logo Nonmelanoma skin cancer

Skin lesions

Nonmelanoma skin cancer

Objectives

  • Recognise solar keratoses, in situ and invasive squamous cell carcinoma and basal cell carcinoma from their clinical appearance and behaviour.
  • Describe how these lesions are removed.

Key points

  • Solar keratoses are found on sun-exposed sites (mainly face, ears and hands).
  • Solar keratoses have a hard scaly surface and no induration.
  • In situ squamous cell carcinoma (Bowen’s disease) presents as one or more slowly enlarging erythematous scaly plaques.
  • Keratoacanthoma is a rapidly growing dome-shaped nodule with a keratinous core.
  • Invasive squamous cell carcinoma (SCC) generally arises within a solar keratosis or within in situ SCC.
  • Invasive SCC presents as an irregular keratinous nodule or a firm erythematous nodule and frequently ulcerates.
  • Nodular basal cell carcinoma (BCC) is a slowly growing pearly nodule that may ulcerate.
  • Superficial BCC presents as one or more slowly growing erythematous shiny plaques, which may be scaly. Superficial BCC may be difficult to distinguish from in situ SCC.
  • Solar keratoses are predominantly treated by cryotherapy, but specialists may treat diffuse lesions with 5-fluorouracil cream or imiquimod cream.
  • In situ squamous cell carcinoma and superficial basal cell carcinoma may be treated surgically but dermatologists may instead use cryotherapy, 5-fluorouracil cream, imiquimod cream or photodynamic therapy.
  • Invasive squamous cell carcinoma and nodular basal cell carcinoma are nearly always treated surgically. Some tumours are treated by radiotherapy.

Introduction

About 45,000 new cases of non-melanoma skin cancer are estimated to occur in New Zealand each year – by far the most common of all cancers. There were 63 deaths in 1996.

Common non-melanocytic skin cancers are described on DermNet.

Keratinocytic tumours

Histology

The histological characteristics of keratinocytic tumours are illustrated below.

Solar keratosis
Hyperkeratosis (thick stratum corneum)
Parakeratosis (retention of cell nuclei in stratum corneum)
Atypical keratinocytes
Inflammatory infiltrate
Solar elastosis (blue-stained dermis)

Bowen’s disease (in situ SCC)
Hyperkeratosis
Parakeratosis
Atypical keratinocytes throughout epidermis
Inflammatory infiltrate

SCC
Invasion of dermis by atypical keratinocytes
Squamous eddies
Inflammatory infiltrate

SCC Close-up
Atypical keratinocytes (pleomorphic hyperchromatic cells)

BCC
Thinned or ulcerated epidermis
Basaloid tumour cells budding from epidermis or follicles

BCC Close-up
Peripheral palisading of nuclei
Mucinous stroma

Factors that predispose to skin cancer

Ultraviolet radiation is the main environmental hazard. Direct damage to DNA and immune suppression contribute to a high risk of skin cancer in outdoor workers, particularly in shorter latitudes.

Human papillomavirus appears to promote skin cancers in immune suppressed patients but probably is not responsible for the majority of skin cancers in the non-immune suppressed population. Other factors responsible for occasional cases of skin cancer include exposure to arsenic, tar, radiation, chronic inflammation (lupus erythematosus, lichen planus etc) and thermal burns.

Some populations are at significantly greater risk of developing non-melanocytic skin cancers.

Genetic factors include:

Immunosuppression results in a greater number of cancers and more aggressive tumours, especially in organ transplant patients.

Other malignant tumours of the skin and its appendages are much less common. They include eccrine, apocrine and hair follicle tumours, vascular tumours (Kaposi’s and angiosarcoma), the neuroendocrine tumour Merkel cell carcinoma and fibrous histiocytoma. Immune cell proliferative diseases include histiocytosis X and cutaneous T-cell lymphoma.