Cancer immunology

[1][2] Cancer immunosurveillance is a theory formulated in 1957 by Burnet and Thomas, who proposed that lymphocytes act as sentinels in recognizing and eliminating continuously arising, nascent transformed cells.

[5] It has also been suggested that immunosurveillance primarily functions as a component of a more general process of cancer immunoediting.

[8][9] Another example of TSAs are abnormal products of mutated oncogenes (e.g. Ras protein) and anti-oncogenes (e.g.

However, some tumor cells may gain more mutations, change their characteristics and evade the immune system.

This condition may lead to the phase of escape, in which the tumor gains dominance over immune system, starts growing and establishes immunosuppressive environment.

He reasoned, the immune system would be able to play a factor via a 'bystander effect' in eradicating chemotherapy-resistant cancer cells.

[43][44][45][2] However, extensive research is still needed on how the immune response is triggered against dying tumour cells.

[2][58] However, advanced cancer patients with immunosuppression have left researchers in a dilemma as to how to activate their T-cells.

The way the host dendritic cells react and uptake tumour antigens to present to CD4+ and CD8+ T-cells is the key to success of the treatment.

Tumor-associated immune cells in the tumor microenvironment (TME) of breast cancer models
Multiple factors determine whether tumor cells will be eliminated by the immune system or will escape detection. During the elimination phase immune effector cells such as CTL's and NK cells with the help of dendritic and CD4+ T-cells are able to recognize and eliminate tumor cells.
Immune checkpoints of immunosuppressive actions associated with breast cancer