Keratinocyte Cancer Flashcards
What are actinic (solar) keratoses?
-Focal areas of dysplasia characterised by erythema and scale that may feel rough when the fingers are rubbed over them
=Smaller and focal
-Marker of UVR exposure occurring at those sites that have received the most cumulative sun exposure, such as the scalps of bald-headed men, the backs of the hands and the nose and ears (just as for SCCs).
=As with most skin cancers, they are most common in those with sun sensitive skin who have had the most UVR exposure
How are actinic keratoses pre-malignant?
-Precursors of squamous cell carcinoma in that a very small proportion of AK progress to squamous cell carcinoma.
-AKs vary in size from 1mm to over 1cm in diameter.
-They are frequently multiple with some patients having 20 lesions or more
Consideration for management of actinic keratoses
-Cosmetic?
-Progression to SCC: Some AKs may progress to SCC and we have little explicit criteria to decide on which ones will regress or fail to progress. Perhaps larger ones are more likely to progress.
-Diagnostic error: You cannot always clinically be certain that a larger AK is not a SCC.
Management of pre-malignant lesions
-Cryotherapy or curette and cautery may suffice, excision may be warranted in some instances
What is intraepithelial carcinoma (Bowen’s disease)?
-Clone of cells is confined to the epidermis and has not breached the basement membrane.
-By contrast with actinic keratoses, in Bowen’s disease / IEC the dysplasia involves the full thickness of the epidermis.
=Further along the pathway of carcinogenesis than an AK.
=Plaque like and larger
-IEC is the result of sun exposure and therefore follows the usual risk factors. However some cases of IEC may be the result of other carcinogenic agents such as arsenic.
How is Bowen’ disease pre-malignant?
-Precursor of squamous cell carcinoma and the rate of progression to squamous cell carcinoma (~10%?) is higher than for actinic keratoses.
-Histopathological confirmation of the diagnosis may be required with an incisional biopsy to assay for any invasion (and hence the presence of an SCC).
-All surgical samples of presumed Bowen’s disease must be sent for histopathological examination.
Clinical features of keratoacanthomas
-Involute and disappear without any treatment.
-Short rapid growth and volcano morphology
-Do not metastasise.
-When they do disappear they tend to leave an unsightly scar.
-Are not premalignant.
-Less common than SCC but more common in usual skin cancer risk group (sun sensitive skin and high UVR exposure)
What are basal cell carcinomas?
-Keratinocyte tumours whose cells histologically resemble the morphology of basal cells
-Malignant epithelial cells that invade through the basement membrane and can destroy underlying structures such as the eye, cranium or nose.
-They can even track along nerves into the brain.
Epidemiology of BCC
-Commonest skin cancer and the commonest cancer (of any type) in most European countries (higher in Australia)
-UVR related= most common in those with sun sensitive skin, who have received the most UVR exposure/ intermittently exposed skin
-Median age of cases is 67, and the sex incidence is equal.
-BCC incidence increases with age
-More common in immunosuppressed (especially organ transplantation)
Clinical features of BCC
-Translucent quality (blue arrow in the images below), and often translucent papules (‘pearly papules’) surround an ulcerated crater/ crust
-Telangiectasis may be prominent.
-Pigmented BCC= grey/brown/firm/ hard=like bone
-Most found on the middle third of the face, but perhaps 30% occur on other sun exposed sites too such as the scalp, back, legs and arms. Very rarely they occur on sun protected sites such as the genitalia
-Typical BCC measures less than 1 cm across but some are much larger (>5cm)
-Appear over a matter of months or over many years growing only very slowly.
Types of BCC
-Nodular
=Classic, well-defined tumour margins, excised using surgery
-Superficial
=more common on back and limbs, no significant induration, largely macular, cryotherapy and chemotherapeutic agents
-Morphoeic
=larger than first appear, Moh’s surgery (also for facial), aggressive and recurrence
Micramod= boost immune system
Overall treatment of BCC
-Confirmatory histopathology is required in virtually all cases
-BCC cannot always be reliably distinguished from a number of related tumours (especially benign appendageal tumours).
-Excision with a 4mm margin.
-Cryotherapy, radiotherapy and topical chemotherapeutic agents
Inherited syndromes in BCC
-Gorlin’s syndrome/ Basal Cell Nevus Syndrome
=autosomal dominant
=mutation in the patched (PTCH ) gene that plays a key role in epidermal physiology.
-Clinically these patients present with a large numbers of BCCs at a young age and show small pit-like abnormalities on their palms as as well a variety of extracutaneous abnormalities and dysmorphic facies
-There may not be any family history as new mutations are common and expressivity varies.
-The first ‘hit’ is inherited and the second is the result of UVR.
What are squamous cell carcinomas?
-Keratinocytes derived tumours
-Capable of metastasis so higher mortality
-They are harder to diagnose than BCCs
-Appear on histological grounds to be more differentiated than basal cells
Clinical features of SCC
-Keratinising nodule that may be ulcerated or show excess ‘keratin’ formation: “ugly” and “untidy” looking - often with a ‘yuck’ factor.
=nodules, and vary in size from ~5mm up to 3 or 4cm or greater.
=Some poorly differentiated SCCs appear to have lost their ‘keratinising’ appearance and resemble a piece of raw steak or jam on the skin’s surface.
-Surrounding skin may show many features of photodamage including dermal atrophy, and increased variation in pigmentation and of the skin vasculature.
-Distribution mirrors cumulative UVR exposure: rates are highest on bald headed men, the tops of the ears, faces and backs of the hands.
