Melanocytes are cells that produce pigment to help protect the skin from ultraviolet (UV) radiation or sunlight. These cells can collect together in the skin to form a mole.
Melanomas are formed when the melanocytes in a mole begin to grow and divide in an uncontrolled and unregulated way. The cells expand outwards or down into the lower layers of the skin where it grows very quickly if left untreated.
Who is at risk?
There are many risk factors that increase the chances of melanoma, including people with fair skin, a high mole count, family history and a pattern of sunburns throughout life, especially during childhood. However, melanoma can be effectively treated if detected early.
Over the past five years new treatments have emerged for people with advanced melanoma. Centenary is focused on better understanding the resistance of certain melanoma to new treatments.
What are the symptoms?
The most common symptoms of melanoma are:
- a new spot on the skin, or a spot that is changing in size, shape or colour
- moles that have features of the ABCDE rule: asymmetry, border irregularity, colour, diameter and evolving
- a sore that does not heal
- itching, scaling, bleeding, oozing, swelling or pain in a mole
- spread of pigment from a spot into the surrounding skin
Please consult with your doctor if you have any concerns about melanoma.
How is it treated?
Melanoma has many treatment options available depending on the stage of the disease.
Stage 1 and 2: The most common treatment for early stage or localised melanoma is surgery, and in the majority of cases, this is the only treatment required.
Stage 3 and 4: More advanced cases of melanoma where the cancer has spread to other parts of the body may require treatments such as chemotherapy, radiotherapy, immunotherapy or targeted molecular therapy.
What is Immunotherapy?
Immunotherapy works by modifying the actions of the immune system to attack the cancer cells. These therapies modulate various components of the immune system.
Checkpoint inhibitors are an immunotherapy which works with the body’s immune system to treat cancer. They work by blocking a pathway that allows tumours to remain hidden from the immune system. This helps to increase the ability of the body’s immune system to detect and fight tumour cells. There are a number of different checkpoint inhibitors used to treat melanoma.
What is Targeted Therapy?
Melanoma is one of the cancers with the highest frequency of genetic mutations. Mutated melanoma cells are targets for this kinds of therapy.
Made up of drugs or other substances targeted therapy blocks the growth and spread of cancer by interfering with specific molecules. It differs from standard chemotherapy because it is designed to act on specific molecular targets and attack cancer cells without harming healthy cells.
This is done by targeting some key differences between cancer cells and other cells. These targets may be genes, so the treatment aims to ‘switch off’ genes that tell cancer cells to grow or to ‘switch on’ genes that tell cancer cells to die. Other targeted therapies deliver substances directly to proteins in the cancer cell to destroy them or prevent growth.
How we are working to improve treatments
Our research looks at improving the effectiveness of treatments for advanced cases of melanoma.
Immunotherapy: Developing a molecular understanding of why up to 50% of melanoma patients do not respond to immunotherapy
Targeted therapy: Looking at new treatments opportunities to improve outcomes for patients who develop resistance to medicines
Clincial trials
Please consult with your cancer specialist for the best treatment options based on the stage of your melanoma has progressed together with other factors such as your age and general health.
Australian Cancer Trials is a free information service that shows you the latest clinical trials in cancer care, including trials that are currently recruiting participants. Australian Cancer Trials aims to help you and your cancer specialist make decisions about your cancer care options, including clinical trials.