Non melanocytic skin tumors
Ref: grabb & smith
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Language: en
Added: Aug 22, 2024
Slides: 63 pages
Slide Content
Non-melanoma skin
cancers
Dr. Sidra memon
PG trainee
Plastic surgery
Definition:
•Non-melanoma skin cancers also
known as keratinocyte carcinomas.
•Are cancers of epithelial layer
(epidermis)
•More common than melanoma
•Incidence:
NMSCs before 40 years of age are
relatively rare.
•BCC most common NMSC.
Basal cell carcinoma:
•Most common skin cancer
•Accounts for 80% of all skin cancers
•Malignant tumor arising from basal layer of
epithelium or from the external root sheath of
the hair follicle.
•Greatest concentration in areas that have the
highest concentration of pilosebaceous units.
•Does not possess cellular aplasia (required for a
true carcinoma & almost never metastasizes)
•Differs from squamous cell carcinoma in that it
does not arise from malignant changes occurring
in pre-existing mature epithelial structures.
PATHOGENESIS:
•Constitutive activation of sonic hedgehog
pathway plays a role in pathogenesis.
Risk factors:
•Exposure to UV radiation & sensitivity of an
individual’s skin to it.
•Light complexion (substantial exposure to
sunlight)/ Fitzpatrick skin types I & II.
•Males
•Family hx
•Smoking
•Human papilloma virus
•Exposure to arsenic & hydrocarbons
•Immunodeficiency (transplant recipients)
•Previous radiation.
•Syndromes association: (bazex synd; gorlin
synd/basal cell nevus synd; xeroderma
pigmentosum)
Bazex syndrome:
Diagnosis of NBCCS is made by having
2 major criteria
or
1 major
and
2
minor criteria.
The
major criteria
consist of the following:
1.more than 2 BCCs or 1 BCC in a person younger than 20
years;
2.odontogenic keratocysts
of the jaw
3.3 or more palmar or plantar pits
4.ectopic calcification
or early (<20 years) calcification of the
falx cerebri
5.bifid, fused, or splayed ribs
6.first-degree relative with NBCCS.
The
minor criteria
include the following:
1.macrocephaly.
2.congenital malformations, such as
cleft lip or palate, frontal bossing,
eye anomaly (cataract,
coloboma, microphtalmia, nystagmus).
3.other skeletal abnormalities, such as
Sprengel deformity,
pectus deformity, polydactyly,
syndactyly
or
hypertelorism.
4.radiologic abnormalities, such as bridging of the
sella turcica,
vertebral anomalies, modeling defects or flame-shaped lucencies of
hands and feet.
5.ovarian
and cardio fibroma or medulloblastoma (the latter is
generally found in children below the age of two).
Gorlin-goltz syndrome / nevoid basal cell
carcinoma syndrome (NBCCS)
Xeroderma pigmentosum:
•Severe sunburn when exposed to only small
amounts of sunlight. These often occur
during a child's first exposure to sunlight.
•Development of many freckles at an early
age
•Rough-surfaced growths (solar keratoses),
and skin cancers
•Eyes that are painfully sensitive to the sun
and may easily become irritated, bloodshot
and clouded
•Blistering or freckling on minimum sun
exposure
•Telangiectasia (spider veins)
•Limited growth of hair on chest and legs
•Scaly skin
•Xeroderma (dry skin)
•Irregular dark spots on the skin
•Corneal ulcerations
Types:
•Tumor type is a key prognostic factor &
guides selection of an appropriate treatment
modality.
1.NODULAR BCC:
most common type
Presents as dome shaped, nodular
papule, pearly surface, scattered
telangiectasias & rolled borders.
enlarges & ulcerates centrally, giving it
classic rodent ulcer appearance.
2.CYSTIC BCC:
variant of nodular BCC.
characterized by cystic mucin filled central
core.
2.PIGMENTED BCC:
characterized by brown or black macules.
D/D: seborrheic keratosis, nodular malignant
melanoma.
3. SUPERFICIAL BCC:
2
nd
most common type.
appears as a demarcated multicentric
erythematous patch.
mostly occur on trunk & extremities.
P
surface is often scaly & ulcerated.
D/D: cutaneous fungal infection, actinic
keratosis, discoid eczema, psoriasis.
5.MORPHEAFORM / SCLEROSING:
most aggressive type.
usually found on head & neck.
difficult to diagnose & manage due to its
insidious onset & infiltrative growth
characteristics.
appears as a poorly defined, flat, indurated
plaque that appears as a scar.
histologically it exhibits thin linear extensions up
to the dermis, so making surgical resection
difficult & recurrence frequent.
Investigations:
•Biopsy definitively establish the
diagnosis & histologic subtype.
•Other workup usually not required as
the risk of metastasis is only <0.05%
•Overall cure rate is >90%
•Recurrence is frequent.
2.Surgical excision:
both low risk & high risk tumors.
Low risk tumors:
simple excisional biopsy can be performed.
clear margin
for tumor size <1cm margin 4-5mm
for tumor size >1cm margin 5-10mm
High risk tumors: (esp.: on face)
Moh’s micrographic surgery is the most definitive treatment
modality for high risk BCC of anatomically complex areas of face.
tumor is serially excised & margins of resection are histologically
examined by moh’s surgeon.
presence of tumor at margin is
noted & further excision of
affected areas is serially
performed & examined until
the margins are clear.
moh’s surgery cure rate in
primary tumor is >98% &
Squamous cell carcinoma:
Epidemiology:
•2
nd
most common skin cancer.
•Accounting for 15-20% of all skin cancers in
U.S.A.
Risk factors:
1.Environmental risk factors:
•Chronic cumulative sun exposure
(both UVA & UVB are implicated in tumor
pathogenesis)
•Mutation in p53 tumor suppressor gene.
•Exposure to hydrocarbons & arsenic.
•Hx of radiation.
•Chronic inflammation (marjolin’s ulcer)
•Chronic immunosuppression.
2.Host risk factors:
•Old age.
•Fitzpatrick skin types I & II.
•Fair hair.
• past Hx of NMSC.
•Infection with HPV.
•Genetic disorders:
(xeroderma pigmentosum,
epidermolysis bullosa, albinism)
Premalignant lesions leading
to CSCC:
•Mostly arise in sun-exposed skin
of head & neck, dorsum of
hands, lower arms & legs.
•SCC can arise from pre existing
premalignant lesions
actinic keratosis
cutaneous horn.
Bowen's disease
Erythroplasia of Qyerat.
Leukoplakia.
Keratocanthoma.
1.Actinic keratosis:
•80% of SCC arise from pre existing actinic
keratosis.
•Presents as a erythematous, rough, scaly
plaque.
•Features associated with malignant
transformation include:
a)Rapid growth.
b)Size >1cm.
c)Ulceration
d)Bleeding
e)Inflammation.
f)Erythema.
2. Cutaneous horn:
•Variant of actinic keratosis.
•Presents as a hyperkeratotic
protuberance shaped like a
cone extending above the
plane of skin.
•Approx.: 15 % of cutaneous
horns contain SCC, so
excision is indicated.
3. Bowen’s disease:
•Cutaneous SCC in situ.
•Presents as a slow growing,
erythematous, scaly patch.
•Diagnosed in older patients
(>60yrs)
•Can occur anywhere in body
including mucosa.
4. Erythroplasia of queyrat:
•cSCC in situ on glans of penis
or labia majora.
•Mostly occur in uncircumcised
man, possibly due to chronic
irritation, infection with HPV &
immunosuppression.
•Presents as a velvety red
plaque.
5. Leukoplakia:
•CSCC in situ on oral or genital mucosa.
•Presents as adherent, white patches.
•Must be differentiated from other
causes of leukoplakia such as chronic
irritation (smoking), candidal infection &
infection with HPV.
•SCC develops in 10-20% of all pt:s with
leukoplakia.
6. Keratoacanthoma:
•Is a rapidly growing nodule
(weeks to months) with a central
ulceration or keratin plug.
•If untreated it may
spontaneously involute.
•It is considered to be a low
grade variant of CSCC, but it is
clinically difficult it from high
grade invasive CSCC, therefore
surgical excision is
recommended.
(note: shave biopsies are not
helpful)
Invasive CSCC:
•It penetrates the basement membrane to reach the
dermis.
•Either arises de novo or associated with actinic
keratosis.
•SCC associated with actinic keratosis has a low
metastatic rate & favorable prognosis.
•De novo invasive SCC occur in immunocompromised
hosts or in areas of chronic irritation (e.g. burns) & is a
high risk variant with a high metastatic rate of up to
14%.
•Well differentiated lesions are firm, raised, pink or
fresh colored papules with frequent keratinization,
scaling, ulceration or crusting on the surface.
•Poorly differentiated lesions are soft, granulomatous
nodules with areas of haemorrhage, necrosis,
ulceration & lacking in keratinization.
Diagnosis:
•Tissue biopsy definitive diagnosis.
•If there are palpable lymph nodes on
examination than fine needle aspiration
should be done.
•Imaging studies usually not
indicated, but should be done in pt:s with
regional lymphadenopathy.
Staging:
•AJCC has introduced a new TNM
classification of CSCC.
•It also comprises high risk features of
tumor.
1.Tumor specific features:
Lesion located on ears, lips, in chronic
wounds or scars.
Horizontal size >2cm.
Depth >6mm.
Poorly differentiated.
Perineural invasion.
Rapidly growing.
Recurrent.
2. Patient specific features:
Immunosuppression as in organ
transplant.
Chronic lymphocytic leukemia.
Small lymphocytic lymphoma.
Epidermolysis bullosa.
HIV/AIDS.
Staging:
Management:
•Treatment options for CSCC are similar to
those of BCC.
1.Direct surgical excision:
Used for both low risk & high risk lesions.
Surgical margin of resection to achieve
histologically negative margins are:
For low risk tumors 4mm
For high risk tumors 6 to 10mm (1cm)
•Moh’s micrographic surgery:
Is the treatment of choice for
lesions in anatomically complex
areas of face or for high risk
tumors.
•Sentinel lymph node biopsy can be done to diagnose
subclinical lymph nodes, metastasis & stage high risk tumors.
•There is no role for adjuvant
therapy in patients who are at risk
for recurrence.
•Systemic chemotherapy is used for
patients with distant metastasis or
advanced local disease not
amenable to surgery or other
treatment modalities.