Skin cancers can be divided into two broad groups :
- Non-melanoma skin cancers (NMSC) – All skin cancers that are not melanomas fall into this group.
These two groups develop from completely different cell lines and tend to behave very differently.
The common types of skin cancer are :
- Basal cell carcinoma (rodent ulcer, BCC)
- Squamous cell carcinoma (SCC)
The main risk factor for developing all of these three types of skin cancer is sun exposure. Tanning beds also increase the risk of skin cancer. BCC and SCC are dose related and risk increases with increased cumulative sun exposure over time. Genetic predisposition also plays a role (If two people have the same amount of sun exposure, one may develop cancers and the other may not).
Melanoma can be traced back to one blistering sunburn in childhood and has a stronger genetic link.
Sun exposed areas are at higher risk for developing skin cancers, especially NMSC. Sometimes; however, cancers develop in non sun exposed areas. The best explanation that we can offer is that diseases don’t read the textbooks!
There are other rarer types of NMSC. Some of these are very aggressive and can be life threatening, while others are far more indolent and less concerning.
Before addressing skin cancers per se, it is important to briefly discuss pre-cancerous skin lesions. Most BCCs and SCCs develop from these.
Precancerous skin lesions
- Actinic keratoses:
These are surface areas of sundamage. If left untreated a percentage of them (10 – 30%) will develop into invasive skin cancers. AKs can be treated with freezing, scraping, topical ointments (Efudix or Aldara) or photodynamic therapy (extensive areas).
- Hypertrophic actinic keratoses
These are common on the scalp, hands and feet. They are raised, thick horn-like plaques, representing areas of advanced actinic keratoses. It can be impossible to distinguish hypertrophic actinic keratoses from SCCs clinically. Because ot their hard, crusted properties, freezing is not usually effective in treating them. Best treated by shave biopsy or excision and suturing.
Bowenoid actinic keratoses:
This is actualy SCC-in-situ, which means very early SCC that is confined to the epidermis (outer layer of the skin only). They usually respond to topical treatment with Efudix (Fluorouracil) or Aldara (Imiquimod), or to curettage and cautery (scraping out and burning the base). In some cases they need to be formally excised and the resultant defect sutured closed.
- Basal cell carcinoma:
The commonest skin cancer that we see, and the best type to have. Although BCC can be very destructive locally if left untreated, it is extremely unusual for it to metastasize to other organs. The best option for definitive treatment is usually surgical excision and repair (There may be exceptions to this). Curettage and cautery, Aldara ointment for superficial BCC and radiotherapy may also be used in certain circumstances.
Large BCCs and BCCs in cosmetically sensitive areas are best treated with surgical excision and intraoperative pathological assessment of the margins to ensure that the cancer has been completely excised before complex reconstruction is performed. This can either involve having a specialist pathologist present in theatre to check the specimen as it is cut out, or a specially trained surgeon/dermatologist can check the specimen themselves (MOHs micrographic surgery). Intraoperative pathologic assessment allows for just enough tissue to be excised to get surgical margins that are clear of cancer.
Squamous cell carcinoma:
Squamous cell carcinoma is the second commonest skin cancer that we see. Although it has a higher incidence of metastasis to other organs than BCC, the incidence is still very low. Intraoral SCCs are far more aggressive and should be treated urgently by a specialst unit. Treatment of SCCs is almost identical to BCCs.
Sometimes BCCs and SCCS grow around nerves. They can spread very rapidly along the nerve sheaths, and it is a concerning feature. Extensive perineural invasion by these cancers is often treated with radiotherapy once the tumour has been excised. This significantly reduces the incidence of further spread and recurrence.
Melanoma is usually more of a concern than BCCs and SCCs. It usually presents as a pigmented skin lesion (flat or raised). Some melanomas have a typical presentation with irregular borders and an irregular pigment pattern with colour variation. These are easy to diagnose clinically. In many cases; unfortunately, melanomas do not present with typical features. They may look completely benign, or may mimic other skin tumours (typically BCCs or benign seborrheic keratoses). Occasionally they present without pigment at all. These atypical presentations are; unfortunately, often not diagnosed until they are in the late stages.
- Melanoma screening:
People with a family history of melanoma, previous melanoma, or lots of moles should be assessed at regular intervals by a dermatologist. Mole mapping is a very useful tool that allows the dermatologist to store images of suspicious moles. These can then be compared with images taken at follow up visits. Any change in mole appearance suggests the need for excision of that mole.
Patients who have had a melanoma-in-situ excised should be seen by their dermatologist every 6 – 12 months for at least 2 years, and then at least once yearly after that.
Patients who have had an invasive melanoma excised should be seen by their dermatogist 3 – 6 times monthly for at least 2 years, and then at least once yearly after that.
- Melanoma-in-situ (MIS):
This is melanoma that is confined to the epidermis of the skin. It is very early (Stage 0) and does not metastasise to other organs. If left untreated it may develop into invasive melanoma. Melanoma-in-situ is treated by surgical excision with clinical margins of 5 mm. (The surgeon measures 5 mm around the edges of the melanoma-in-situ, so the diameter of the final defect is 10 mm plus the diameter of the melanoma-in-situ eg. A MIS with a diameter of 7 mm will have a 17 mm resultant defect diameter – 5mm + 7mm + 5mm).
- Treatment of invasive melanoma:
Invasive melanoma is best diagnosed by excision of the entire suspicious lesion. In certain cases it is not practical to excise the entire suspicious lesion. In these cases an incision biopsy of a section of the lesion can be done. The pathologist will make the diagnosis and give the depth of the melanoma. This is called the Breslow depth. Further treatment is related to the Breslow depth. The diameter of the melanoma has no impact on treatment per se. Treatment is primarily surgical, but depending on the Breslow depth, your surgeon may refer you to an oncologist postoperatively, either for further treatment, or just for further investigations.
- Breslow depth less than 1 mm :
Excise with 1 cm margins and down to the next fascial layer.
- Breslow depth 1 – 2 mm :
Excise with 1 – 2 cm margins and down to the next fascial layer.
- Breslow depth > 2 mm :
Excise with 2 cm margins and down to the next fascial layer.
- Sentinel lymph node biopsy:
For melanomas with a Breslow depth of greater than 0.8 – 1 mm a sentinel lymph node biopsy should be considered. This is done at the same time as excision of the melanoma.
Please see the seprate document called “Sentinel lymph node bioipsy” for an explanation of this procedure.
Repair of the defects after wide excision of a melanoma is either by:
- Direct advancement of skin flaps and closure as a straight line.
- Closure with a transposition skin flap, where skin is moved from adjacent areas, but still connected on one side to maintain blood supply.
- Skin graft.
- Combination of skin flap and skin graft.