The Melanoma Story: What Am I?

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 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

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

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.
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 the 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.

Show References


  • Melanoma risk factors, Melanoma Institute Australia, viewed 12 May 2016, https://www.melanoma.org.au/
  • Beer, TW 2014, Common sense pathology: Sampling suspicious pigmented lesions, viewed 4 February 2016, https://www.rcpa.edu.au/get…spx
  • 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
  • Carrera, C, Puig-Butillè, JA, Aguilera, P, Ogbah, Z, Palou, J, Lecha, M, Malvehy, J, Puig, S 2013, ‘Impact of sunscreens on preventing UVR-induced effects in nevi,’ In vivo study comparing protection using a physical barrier vs sunscreen’, JAMA Dermatology, vol 149, no 7, pp. 803-813, viewed 30 October 2015 http://archderm.jamanetwork.com/a…10
  • Cichorek, M, Wachulska, M, Stasiewicz, A & Tymińska, A 2013, Skin melanocytes: biology and development, Advances in Dermatology and Allergology, pp. 30–41, viewed 10 March 2016, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834696/
  • Duman N, Erkin G, Gököz Ö, Karahan S, Kayıkçıoğlu AU, Çelik, İ 2015, Nevus-Associated versus de novo Melanoma: Do They Have Different Characteristics and Prognoses? Dermatopathology; vol 2, pp. 46-51, viewed 19 January 2016, https://www.karger.com/Article/FullText/375490#
  • Green, AC, Williams, GM, Logan, V & Strutton, GM 2011, Reduced melanoma after regular sunscreen use: Randomized trial follow-up., viewed 12 May 2016 http://jco.ascopubs.org/content/29/3/257.full.pdf+html
  • Green, AC, Wallingford, SC, & McBride, P 2011, ‘Childhood exposure to ultraviolet radiation and harmful skin effects: Epidemiological evidence,’ Progress in biophysics and molecular biology, pp. 349–355, viewed 27 March 2016, http://doi.org/10.1016/j.pbiomolbio.2011.08.010
  • LeLeux, TM 2015, Pathology of benign melanocytic nevi, viewed 4 February 2016, http://emedicine.medscape.com/articl…wall
  • Macdonald JB, Dueck AC, Gray RJ, Wasif N, Swanson DL, Sekulic A, Pockaj, BA 2011, Malignant melanoma in the elderly: Different regional disease and poorer prognosis, pp. 538-543, viewed 27 March 2016, http://www.jcancer.org/v02p0538.htm
  • Noonan, FP, Zaidi, MR, Wolnicka-Glubisz, A, Anver, MR, Bahn, J, Wielgus, A, Cadet, J, Douki5, T, Mouret, S, Tucker, MA, Popratiloff, A, Merlino, G & De Fabo, EC 2012, Melanoma induction by ultraviolet A but not ultraviolet B radiation requires melanin pigment, Nature Communications, http://www.nature.com/ncomms/journ…s1893.pdf
  • Pearson, G, Robinson, F, Gibson, Tb, Xu, BE, Karandikar, M, Berman, K & Cobb, MH 2001, Mitogen-activated protein (MAP) kinase pathways: Regulation and physiological functions, Endocrine Reviews, vol 22, no 2, pp. 153–183, viewed 23 November 2015,
  • Thompson, JF, Scolyer, RA, Kefford, RF 2012, Melanoma. A management guide for GPs, pp. 470-473, viewed 20 January 2016 http://www.racgp.org.au/afp/2012/july/melanoma-guide/
  • Zhao, C, Snellman, E, Jansen, CT & Hemminki, K 2002, ‘Ultraviolet photoproduct levels in melanocytic nevi and surrounding epidermis in human skin in situ,’ Journal of investigative dermatology 118, pp. 180–184, viewed 12 May 2016 http://www.nature.com/jid/journal/v118/n1/full/5601376a.html

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