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PH-SD17

Non-melanocytic skin tumours

How ultraviolet light mutates keratinocytes, how benign seborrhoeic keratosis differs from the dysplasia of actinic keratosis and Bowen disease, and why squamous cell carcinoma can spread to nodes while basal cell carcinoma destroys locally.

  • Free preview
  • 5 steps · 9 questions
  • 3D anatomy, affected parts marked

By the end, you can

  • Explain how ultraviolet light causes the characteristic mutations of skin cancer and why TP53-mutant clones expand.
  • Distinguish seborrhoeic keratosis, actinic keratosis and Bowen disease by their microscopic appearance and behaviour.
  • Describe the gross and microscopic appearance of cutaneous squamous cell carcinoma and basal cell carcinoma.
  • Explain how Hedgehog pathway activation drives basal cell carcinoma and why it rarely metastasises.
  • Explain what grade and stage measure in keratinocyte cancers, and outline Merkel cell carcinoma.

What it is

Non-melanocytic skin tumours arise from the epidermis and its appendages rather than from melanocytes. The large group are tumours of keratinocytes: benign (seborrhoeic keratosis), dysplastic precursors (actinic keratosis, squamous cell carcinoma in situ) and the two commonest human cancers, basal cell carcinoma and cutaneous squamous cell carcinoma, together called keratinocyte carcinomas. Rarer tumours include Merkel cell carcinoma and adnexal tumours.

4 types to tell apart
Benign keratinocyte tumours
Seborrhoeic keratosis: uniform basal-like cells with horn cysts, no atypia, not a precursor of carcinoma.
Squamous precursors
Actinic keratosis (atypia in the lower epidermis) and Bowen disease (squamous cell carcinoma in situ, atypia through the full thickness).
Keratinocyte carcinomas
Basal cell carcinoma (Hedgehog-driven, locally invasive, rarely metastasises) and cutaneous squamous cell carcinoma (can reach lymph nodes); keratoacanthoma is usually regarded as a variant of well-differentiated squamous cell carcinoma.
Merkel cell carcinoma
A rare, aggressive neuroendocrine carcinoma, mostly driven by Merkel cell polyomavirus, otherwise by ultraviolet damage.

US spelling: tumours → tumors, tumour → tumor.

Normal function

The epidermis: keratinocytes renewed from the basal layer

The epidermis is a keratinising stratified squamous epithelium made mostly of keratinocytes. Stem cells in the divide; their daughters rise through the , joined by desmosomes, and the , then die and flatten into the and are shed, a journey of about a month. Stem cells in the hair follicle can also renew the epidermis.

Among the basal cells sit melanocytes (their tumours have their own lesson) and Merkel cells, touch receptors with neuroendocrine granules. Below the basement membrane, the holds the capillaries and lymphatics an invasive tumour would need to reach.

Melanin over keratinocyte nuclei absorbs ultraviolet (UV) light, and badly damaged keratinocytes normally die by apoptosis under the control of p53. Skin cancers arise when this protection is overwhelmed over decades.

Point to it on the model