Basal cell carcinoma (BCC) is the commonest human malignancy in Caucasians, it is
less common in those with pigmented skin. The incidence varies from over 1500 in
100 000 in Queensland, Australia, to 200–300 per 100 000 in the United Kingdom, and
2–3 per 100 000 in Hong Kong Chinese. There is a male predominance, but the incidence
in females is increasing.
The tumour arises in hair-bearing skin, particularly on the face where sun exposure
is the highest; over three-quarters arise on the face, one-quarter on the nose. The
lesion is generally slow-growing, but is locally destructive, hence the common name of
‘rodent ulcer’.
Despite their name, BCCs probably do not arise from the basal cells of the epidermis
but from the pluripotential cells in the epidermis; this is supported by the occasional
observation of appendigeal differentiation in these tumours. The typical
features are raised pearly edges and telangiectasia (small blood vessels) with or
without a central ulcer. Histologically, there are undifferentiated cells in nodules with
peripheral palisading (‘picket fence pattern’).
There are a number of morphological subtypes of BCC:
• Nodular—less than 5% of BCCs in Caucasians are pigmented (can look very
similar to malignant melanoma), but pigmented carcinomas are more common
in darker-skinned races. (Three-quarters of BCCs in Chinese patients are
pigmented)
• Superficial—commoner on the trunk. Multiple lesions in a patient should raise the
possibility of arsenic poisoning as a cause
• Morpheaform/sclerosing—often a scar-like lesion with ill-defined margins
• Infiltrative.
The latter two subtypes are more aggressive in behaviour. The overall
rate of metastasis is extremely low but there have been several reports in the
literature.
Sun exposure (ultraviolet B)—the strongest association is repeated sunburn
in childhood with a lag time of 20–50 years; the field effect is demonstrated
by the almost 50% risk of developing a further BCC in the subsequent 5
years. Psoralen ultraviolet A (PUVA) treatment for psoriasis is another risk
factor.
Other risk factors include:
• immunosuppression
• exposure to carcinogens such as hydrocarbons/arsenic (occupational, medicinal
or environmental—contaminated water supplies are often implicated)
• irradiation
• genetic conditions such as xeroderma pigmentosa or syndromes such as
Gorlin’s syndrome. It has a multitude of alternative names, including BCC
syndrome which is inherited in an autosomal dominant manner. Patients
have a predisposition to developing carcinomas from puberty onward,
particularly BCCs. Other associated feature include jaw cysts, bifid ribs, pits
in the palms and soles, prominent brow with hypertelorism, partial agenesis
of the corpus callosum with learning difficulties.
• pre-existing sebaceous naevus.
less common in those with pigmented skin. The incidence varies from over 1500 in
100 000 in Queensland, Australia, to 200–300 per 100 000 in the United Kingdom, and
2–3 per 100 000 in Hong Kong Chinese. There is a male predominance, but the incidence
in females is increasing.
The tumour arises in hair-bearing skin, particularly on the face where sun exposure
is the highest; over three-quarters arise on the face, one-quarter on the nose. The
lesion is generally slow-growing, but is locally destructive, hence the common name of
‘rodent ulcer’.
Despite their name, BCCs probably do not arise from the basal cells of the epidermis
but from the pluripotential cells in the epidermis; this is supported by the occasional
observation of appendigeal differentiation in these tumours. The typical
features are raised pearly edges and telangiectasia (small blood vessels) with or
without a central ulcer. Histologically, there are undifferentiated cells in nodules with
peripheral palisading (‘picket fence pattern’).
There are a number of morphological subtypes of BCC:
• Nodular—less than 5% of BCCs in Caucasians are pigmented (can look very
similar to malignant melanoma), but pigmented carcinomas are more common
in darker-skinned races. (Three-quarters of BCCs in Chinese patients are
pigmented)
• Superficial—commoner on the trunk. Multiple lesions in a patient should raise the
possibility of arsenic poisoning as a cause
• Morpheaform/sclerosing—often a scar-like lesion with ill-defined margins
• Infiltrative.
The latter two subtypes are more aggressive in behaviour. The overall
rate of metastasis is extremely low but there have been several reports in the
literature.
Sun exposure (ultraviolet B)—the strongest association is repeated sunburn
in childhood with a lag time of 20–50 years; the field effect is demonstrated
by the almost 50% risk of developing a further BCC in the subsequent 5
years. Psoralen ultraviolet A (PUVA) treatment for psoriasis is another risk
factor.
Other risk factors include:
• immunosuppression
• exposure to carcinogens such as hydrocarbons/arsenic (occupational, medicinal
or environmental—contaminated water supplies are often implicated)
• irradiation
• genetic conditions such as xeroderma pigmentosa or syndromes such as
Gorlin’s syndrome. It has a multitude of alternative names, including BCC
syndrome which is inherited in an autosomal dominant manner. Patients
have a predisposition to developing carcinomas from puberty onward,
particularly BCCs. Other associated feature include jaw cysts, bifid ribs, pits
in the palms and soles, prominent brow with hypertelorism, partial agenesis
of the corpus callosum with learning difficulties.
• pre-existing sebaceous naevus.
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