Skin Cancers
Dr Tim Bracey
SpR Histopathology
Derriford Hospital
Learning Objectives
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Normal structure and function of the
skin
Premalignant Epidermal Disease
Squamous Cell Carcinoma (SCC)
Basal Cell Carcinoma (BCC)
Melanoma and other melanocytic
lesions
Functions of the Skin
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SKIN IS THE LARGEST ORGAN IN
BODY!
Protection:
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Thermoregulation:
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Insulation- hair & fat; Heat loss via sweat glands
Metabolic functions:
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UV-light, micro-organisms, mechanical, chemical
& thermal insults
Vitamin D synthesis
Sensation:
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Largest sensory organ in the body with receptors
for touch, pressure, pain and temperature.
Normal Skin
Normal Skin
Understand the terminology
commonly used in reporting skin
cancers
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Solar elastosis
Acanthosis
Dysplasia
Hyperkeratosis
Parakeratosis
Solar Elastosis
The accumulation
of abnormal
elastic fibres in
the dermis in
response to longterm sun
exposure
(Sometimes called
“Actinic
Damage”)
Acanthosis
Increased thickness of
the spinous layer of
the epidermis. This
is usually associated
with enlargement
and down growth of
the rete pegs
Basically “hyperplasia”
Mild Dysplasia
Severe Dysplasia
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Can still call this “actinic keratosis” in presence of
sun-damage but more correctly called “in situ SCC”
Solar (actinic) Keratosis
Circumscribed, scaly lesions on sun exposed
skin
( Head &Neck area, Hands)
! May resolve or remain unchanged for years
! 10-20% Gradually Transform to cancer if left
untreated
! Pathology
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Dysplasia of epidermis
Hyperkeratosis and Parakeratosis
Dermal chronic Inflammation
Solar Damage
Solar (actinic) Keratosis
Solar (Actinic) Keratosis
Squamous Cell Carcinoma
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Arises from Dysplasia
Invasion: Breach of Basement
Membrane
Second most common Skin cancer in
Caucasians
Clinically:
Shallow ulcers with a keratinous crust in
back ground of actinic damage
! Sometimes as a nodular tumour
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Squamous cell carcinoma
SCC - Invasion
SCC - Invasion
SCC - Grading
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Grading
Well Differentiated
! Moderately Differentiate
! Poorly Differentiated
! Undifferentiated
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Officially: Amount of Keratin
Production
Reality : Also on Cytological Atypia
SCC – Moderately
Differentiated
SCC – Poorly Differentiated
SCC Complications
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Recurrence
Aggressive histology (poorly
differentiated)
! Thickness of tumour
! Narrow Surgical Margins
! Perineural invasion
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Metastases (lymph nodes, lungs)
Location – ear and lip worse than other
sun-exposed areas
! Scar cancers highest risk of metastasis
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SCC in chronic leg ulcer
Basal Cell Carcinoma
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Most common Skin Cancer in
Caucasians (Ratio of BCC: SCC = 5:1)
Rare in Black skinned individuals
Cause
Sun Exposure
! Rarely: Scars: Burns, Radiation,
Vaccination
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Basal Cell Carcinoma
BCC - Histology
BCC - Pathology
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No “in-situ” precursor lesion
Background of Solar Damage
Epidermal attachment in majority of
cases
Nests and islands of basaloid cells
Peripheral pallisading
Numerous Mitoses and Apoptotic
bodies
Typical stroma with chronic
inflammation
BCC - Morphology
BCC can mimic other benign
and malignant lesions
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Due to diverse morphology
Cystic Change
! Calcification
! Pigmentation
! Ossification (Bone formation)
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BCC – Cystic Change
BCC - Calcification
BCC - Pigmentation
BCC - Complications
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Recurrence
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Depends on excision margins
! “Adequately” excised
– 1.2%
! Within 1mm from margin – 12%
! At margin – 33%
Common in lesions on nose & nasolabial
fold
! Multifocal Subtypes
! Residual BCC only found in 60% of reexcisions
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Superficial multifocal BCC
Superficial multifocal BCC
Morpheaform BCC
BCC Invading Into Bone
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BCC almost never metastasizes!
BCC – complications 1
BCC – complications 2
Standard pathology vs Mohs
Nearest peripheral and deep
margin assessed in each section
Melanocytic Skin Lesions
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Lesions with increased basal melanin
pigment (epulis “freckle”)
Lesions with basal melanocyte
proliferation (“lentigo”)
Melanocytic naevi
Malignant melanoma
Epulis
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Most common
pigmented lesion
1 – 10 mm
Tan-red macules
Appear early in
childhood after sun
exposure
Epulis
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Increased melanin
pigment in basal
keratinocytes
No increase in the
number of
melanocytes
Simple Lentigo
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Brown macule
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Found anywhere on
the body
Simple Lentigo
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Variable basal hyperpigmentation
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Increased number of
single melanocytes in
the basal layer.
Solar Lentigo
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Dark –brown macules
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Develop on sun
exposed skin
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Middle aged to
elderly individuals
Solar Lentigo
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Sun damaged skin
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Club-like elongation
of the rete ridges
May become into
seborrhoeic keratoses
(debatable)
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Melanocytic Naevi
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Junctional naevus
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Compound naevus
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Intra-dermal naevus
Junctional naevus
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Well-circumscribed
brown to black
macule
Appears during early
childhood or
adolescence
Anywhere on the
body
Junctional Naevus
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Discrete nests of
melanocytes at
dermal-epidermal
junction.
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Matures into
compound naevus
and later into
intradermal naevus.
Compound naevus
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Both junctional nests
and intra-dermal
nests.
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Dermal component
may show
‘maturation’
Intra-dermal Naevus
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Naevus cells confined
to dermis.
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In deeper parts of the
naevus the cells may
assume a ‘neuroid’
appearance.
Dysplastic Naevus
Malignant Melanoma
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Lentigo Malignant Melanoma (5 – 15 %)
Acral Lentiginous Melanoma (5-10%)
Superficial Spreading Melanoma(50-70%)
Nodular Melanoma(15-35%)
Desmoplastic Melanoma (rare)
Miscellaneous (rare)
Lentigo Malignant Melanoma
Acral Lentiginous Melanoma
Superficial Spreading
Melanoma
Nodular Melanoma
Risk Factors for Melanoma
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Skin & Hair colour
Numerous freckles
Tendency to burn / tan poorly
Presence of numerous / atypical naevi
Severe / blistering sunburn
Tanning salons
Genetic factors (CDKN2A & CDK4)
Immunosuppression.
Prognostic Factors In
Melanoma
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Adverse
Increased Breslow Thickness
! Ulceration
! Satellite deposits
! Vascular Invasion
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Conflicting Reports
Histological subtype
! Clark level
! Co-existing naevus
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ABCDE of melanoma
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Asymmetry
Border
Colour variegation
Diameter
Enlarging
Erythema
Elevation
Ulceration
Conclusion and learning
points
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BCC, SCC and melanoma are all common!
All can cause significant morbidity and
mortality
Skin cancers can be cured when identified
and treated in early stages
Learn to recognise the common subtypes!