What am I?
I present in shades of pigment – from black, to skin-toned. My size ranges from millimetres to centimetres. Flat and masquerading as a freckle, or raised and mole-like, I may be completely symptomless. In Australia and New Zealand, I have the highest reported rates worldwide. I am the product of the uncontrolled growth of melanocytes.
I am a melanoma.
Melanoma may arise from pre-existing benign nevi (moles) and mostly develop as new lesions. Gene mutations, enabling benign nevi to form, are compounded by accumulated mutations, advancing melanoma development and invasion.
Though nevi do develop on sun-protected sites, there is a confirmed association between Ultra Violet Radiation (UVR) and melanocytic nevi development and behaviour. UVR often from intense intermittent exposure, initiates melanoma progression by effecting melanocyte size, number and activity. UVR induced DNA damage impairs signalling between keratinocytes and melanocytes and can lead to the formation of nevi formation that have a higher risk of acquiring further mutations and becoming melanoma.
Children at Risk of Melanoma
Children are vulnerable to UVR outdoor due to a combination of UV exposure patterns and young active melanocytes and melanocyte stem cells, positioned closer to the skin’s surface than in adults which are susceptible to DNA change.
- The largest increase in skin nevus numbers occurs before adolescence
- Chronic exposure triggers nevi development through to adulthood
- Intermittent exposure is significant in melanoma development, and adult exposure also contributes
Melanoma Risk Factors
Sources of melanoma risks arise from combined environmental, genetic and host factors, including:
- Fair complexion: skin, eyes and hair
- Nevus Count: a high number of moles or unusual moles
- Previous melanoma or skin cancer
- Sunburn: particularly blistering burns and especially in childhood and adolescence
- Ultra Violet Radiation exposure: occupational, activities/sport, tanning activities
- Family history: close family; parents, sibling, child
- Age/gender: males over 55 years; as we age our risk rises (Melanoma site presentations differ between genders)
There are several different melanoma subtypes, all with differing clinical presentation, pathological and disease characteristics and potential clinical outcomes.
This is due to the many genes and mutation types implicated in melanoma development and progression.
Diagnosis Recommendations and Treatment Options for Melanoma
Clinical examination, including dermoscopy (magnification with a light), enables vision of structure and pigmentation deep into the epidermis and upper dermis.
A partial biopsy is problematical as it may misrepresent the pathology of the entire lesion, leading to delayed or erroneous diagnosis. Excision biopsy with 2 mm margins is recommended whenever possible; Lesion thickness (Breslow thickness) determines wider excision margins.
Risk of metastatic disease rises as a tumour progresses from in-situ (above epidermal basal layer) to invasive (breaking through that layer), and Breslow thickness increases. This vertical measurement is the main prognostic indicator for primary melanoma. Other indicators include presence of ulceration (a bleeding or ulcerated lesion) and tumour mitosis rate, noted in the pathology report.
Whilst Sentinal Lymph Node biopsy identifies regional lymph node metastases, its value is prognostic, informing management decisions; the procedure does not influence long-term survival and is not considered routine care. Radioactive tracer, injected around the primary melanoma, locates regional lymph nodes. Identified nodes closest to the lesion are examined for metastatic cells.
Disease staging is important for treatment and management decisions. Advanced melanoma is an aggressive disease. Treatments beyond wide excision for early and local disease have delivered disappointing outcomes.
Now, therapies targeting inhibitors of mutations or enzymes that enable tumour growth, and immunotherapy that assists the patient’s immune response against a tumour, are able to arrest metastatic disease and improve overall survival.
With increasing knowledge, Melanoma is more understood as a condition with complex genetic associations. Ultra violet light is a prime trigger; nurses can raise the profile of skin care and sun avoidance on individuals, impacting directly on recognition of early lesions and reducing the UV exposure that drives a large percentage of these tumours.
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- Australian Cancer Network Melanoma Guidelines Revision Working Party 2008, Clinical practice guidelines for the management of melanoma in Australia and New Zealand, Cancer Council Australia and Australian Cancer Network, Sydney and New Zealand Guidelines Group, Wellington, viewed 27 March 2016 http://www.cancer.org.au/conten…ma.pdf
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Jan Riley RN, MNurs(NP) is a specialist dermatology nurse based in regional New South Wales, Australia. Her postgraduate studies include a Certificate in Dermatology Nursing (USA), Master of Nursing (NP) and Certificates in Dermoscopy and Skin Cancer Medicine. Driven by a passion for “all things skin”, Jan is a staunch and passionate mentor and advocate, who is always ready and willing to share knowledge and inspire nurses to understand skin’s impact on daily lives. Her active participation in a range of professional activities has greatly assisted to raise the profile of dermatology and skin disease in the community. Jan currently develops and presents skin education modules through a co-directed nurse education company (Dermatology Nurse Education Australia) for nurses across all areas of care delivery.