Cancer immunology is an interdisciplinary branch of biology that is concerned with understanding the role of the immune system in the progression and development of cancer; the most well known application is cancer immunotherapy, which utilises the immune system as a treatment for cancer. Cancer immunosurveillance and immunoediting are based on protection against development of tumors in animal systems and (ii) identification of targets for immune recognition of human cancer.
Cancer immunology is an interdisciplinary branch of biology concerned with the role of the immune system in the progression and development of cancer; the most well known application is cancer immunotherapy, where the immune system is used to treat cancer. 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. Cancer immunosurveillance appears to be an important host protection process that decreases cancer rates through inhibition of carcinogenesis and maintaining of regular cellular homeostasis. It has also been suggested that immunosurveillance primarily functions as a component of a more general process of cancer immunoediting.
Tumors may express tumor antigens that are recognized by the immune system and may induce an immune response. These tumor antigens are either TSA (Tumor-specific antigen) or TAA (Tumor-associated antigen).
Tumor-specific antigens are antigens that only occur in tumor cells. TSAs can be products of oncoviruses like E6 and E7 proteins of Human papillomavirus, occurring in cervical carcinoma, or EBNA-1 protein of EBV, occurring in Burkitt’s lymphoma cells.  Another example of TSAs are abnormal products of mutated oncogenes (e.g. ras) and anti-oncogenes (e.g. p53). 
Tumor-associated antigens are present in healthy cells, but for some reason they also occur in tumor cells.  However, they differ in quantity, place or time period of expression. Oncofetal antigens are tumor-associated antigens expressed by embryonic cells and by tumors. Examples of oncofetal antigens are AFP (α-fetoprotein), produced by hepatocellular carcinoma, or CEA (carcinoembryonic antigen), occurring in ovarian and colon cancer. More tumor-associated antigens are HER2/neu, EGFR or MAGE-1.
Cancer immunoediting is a process in which immune system interacts with tumor cells. It consists of three phases: elimination, equilibrium and escape. These phases are often referred to as “the three Es” of cancer immunoediting. Both, adaptive and innate immune system participate in immunoediting.
In the elimination phase, the immune response leads to destruction of tumor cells and therefore to tumor suppression. However, some tumor cells may gain more mutations, change their characteristics and evade the immune system. These cells might enter the equilibrium phase, in which the immune system doesn’t recognise all tumor cells, but at the same time the tumor doesn’t grow. This condition may lead to the phase of escape, in which the tumor gains dominance over immune system, starts growing and establishes immunosuppressive environment. 
As a consequence of immunoediting, tumor cell clones less responsive to the immune system gain dominance in the tumor through time, as the recognized cells are eliminated. Therefore the tumor consist of cells with decreased immunogenicity and can hardly be eliminated. This phenomenon was proven to happen as a result of immunotherapies of cancer patients.
Tumor cells have developed various mechanisms to escape immune surveillance.
CD8+ cytotoxic T cells are a fundamental element of anti-tumor immunity. Their TCR receptors recognise antigens presented by MHC class I and when bound, the Tc cell triggers its cytotoxic activity. MHC I are present on the surface of all nucleated cells. However, some cancer cells lower their MHC I expression and avoid being detected by the cytotoxic T cells. This can be done by mutation of MHC I gene, or by lowering the sensitivity to IFN-γ (which influences the surface expression of MHC I).On the other hand, a complete loss of MHC I is a trigger for NK cells. Tumor cells therefore maintain a low expression of MHC I. Another way to escape cytotoxic T cells is to stop expressing molecules essential for co-stimulation of cytotoxic T cells, such as CD80 or CD86.
By expressing FasL on its surface, tumor calls may induce apoptosis of T lymphocytes by FasL-Fas interaction.
Moreover, tumor cells may induce production of regulatory T cells by a contact dependent or independent stimulation. In a healthy tissue, functioning Tregs are essential to maintain self-tolerance. In a tumor, however, Tregs form an immunosupresive microenviroment.[26
Obeid et al. investigated how inducing immunogenic cancer cell death ought to become a priority of cancer chemotherapy. He reasoned, the immune system would be able to play a factor via a ‘bystander effect’ in eradicating chemotherapy-resistant cancer cells. However, extensive research is still needed on how the immune response is triggered against dying tumour cells.
Professionals in the field have hypothesized that ‘apoptotic cell death is poorly immunogenic whereas necrotic cell death is truly immunogenic’. This is perhaps because cancer cells being eradicated via a necrotic cell death pathway induce an immune response by triggering dendritic cells to mature, due to inflammatory response stimulation. On the other hand, apoptosis is connected to slight alterations within the plasma membrane causing the dying cells to be attractive to phagocytic cells. However, numerous animal studies have shown the superiority of vaccination with apoptotic cells, compared to necrotic cells, in eliciting anti-tumor immune responses.
Thus Obeid et al. propose that the way in which cancer cells die during chemotherapy is vital. Anthracyclins produce a beneficial immunogenic environment. The researchers report that when killing cancer cells with this agent uptake and presentation by antigen presenting dendritic cells is encouraged, thus allowing a T-cell response which can shrink tumours. Therefore, activating tumour-killing T-cells is crucial for immunotherapy success.
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.
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