2nd most common skin malignancy. Age
Peak incidence 40-80 years.
Increasing in young due to childhood sun over-exposure. Sex
M>F; occupational. Geography
Risk Factors Environmental:
Exposure to UVB is central.
- more exposure = more SCC
Carcinogens (cigarette smoke, pesticides, radiation).
Fair hair, fair skin, blue eyes.
Precursors: SCCs arise in an area that have had premalignant change.
- precursors are solar (actinic) keratosis, Bowen's disease (in situ
SCC); see below. - may occur in scars (Marjolin's Ulcer; see below).
Past hx of skin cancers.
HPV for mucocutaneous surfaces.
Xeroderma pigmentosum, albinism.
Immunosuppression after kidney transplants may lead to multiple /
confluent SCCs (perhaps virally-related): - associated drugs: prednisone, cyclosporine, eosothyoprin
Other acquire cell-mediated immune deficiencies:
- lymphomas, leukemias, autoimmune diseases.
Aka senile / solar keratoses.
Arise from sun damaged skin.
- mostly elderly men who ignore them.
- often on hands / face and helix of ears.
- 6-10% lifetime SCC risk
- watch for any change in size or appearance.
Areas of epidermal dysplasia usually on sun-exposed fair skin.
Give rise to painless cutaneous scaling.
- raised plaque of skin with keritonous layer.
- should be confined to skin; if tethered suspect invasive SCC
- local lymph should not be enlarged.
Must rule out SCC
Remove then with liquid nitrogen / diathermy preceded by curettage
(more scarring with diathermy).
- multiple lesions treated with 5FU cream; not radiotherapy.
- further sun protection essential.
Similar in appearance to SCC
But rapid growth for 1-2m then involution for 1-2 months
Treated by excision biopsy
- must rule out SCC
Intraepidermal SCC (SCC in situ)
Premalignant (3-5% transform)
Frequent in elderly.
Persistent, progressive, usually flat, scale / crusted plaque.
- often flat pink papular pactures covered in crusts.
- often mistaken for eczema
- when crusts removed, oozy bloody papilliferous surface.
Rule out invasion.
If diagnosis uncertain, biopsy & lack of response to steroid may
Excision is best
- recurrence if not taken deep enough or skin appendage structures
- radiotherapy has to be full tumour doses.
- chemo with 5FU may be effective if very large or field change.
- cryotherapy / curettage & cautery often undertaken instead.
SCC arising in a longstanding ulcer or scar.
- commonest in a venous ulcer or a burns scar.
Similar to other SCC, but not usually so florid.
Edge not always raised; may be subtle & masked.
View unusual nodules / changes in a chronic lesion with suspicion
- particularly if enlarging / discharging foul matter.
Lymph is usually involved late as local drainage damaged in scar.
Invade locally but rarely metastasise
More commonly on palm and soles - 'carcinoma ciniculatum'.
Pathogenesis Role of UV radiation UVB thought to cause
i) Direct carcinogenesis
- keratinocytes in the basilar layer affected.
- tumor promotion & growth result from unrepaired mutations.
ii) Depression of cutaneous
- inhibition of tumor rejection.
- p53 tumor suppressor genes mutated in >90% of SCCs.
Routinely begin as solar keratoses (see below)
- best differentiated by feeling the lesion; base has concerning
thickness to palpation
- appear on chronically sun-damaged skin.
- 80% arise on arms, head and neck.
When develops a plaque-like thickening, termed Bowen's disease (see
Later invades epidermis, dermis and adjacent tissues.
- overall conversion rate low, ie ~1/1000 lesions/year.
Histology shows invasive nests of cells.
- spread in all directions.
- clusters of cells show concentric rings of flattened squamous
- often called 'epithelial pearls'.
Variable central keratinisation.
Horn cell formation.
No peripheral palisading as for BCC.
Cells vary from large, well differentiated cells to anaplastic cells.
3-10% metastasise (when not treated).
- ie rare unless lesions are large and neglected
- very rare for tumours less than 0.5cm.
- lip / ear lesions metastasise earlier, even when well
First spreads to regional lymph nodes.
- nb these may be enlarged simply due to associated infection
And then may spread systemically.
Once SCC has metastasised to nodes the 5 year survival is 35%.
- but rare to die of SCC (~1/500).
Similar risk factors to BCC
- tumor size (>2cm face; >1cm head/neck; >0.6cm other)
- depth of invasion
- perineural invasion
- immune status of pt
- borders poorly defined
- earlier recurrence
- pst radioRx / inflammation
- rapid growth
- mod-poor differentiation.
Initially an area of crusting
- usually hyperkeratotic
- may be clinically indistinguishable from solar keratoses.
Progress to form a palpable scaly nodule or plaque - irregular in
May ulcerate centrally with a pink rolled edge.
Spreads as above.
They appear more inflammatory, feel more indurated and ulcerate
sooner than BCC.
One key to diagnosis is surface keratin.
Initially indistinguishable from solar keratosis.
Other Differential Diagnoses Keratoacanthoma
Overgrowth of hair follicle cells
- produce a central plug of keratin.
Rapidly growing, often for 6-8 wks
- are benign
lesions that regress spontaneously over months when the plug
- may leave a small scar.
Can look very similar to SCCs.
- conical 'volcanic' appearance.
- have an irregular crater centre and keratotic plug
- undamaged surrounding skin helps make distinction possible.
- usually solitary, on face or hands
- rubbery feel, with hard central core.
- necrotic centre may be brown or black.
Excision to confirm.
Either surgery or radiotherapy.
Limit UV exposure.
Precancerous lesions in high risk pts (e.g. AKs) should be
- shave excision or topical therapies (cryotherapy, photodynamic
therapy, topical 5FU)
- lesions resistant to nonsurgical therapy should undergo excision
If the frequency and severity of skin tumours becomes life
theratening, reduction of immunosuppresion meds must be considered
in some transplant pts.
Surgical vs 'Field
Field treatments work on a generalized area, but don't define
Consider carefully in terms of lesion, patient and risk factors for
Surgical excision preferable for most. Surgical
Cure rate ~90% at 5y.
Re-excision for +ve margins.
Margins As per BCC
Low risk = 4-6mm
High risk = 10mm
- primary risk factors are site and size
- Ie trunk / extremities >2cm, head/neck >1cm, eyes ears, nose
mouth, hands feed >6mm
- immunocompromised, radiotherapy,
- poorly differentiated, adenoid, adenosquamous or desmoplastic
Moh's micrographic surgery
99.5% cure rate
Serial transverse slices under frozen section until clearly free of
- recommended for lesions of high-risk of recurrence in
anatomic areas where preservation of tissue important (eye, nasal
ala, mouth, ear).
Nodes palpable Need FNA
Note negative FNA with suspicion does not rule out metastatic spread
--> repeat FNA or proceed to open biopsy.
Technical Notes Mark edges to include appropriate oncologic margin.
Excision line injected with local + adrenaline
Excise before planning closure
Orient specimen for histologic margins
Incise down to deep fascia, beveling blade to prevent undermining.
Atraumatic handling with toothed forceps.
Reconstruction and closure Small defects closed with ellipse.
- Avoid long ellipses as enlarge the scar, which will need total
reexcision if margins +ve
Fashion along skin tension lines
Deep dermis closure with buried 3-0 vicryl
Then epidermis with prolene 5-0 to 6-0, removed at 5-7d
Chronic steroids or wound beds irradiated --> epidermal suture
closure with 10-14d tensile strength.
Small low risk lesions closed at excision
High-risk lesions with dubious margins:
- secondary intention, primary closure or skin graftin.
Local flap closures when margins are in question is contraindicated.
Avoid wide undermining unless known that tumour margins negative
Definitive reconstruction when histopath is back.
- most can be closed with V-Y closure, rotation flap, transposition
flaps, or advancement flaps.
- larger defects with pedicled flaps, or free-flaps.
- pectoralis myocutaneous flap commonly used in head and neck but
not well suitable to defects superior to the mandible.
Free tissue transfer recommended in radiotherapy fields, when
separating skin from saliva or CSF covering vital structures.
- allow to mature for 3m before considering reexcision
- if crosses tension lines, can contract and be unacceptable.
- Z-plasty can align the scar
- patients with keloid should be aggressively managed with silicone
dressings and steroid injections; performed at initial resection and
Alternatives to Excision
1. Electrodissection and curretage
- low risk lesions / multiple lesions
- tension on the underlying dermal sling; sequentially smaller
curettes followed by cautery
- low risk BCCs / superficial BCCs and AKs
- respond to topical 5FU cream, b.d. for 4-8 weeks
- also used in Bowen's disease though not well established evidence
- inflammatory reaction with burning, redness oozing
- 5% imiquimod; apoptosis promoter for low-risk lesions' 1cm margin
for 8h (overnight) 5x per week for 6-12w
--> cure in 80% superficial BCC and 66% nodular BCCs
--> brisker skin reactions.
Oral retinoids effective as well.
4. Radiation therapy
Primarily or post-operatively for very high risk lesions
Suitable for pts >50y who want to avoid surgery (deformity, or
Outcomes below surgery (local control 80-90%)
- and recurrences are aggressive.
Primay radiotherpya produces local tissue effects; dermatitis and
- can be more severe skin breakdown
Adjuct for inovlved margins where further excision has unacceptable
Cryotherapy, electrodesiccation, 5FU
Usually for small lesions (2-5mm)
Local control >90% for cryotherapy.
- heal slowly and leave a pale scar.
Highly effective for BCC and SCC
- also useful for difficult areas / skin at high risk of recurrence.
Adjunct to lymph node dissection for metastatic disease
- recommended for multiple lymph node involvement OR extra-capsular
Generally reserved for elderly pts unsuitable for surgery / certain
FAQs Do I need to conduct routine follow-up
No, unless they have Gorlin's syndrome.
exposure UVB is
thought to be responsible via a direct mutagenic effect on
keratinocytes in the basilar layer of the epidermis depression
the intensity and duration of immunosuppression is associated
with disease. Immunosuppressive
leukemia, lymphoma and auto-immune disease. HPV is causative factor
acral and peri-ungual regions
sunlight induced damage
inability to repair DNA damage
partial or complete deficiency of melanin production
keratosis with small oozing ulcer
Widely ulcerated with raised indurated
Tend to be poorly diff.
of squamous cells invading BM of dermis
nucleus, eosinophilic cytoplasm
pearls of central keratin surrounded by prickle cells
Can be mistaken
genitalia and occasionally skin
Invade deeply and
Can progress to
high grade SCC after XRT
T3 >5 or
deep dermal invasion
of other extra-dermal structures (skeletal muscle, bone, tendon)
movable contralateral or bilateral
of lymph node
metastasis depends on site of origin
Sundamaged skin 3%
Ear lips forehead
common on non-exposed skin than BCC
biopsy is important before
treatment of any skin cancer.
Most non-melanoma skin cancers are small low
that respond with a 90-95% success rate to standard treatment.
with margins clear of carcinoma typically
5-10mm of normal appearing
skin for low risk SCC (the evidence regarding the adequacy of
margins is less
clear than melanoma).
Can be used for 1° treatment
Avoid pinna (radionecrosis) and scalp
Cosmetic results good to excellent
especially for preserving large
areas of skin in head and neck region.
small amount of
hypopigmentation or telangiectasia in the treatment
Recurrence after surgery
where re-excision is not
basal cell nevus
may induce more tumors in Rx
Adjuvant XRT to primary site and draining
lymph nodes may also be used
when many high risk factors (see Mohs) are present, or there is
Mohs may reduce recurrence
rate when there are risk
factors for subclinical invasion and recurrence.
oTumour is on the
hand/foot, genitals, in front or
behind ear, temple, mandible or chin, lip, nose, peri-orbital
region or central
face and >6mm
oCheek, forehead, scalp or
neck and >10mm
oTrunk or extremity and
oClark level V or >4mm
oAssociated with scars or
Can be used for well defined in situ
abnormal cold tolerance
only for treatment of lesions on hands and
sclerosing basal cell
nasi, nasolabial fold,
upper lip vermillion border
especially around the periorbital region,
temple, and forehead
Treated tumors usually exude necrotic
material, after which an eschar
forms and persists
for about 4 weeks
Permanent pigment loss at the treatment
site is unavoidable
Atrophy and hypertrophic scarring have
been reported, as well as
instances of motor and
Can be used for Rx of in-situ lesions and
small superficial lesions
Excision and block dissection
burns and irradiated skin aggressive and frequently metastasise