Treatment of breast cancer tumor immunity

By | April 6, 2012

Treatment of breast cancer immunology, cancer immunotherapy is a relatively new field, including tumor-specific therapy, such as tumor vaccines, and non-specific immune regulation such as cytokines (cytokine, CK), T cell therapy.
(A) of the tumor vaccine
Tumor vaccine theory is based on the existence of human tumor cell tumor-associated antigen. Has been demonstrated in human tumor antigens: embryonic antigens, such as AFP, CEA, PSA, MAGE-I; virus-related antigens, such as EB virus EBNA-1 gene product, SV40T antigen, human papilloma virus E6 and E7 gene product; differentiation antigens, such as MART a 1, TRP-I, enzyme neuraminidase; mutations of oncogenes and anti-cancer products, such as P2Iras, PI85, mp53; after chromosomal translocation fusion protein, such as the P210 protein ; common tumor antigen, such as heat shock proteins, tumor straw liquid core skin MU-L tumor-associated antigens, especially tumor-specific antigen immunogenicity and the ability to induce humoral and cellular immune responses, in particular, can induce specific cell toxic T cells (CTL).
Breast cancer treatment in which immune CD8 + T cells can directly dissolve tumor cells, it is activated after the main release of perforin, the tumor cell membrane calcium channels out of balance, leading to electrolyte / disorders, cell edema and apoptosis, the release of the enzymes to digest the tumor cells. CD8 + T cells release cytokines and activate macrophages, further release of cytokines, inhibition of tumor growth.
T cells (including CD8 + CTL and CD4 + T helper cells) cellular immune activation is the key. T cell activation in addition to tumor antigens and MHC complexes first signal, there must be a total of the second signal stimulating factor, one of the most important and critical is B7 molecules. It is expressed in activated B lymphocytes, dendritic cells and macrophages, and T cells, CD28, CTLA-4 receptor binding, activation of CD4 + and CD8 + T cells, resulting in cellular immunity.
Because tumor cells do not express B7, so that the body of its immune tolerance. If the increased expression of B7 or B7 leaders and the tumor cells or CD28 and CD28 with CD3 antibody to activate T cells, T cells can enhance the role of killing tumor cells.
Adjuvant as a carrier, can stimulate monocytes and macrophages activity, while the release of anti-tumor cytokines, soluble antigen will be presented to other immune activity of T "B cells, to produce the immune response , breaking the body's immune tolerance of tumor. but also must be applied immunomodulatory agent, to remove the inhibition of T cell (Ts) (the current routine use of cyclophosphamide).
Tumor cells to tumor cells as vaccine immunogens. The early study of autologous or allogeneic tumor cells live tumor cell vaccine preparation of survival, but only in animal experiments. After using the ray or ultraviolet radiation, high temperature treatment, anti-cancer drug inactivation, hydrolysis and other methods to change their tumorigenicity, retain their immunogenicity and adjuvanted BCG vaccine prepared from inactivated tumor cells, was used in a variety clinical treatment of cancer, but the effects are unstable. In recent years, use of retroviral or adenoviral vector will be the leaders of foreign genes into tumor cells genetically engineered vaccine. Transfected travel, MHC genes are genes, B7 molecules, cytokines, adhesion molecules.
Treatment of breast cancer tumor immunity, the cytokine into tumor cells, on the one hand slowly and continuously secreted antigen, while the secretion of cytokines, reducing the tumorigenicity of tumor cells, increased immunogenicity. This as a vaccine, once again attack the tumor's growth capacity. Leaders present successful tumor cell cytokines IL-2, IL-3, IL-4, IL-6, IL-7, IFN a , TNF a , M-CSF, GM-CSF and so on. In addition, transduction MHC-I, MHC-II and B7 have demonstrated enhanced immunogenicity and killing tumor cells. Tumor cell vaccine for clinical is still in the testing stage.

Leave a Reply

Your email address will not be published. Required fields are marked *