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  • New Zealand has the highest incidence of melanoma cancer in the world. Although there are no cures for advanced melanomas at this stage, our scientists are trying to see if they can use the body’s own immune system to fight the disease.

    What is melanoma?

    Melanoma is a type of skin cancer that is associated with overexposure to UV rays in sunlight. It gets its name from the cell it develops in – a type of skin cell called a melanocyte. Melanocytes are pigment-producing cells and give rise to moles. This is why melanoma is usually linked to changes in mole colour and size.

    A superficial melanoma can be surgically removed, but if it is left to grow into the tissue below the upper skin layer, it can spread throughout the body and become deadly. When it is at this stage, it is called a metastatic melanoma. There are very few treatment options available for someone who has been diagnosed with metastatic melanoma. Late-stage disease is usually fatal.

    This article explains how melanoma form.

    Why is melanoma difficult to treat?

    One of the reasons that melanoma is so difficult to treat is that the tumour cells for each person have slightly different protein structures on their surfaces, called epitopes. It is difficult to make a drug that can target all of these different epitopes, especially because new types are showing up all the time!

    Activating the body’s own defences

    In rare cases, an advanced melanoma can shrink on its own – the person’s immune system fights the melanoma. This makes melanoma an unusual cancer, because the immune system seems able to respond to it, trying to rid the body of tissue damaged by the disease, but this response is variable and not often successful, especially if the cancer is spreading faster than the immune system can respond.

    A group of researchers at New Zealand’s Malaghan Institute of Medical Research are investigating whether they can use the body’s own natural immune response to develop individualised treatments that target the particular type of melanoma a person has. This takes the form of a vaccine that helps increase the immune system’s ability to fight the cancer cells.

    There is a big difference between the planned melanoma vaccine and a traditional vaccine. A traditional vaccine protects a person from getting a particular disease (e.g. if they get infected by a particular virus. Thanks to the vaccine, the immune system already has the instructions it needs to build the antibodies needed to disable the infectious agent (e.g. the virus).

    How the vaccine will work

    The melanoma vaccine doesn’t provide protection prior to exposure but will sensitise the immune system to the tumour so that an immune response is initiated. The vaccine will be made from dendritic cells obtained from the patient’s blood and peptides common to melanomas. The mixture is kept in the lab for a short time, allowing the dendritic cells time to ‘recognise’ the tumour peptides. Once injected back into the patient, the immune system receives an alert. The vaccine also contains an immune-boosting adjuvant to maximise T-cell (a type of white blood cell) activation.

    In 2013, the Malaghan Institute conducted their own clinical trials to test their vaccines ability to induce effective anti-tumor immune responses in patients. In 2017, the data gathered from those trials is still being analysed and a larger Phase II trial is also underway. The Phase II trial will examine the quality and size of the generated immune responses in cancer patients.

    Activity ideas

    In this activity, students examine the lifestyle factors that contribute to skin cancer and prepare information about skin cancer for a child or teenage audience.

    In this activity, students define 4 key cancer terms. The aim is to produce accurate definitions identifiable by their peers.

    Useful link

    The Malaghan Institute have more than 90 researchers and support staff working in their core programmes – cancer, asthma and allergy, arthritis, multiple sclerosis and infectious diseases.

      Published 15 November 2007, Updated 29 March 2017 Referencing Hub articles
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