Emily's Melanoma
Risk calculator

Risk calculator for health professionals

Terms and conditions

To use this melanoma risk calculator you must agree with the following terms and conditions of use.

The calculator is not intended to be used as a substitute for an independent health professional's advice.
Please read the disclaimer for more information.

Emily's risk assessment tool aims to give an estimation of an individual's risk of developing melanoma over a 5 year period.

This model does not predict mortality or the risk of spread of melanoma once diagnosed.

The model is designed for use by doctors in the clinical setting to assist in the communication of risk to their patients. It is highly recommended that you discuss your personal risk factors and results of your risk assessment with your doctor.

Australian immigrants may be at lower risk of melanoma compared to individuals born in Australia. Melanoma risk is very low for Indigenous and darker skinned Australians. Our tool provides a crude guide only for such individuals.

During the development of this model, we have highlighted shortfalls in our current understanding of some risk factors, namely past history of melanoma, risk for number of family members affected, and number of non-melanoma skin cancers. This tool may be updated as new information becomes available.

For information on risk factors not currently included in this risk model, please click here.

This model needs to be validated in order to find values that define risk groups appropriately in the Australian setting.

Personal details

Melanoma incidence rates increase with age in both sexes, with a sharper rise in incidence rates observed in males over 60. The overall increase in incidence of melanoma is almost entirely attributable to rising incidence in people over 60 years. Melanoma is rare under 15 years of age.

In Australia, melanoma is the most common cancer among those aged 15-59.

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Melanoma incidence in males
Melanoma incidence in females

Australia and New Zealand have the highest rates of melanoma in the world. In Australia, 1 in 14 males and 1 in 22 females will develop invasive melanoma in their lifetime (to age 85).

Melanoma is now the third most common malignancy in Australia for both sexes, behind colorectal, breast and prostate cancer. Incidence is rising steadily at 3-4% per year1. The rise in incidence is much steeper in men than women.

Melanoma is most commonly found on the trunk in males and limbs in females. Prognosis is a little better in women.

Mortality is rising in men over 60 years but stable in women1.


Map of Australia showing zones of differing risk

In Australia, incidence of melanoma increases with proximity to the equator.

Latitude of residence correlates well with UV exposure even though it does not account for individual behaviours or migration from areas of different UV indices. The effect of latitude is greatest on skin areas intermittently exposed to the sun.

For the purposes of this risk model, Australia has been divided into 3 zones based on latitudes of the eastern states.

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Melanoma incidence in males
Melanoma incidence in females

Data taken from Victorian, NSW and Queensland Cancer Registries.

Naevi (moles)

Common naevi are well defined, raised or macular and are usually pigmented. The majority appear after birth and prevalence varies with age. Numbers increase during childhood and slow in early adulthood. Melanocyte number and function declines from middle age, resulting in fewer common naevi. Counts may therefore be less predictive in the elderly.

Naevus counts are primarily genetically determined, though UV exposure plays a role in initiating naevus development and growth. Naevi counts tend to be higher on arms and legs of females, and backs for males. This is consistent with the distribution of melanoma in males and females.

Naevus count on the arms (from elbow to shoulder, not forearm) correlates well with total number of naevi and is simpler to assess that total body count.

A widely accepted definition of clinically atypical naevi requires a macular component in at least one area, and at least three of:

  • border not well defined,
  • size 5mm or more,
  • colour variegated,
  • uneven contour,
  • erythema.

The presence of clinically atypical naevi is more strongly correlated with risk for melanoma than common naevi4.

It is important to note that, whilst atypical naevi are a significant risk factor, the majority of melanomas (43 - 77%) arise de novo and dysplastic naevi do not warrant prophylactic excision.


Freckles are areas of increased melanin pigmentation. They are more common in children and those with red hair, and fair skin. This model uses freckles in adulthood as a risk factor (RR=2.05)6. Childhood studies report higher relative risks.

Freckles reflect melanocyte overactivity as a result of UV exposure. They fade in the winter months. They must be distinguished from solar lentigines which persist indefinitely and result from a severe sunburn or chronic solar damage. Freckle density is greater with proximity to the equator, hence there is a correlation with latitude6.

Melanoma risk increases with freckle density, usually assessed on the shoulders and upper back. This risk is independent of the risk associated with naevi, phenotype and phototype.

Hair colour was selected for this risk model as an easily assessed phenotypic characteristic. Red hair has also been shown to be the phenotypic trait best representing the presence of MC1R variants, a known genetic marker of melanoma risk5.

This is most accurately assessed by considering hair colour at age 20. Redheads are at greatest risk with almost three times the risk of darker haired people. Blond or fair haired people have 1.5 times the risk6.

Personal history

The risk of developing a second melanoma is in the order of 0.5% per year (or 4.5% risk over 10 years)12. Risk for a further melanoma increases progressively with increasing numbers of primary melanomas. Following 2 primary melanomas the risk for a third is of the order of 3% per year.

The risk of a second melanoma is higher in males over 70. Incidence of second primaries also peaks around the ages of 25-34, which may reflect the association with cases of familial melanoma. Those diagnosed with their first melanoma before age 45 have about twice the risk of a second primary as the older group. It has been reported that 10.5% people with multiple melanoma have a positive family history.

From the few studies available, it is difficult to assess the extent to which past history acts as an independent risk factor. There is evidence that it is a strong risk factor and we felt it was important to include it in this model. In the context of the other six predictors, however, its effect may be over-stated. While this impacts on absolute risk prediction it has little or no bearing on the model's ability to discriminate between individuals of high and low risk.

Basal cell carcinomas are the most common malignancy in white populations. Both basal cell and squamous cell carcinomas are important risk factors for melanoma. They share common risk factors with melanoma, specifically sun exposure and phenotype. A shared pathway of induction is likely. UV radiation causes DNA damage and mutations in tumor suppressor and proto-oncogenes responsible for unrestricted cell turnover.

Family history

Family history is a complex risk factor for melanoma. It is difficult to tease out the proportion of risk that can be attributed to susceptibility genes versus pigmentary characteristics (also genetically determined) and environmental factors. Despite this, studies consistently show that melanoma in a first degree relative (parent, sibling, child) increases risk of melanoma approximately 2 fold6.

Melanoma risk increases with increasing numbers of affected family members. Individuals with known mutations that predispose to melanoma make up a small proportion (around 2%) of individuals with a positive family history.

There are two main tumour suppressor genes linked with susceptibility to melanoma. Mutations in CDKN2A may be found in 25 to 40% of members of melanoma-prone families, with CDK4 mutations much less common. An Australian study found mutations in CDKN2A in 10.3% of a high risk population, and estimated that only 0.2% of melanomas in Australia were due to CDKN2A mutations8. The likelihood of finding a mutation in CDKN2A rises from about 5% in families with 2 affected members, to 20-40% if 3 or more family members are affected9. Furthermore, residence in areas with high rates of melanoma significantly increases the penetrance (ie. probability of developing melanoma amongst mutation carriers).


Reference: 1
Australian Institute of Health and Welfare. Melanoma Incidence and Mortality. In; Cancer in Australia: an overview, 2006 [WWW document]. URL www.aihw.gov.au/publications/index.cfm/title/10476 [Accessed on 17 December 2008].
Reference: 4
Gandini S, Sera F, Cattaruzza MS et al. Meta-analysis of risk factors for cutaneous melanoma: I. Common and atypical naevi. Eur J Cancer 2005; 41: 28-44.
Reference: 5
Palmer JS, Duffy DL, Box NF et al. Melanocortin-1 receptor polymorphisms and risk of melanoma: is the association explained solely by pigmentation phenotype? Am J Hum Genet 2000; 66: 176-86.
Reference: 6
Gandini S, Sera F, Cattaruzza MS et al. Meta-analysis of risk factors for cutaneous melanoma: III. Family history, actinic damage and phenotypic factors. Eur J Cancer 2005; 41: 2040-59.
Reference: 8
Aitken JF, Duffy DL, Green A et al. Heterogeneity of melanoma risk in families of melanoma patients. Am J Epidemiol 1994; 140: 961-73.
Reference: 9
Kefford RF, Newton-Bishop J, Bergman W, Tucker MA, Counselling and DNA testing for individuals perceived to be genetically predisposed to melanoma: A concensus statement of the Melanoma Genetics Consortium. Journal of Clinical Oncology 1999 Oct; 17(10): 3245-51
Reference: 12
Second Primary Cancers in Victoria. Cancer Council of Victoria Epidemiology Centre 2009. www.cancervic.org.au/about-our-research/cancer-statistics/second-primary-cancers-victoria