of Bcl-2; 4) the accumulation of Akt and NF-kB. II. APC secretes IL-1 that activates CD79 α (B lymphocytes) cells. IL-1 which is excreted by APC and CD79α cells induces the accumulation of NF-kB in cell. NF-kB starts the following processes: 1) the accumulation of Akt, EZH2 and BLIMP-1; 2) the activation of Bcl-2. Akt activates Bcl-2 and blocks FOXO3A, which is responsible for the transcription of ERS. EZH2 and BLIMP-1 also block the ERS transcription. As a result ER disappears. Because PR is formed after ER then they disappear too. BCL 2 is an estrogen-responsive gene, so the amount of Bcl-2 is also reduced