Cancer immunology

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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.[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.[3][4] Cancer immunosurveillance appears to be an important host protection process that decreases cancer rates through inhibition of carcinogenesis and maintaining of regular cellular homeostasis.[5] It has also been suggested that immunosurveillance primarily functions as a component of a more general process of cancer immunoediting.[3]

Immunoediting induces selection for certain tumour cells, which loose dominant tumour-specific antigens allowing the tumour to progress. It has three main phases: elimination, equilibrium and escape.[2][6]

Cancer immunology and chemotherapy[edit]

Obeid et al.[7] 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.[8][9][10][11] However, extensive research is still needed on how the immune response is triggered against dying tumour cells.[2][12]

Professionals in the field have hypothesized that ‘apoptotic cell death is poorly immunogenic whereas necrotic cell death is truly immunogenic’.[13][14][15] 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.[16][17] On the other hand, apoptosis is connected to slight alterations within the plasma membrane causing the dying cells to be attractive to phagocytic cells.[18] However, numerous animal studies have shown the superiority of vaccination with apoptotic cells, compared to necrotic cells, in eliciting anti-tumor immune responses.[19][20][21][22][23]

Thus Obeid et al.[7] 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.[11][24]

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.[11][25]

The role of viruses in cancer development[edit]

Various strains of human papillomavirus (HPV) have been found to play an important role in the development of cervical cancer. The HPV oncogenes E6 and E7 that these viruses possess have been shown to immortalise some human cells and thus promote cancer development.[26] Although these strains of HPV have not been found in all cervical cancers, they have been found to be the cause in roughly 70% of cases. The study of these viruses and their role in the development of various cancers is still continuing, however a vaccine has been developed that can prevent infection of certain HPV strains, and thus prevent those HPV strains from causing cervical cancer, and possibly other cancers as well.

A virus that has been shown to cause breast cancer in mice is mouse mammary tumor virus.[27][28] It is from discoveries such as this and the role of HPV in cervical cancer development that research is currently being undertaken to discover whether or not human mammary tumour virus is a cause of breast cancer in humans.[29] [clarification needed]

See also[edit]


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