Squamous cell carcinoma (SCC), the second most common non-melanoma skin cancer (NMSC), has several features distinguishing it from basal cell carcinoma (BCC). Awareness of these differences can assist with timely referral and treatment, thereby reducing morbidity associated with aggressive tumours and enhancing overall patient outcomes. Therefore, all healthcare professionals should be able to identify lesions and refer appropriately.
SCC is caused by a range of factors, including:
- Direct ultraviolet (UV) exposure to skin (typical sites include: dorsum of hands, ears, bald scalp, and lower lip)
- Reduced immune function (e.g. SCCs typically outnumber BCCs in transplant patients due to decreased immune function)
- Exposure to ionising radiation or chemical carcinogens
- Human papilloma virus (HPV) infection
- Individual response to chronic inflammation (such as a burn site)
- Genetic susceptibility or defective genetic repair mechanisms
- Individuals with a fair complexion have an increased vulnerability.
There are a number of things to look for when identifying potential SCCs. Surface changes may include:
- Shallow ulcer, raised edges
- Cutaneous horn
- A symptomatic lesion; developing pain rather than itch in an existing lesion alerts the clinician to possible tumour progression
- Persistent lesion over an extended time, e.g. under a nail or genital.
Dysplasia is the abnormal growth of a pre-existing lesion, from which SCCs can develop. Initially, dysplastic keratinocytes above the epidermal basal layer behave abnormally resulting in a focally thickened stratum corneum (SC); i.e. an actinic keratoses (AK).
If the atypical keratinocytes demonstrate advancing dysplasia and dysfunction that fully infiltrates the epidermis, this becomes SCC in situ, Bowen’s disease or intra epidermal carcinoma. Specific histological definition can highlight the lesion’s level of abnormality. Well differentiated SCC’s most closely resemble normal tissue and are more predictable in behaviour than moderately well or poorly differentiated – the most unpredictable tumours with poorer outcomes. These less dysplastic, well differentiated lesions retain some normal tissue function and can produce keratin, which may appear initially as a cutaneous horn (spiky, hard and often painful to the touch.)
Diagnosis and Treatment
Careful diagnosis of lesions thick or larger than 2cm, previously treated (recurrent), or biopsy results showing suspected perineural invasion, will dictate appropriate therapy. It’s important to note that tumour sites around the ear or cheek, cases of immunosuppression and other high risk tumours displaying increased risk of metastasis and local tissue involvement, can cause death. Metastatic disease can also result from poorly treated, advanced or neglected tumours.
Treatment of SCCs aims to completely remove the tumour in order to avoid recurrent disease or metastasis. The appropriate mode of treatment is determined by biopsy. Depending on patient characteristics, low risk tumours (e.g. well defined, well differentiated, small, thin and well sited) can be treated with destructive modalities like curettage, cautery or topical creams. High risk tumours require complete excision. Challenging sites, thick, invasive lesions and lymph node involvement requires referral for comprehensive management.
In summary, it is imperative that nurses working in all health settings have up-to-date knowledge of tumour types, in particular squamous cell carcinomas.
- Munroe, MM 2015, Cutaneous Squamous Cell Carcinoma, viewed 15 November 2015, http://emedicine.medscape.com/article/1965430-overview#showall
- Ratushny, V, Gober, MD, Hick, R, Ridky, TW, Seykora, JT 2012, ‘Keratinocyte to cancer: the pathogenesis and modelling of cutaneous squamous cell carcinoma’, The Journal of Clinical Investigation, vol. 122, no. 2, pp. 464–72, viewed 15 November 2015 http://doi.org/10.1172/JCI57415
- Veness, MJ 2007, ‘High-Risk Cutaneous Squamous Cell Carcinoma of the Head and Neck’, Journal of Biomedicine and Biotechnology, 80572, viewed 8 December 2015, http://doi.org/10.1155/2007/80572
- Weedon, D ed. 2010, Weedon’s Skin Pathology, 3rd edn, Churchill Livingstone Elsevier online, (no city name disclosed), pp. 682-90.