Skin malignancies

DR.C.SRINIVASAN
PROFESSOR
LAYERS OF SKIN

• EPIDERMIS
• DERMIS
 CLASSIFICATION OF SKIN TUMOURS
Benign Malignant
• Epidermal • Squamous cell
• Seborrhoeic keratosis. carcinoma.
• Trichilemmal tumour. • Basal cell carcinoma.
• Sebaceous adenoma. • Melanoma.
• Sebaceous epithelioma. • Malignant skin adnexal
• Hydrocystoma, tumour.
syringoma, spiradenoma • Secondaries in the skin.
Sister Joseph nodules
around umbilicus.
 EPITHELIOMA
• ORIGIN: Malignant tumour of the keratinizing cells of the
epidermis or its appendages.
• 2nd most common cancer of skin.
• Commom in males.
• It accounts for 90% of head and neck cancers and 20% of
skin cancers

COMMON SITES:
• Dorsum of hand, limbs, face and skin of abdominal wall.
• SCC can occur in lips, mouth, pharynx, oesophagus, anal
canal, glans penis, uterine cervix, urinary bladder,
metaplastic areas of respiratory epithelium
 PREMALIGNANT CONDITION OF SKIN
• Leukoplakia
• Bowen s disease
• Pagets disease
• Erythroplasia of queyrat
• Chronic scars
• Senile keratosis
• Solar keratosis
• Radiation dermatitis
• Xeroderma pigmentosum
• Lupus vulgaris
• Viral cause--- HPV 5 and 16
• Immunosuppression
 PREDISPOSING FACTORS OF SCC
Exposure to UV B rays causes SCC by
1. Direct carcinogenic effects on keratinocytes in
basal layer of the epidermis.
2. Depression of the cutaneous immune
surveillance response.
 Fair complexion: albinism
 Immunosupression: Patients with HIV/AIDS and
immunosuppressing drugs
• Smoking and alcohol

• Age : with increasing age

• Familial associated inherited conditions: xeroderma

pigmentosum.

• Occupational exposure : Arsenic exposure

• Long standing leg ulcers

• Viruses: HPV 5 and 16 is associated with genital and

cervical cancer.
• KANGRI CANCER: due to constant placing of
the hot charcoalpot over the abdominal wall
to control cold.. Seen in kashmir
• KANG CANCER: due to sleeping over oven bed
to control cold.. Common site buttock and
heel..
• CHIMNEY SWEEP CANCER: seen in scrotum
due to constant irritation by tar(hydrocarbons)
 MACROSCOPIC TYPES OF SCC
• Ulcerative
• Proliferative
• Ulceroproliferative
CLINICAL FEATURES
• An ulcerative or ulceroproliferative lesion.
• Raised and everted edge.
• Indurated base and edge.
• Copious bloody foul smelling discharge
 Spread of SCC
• Main spread is LYMPHATIC reaching the lymph node.
hard, nodular, initially mobile  eventually fixed to
underlying structures

• LOCAL SPREAD – subcutaneous tissue, tendons, muscles,

bones and vasculature.
Involvement of blood vessels cause thrombosis and
ischemia.
Subcutaneous spread may involve the nearby nerves
causing neuritis
• Blood spread: occurs very rarely.
 INVESTIGATION
• EDGE BIOPSY: the edge of
ulcer is growing part which
will show malignant cells.

MICROSCOPIC PATHOLOGY OF
SCC:
• EPITHELIAL or KERATIN
PEARLS – squamous cells
arranged in concentric
manner such as onion skin.
• Plasma cell infiltraion
• Positive for cytokeratin 1 and
10
BRODER’S CLASSIFICATION

• I: Well differentiated: 75% or more keratin

pearls
• II: Moderately differentiated: 50-75% keratin
pearls
• III: Poorly differentiated: 25-50% keratin pearls
• IV: Undifferentiated/anaplastic: <25% keratin
pearls. It is seen in 20% of SCCs
 Investigation
• FINE NEEDLE
ASPIRATION(FNA)
BIOPSY to determine if cancer
cells have spread to the
lymph nodes. 
• If distant spread of cancer is
suspected then imaging like
Chest X-ray, CT scan and MRI
scan can be done
 TREATMENT
 Depend on the site, size
and location of SCC lesion.
• SURGICAL

• NON-SURGICAL.
 Surgical treatment
SURGICAL EXCISION: WIDE LOCAL EXCISION
• For lesion less than 2cm diameter– 4mm
margin is adequate.
• For lesion more than 2cm –1cm margin is
recommended.
• If cancer is large, a Flap(free flap, island flap,
local flap) or Graft(SSG) may be needed to
cover the defect post-surgery.
• If lesion involving bones– Amputation
 MOHS (Microscopically Oriented Histographic
Surgery)

• for recurrent tumors

and primary lesions
which are ill-defined
and deep is
recommended
 CRYOTHERAPY
• liquid nitrogen to cool small
squamous cell carcinomas (SCCs) to
temperatures that can kill the cancer
cells
• Indication: In situ squamous cell
carcinomas and actinic keratoses
• Safe and low-cost procedure.
• 5 year survival rate for superficial
early stage SCC in situ can be as high
as 95%.
PHOTODYNAMIC THERAPY
• a photosensitizing drug,
light, and oxygen are
used to induce targeted
cell death of cancerous
or abnormal tissue.
• Indication : SCC in situ
and actinic keratosis
• SCC in situ and actinic
keratosis
 RADIATION THERAPY
Indication
• tumours are not adherent to deeper
planes or cartilage as SCC is
radiosensitive.
• Unfit patient
• Recurrence
• A dose of 6000 cGy units over 6
weeks; 200 units/day is used.

SIDE EFFECTS: localized redness,

erosions,alopecia, localized pain, skin
atrophy, pigmentation changes.
CHEMOTHERAPY
• Systemic chemotherapy will be used for
advance SCC that has spread to other organs.
 TOPICAL TREATMENT
• Topical imiquimod is an immune
modulator
INDICATION:
Gential warts, actinic keratosis,
Bowen disease and superficial
SCC.
• It should be applied 3 times per
week for 4-6 weeks.
SIDE EFFECTS : increased redness,
swelling, and erosions or
ulcerations.
 TOPICAL CHEMOTHERAPY
• Agents like 5-fluorouracil
• Used for the treatment of
actinic keratosis, SCC in situ
and superficial BCC.
• Applied daily for about a
month.
SIDE EFFECTS:
skin irritation and redness over
the application site.
 Prognostic factors
• Site of tumour: Ears and lips are having bad
prognosis. Extremities fare worse than the trunk.
• Depth of invasion: less than 2mm metastasis
unlikely. More than 6mm—15% will have
metastasis.
• Surface size --- Tumour size > 2 cm is worse
• Tumour border—illdefined border is worse
• Immunosuppression: bad prognosis
• Differentiation—poorly differentiated is worse
• Perineural involvement: worse prognosis
MARJOLIN’S ULCER – variant SCC

• It is a curable malignancy

• well-differentiated squamous cell carcinoma

• occurs in chronic scars like burn scar, scar of venous ulcer.

• It develops in a scar due to chronic irritation and there are no lymphatics in scar
tissue, it will not spread to lymph nodes.

• Once it reaches the normal skin it may behave like any other squamous cell
carcinoma, i.e. it will spread to lymph nodes.

Clinical Features:
• Indurated, painless, nontender, ulcer with raised and everted
edge.
MARJOLIN’S ULCER
Investigation : Biopsy from the edge confirms the
diagnosis.

Treatment
• Wide excision.
• In case of large ulcer: amputation is required.
• Radiotherapy should not be given as it may turn
into poorly differentiated squamous cell
carcinoma.
 VERRUCOUS CARCINOMA
• Dry, exophytic, warty growth.
• No lymph node spread.
• No blood spread.
• Surgery is the treatment—wide excision.
• No radiotherapy.

Examples:
Giant condyloma acuminatum (Buschke-
Lowenstein tumour, Verrucous carcinoma of
genitalia).
 BASAL CELL CARCINOMA
• Basal cell carcinoma is also called BCC,
BASALIOMA or RODENT ULCER.
• It is the commonest skin cancer.
• Origin: Malignant tumor of pluripotential
epithelial cell arising from basal epidermis and
hair follicle—affecting the pilosebaceous skin.
• It is low grade and locally invasive
• More common in white skinned peoples than
black
• Common in males and elderly.
 PREDISPOSING FACTORS
• UV light (most important)
• Arsenical compounds
• Coal tar
• Aromatic hydrocarbons
• Infrared rays
• Genetic skin cancer syndromes:
Basal cell naevus syndrome (Gorlin
syndrome) with BCC, medulloblastoma; bifid ribs.
 COMMON SITES
• Common site is face—
above the line drawn
between angle of mouth
and ear lobule (90%)—
ONGHREN’S LINE.
• It can occur in muco-
cutaneous junctions.
• It is called as tear cancer
because it is commonly
seen in area where tears
roll down.
• Medial canthus of the eye
• Lateral canthus of the eye
• Nasolabial fold
• Nose
• Eyelid
• Cheek
• Ear.
It can also occur in other sites like scalp, neck,
arms and hands.
• Locally malignant.
• It does not spread through
lymphatics nor through the
blood.
• But it erodes deeply into local
tissues including cartilages,
bones causing extensive local
destruction.
• Hence the name “RODENT
ULCER”.
 TYPES OF BASAL CELL CARCINOMA

MARCOSCOPIC
• Localized: Nodular, nodulocystic, cystic,
pigmented and nevoid.
• Generalized: Superficial (multifocal or
superficial spreading)
• Infiltrative (morpheic).

NODULOCYSTIC AND NODULOULCERATIVE is

the commonest form 70-90%
 CLINICOPATHOLOGICAL TYPES

• SUPERFI CIAL TYPE—small buds of tumour

masses.
• MORPHEIC TYPE—dense stroma with basal
cells and type IV collagen; spreads rapidly.
• Fibroepithelioma type-- Pinkus shows
elongated cords of basaloid cells with mesh
work.
 CLINICAL FEATURES
• Ulcer on the face which is non-
tender, dry, slowly growing,
non-mobile, with raised and
beaded edge with central scab,
often with central depression
or umbilication.
• No lymph node or blood
spread occurs.
• Local destruction by infiltration
is the hallmark.
• Lesion may be pigmented or
nonpigmented
 INVESTIGATION
EDGE BIOPSY
• Site of beading signifies
the area of active
proliferating cells.
MICROSCOPIC PATHOLOGY:
• It contains outer
palisading columnar cells
with central polyhedral
cells
• X-Ray of the part
• CT scan
 HIGH-RISK BCC

BCC can be low risk or high-risk

• Size > 2 cm
• Near the eye/nose/ear
• Ill-defi ned margins
• Recurrent tumours
• Immunosuppressed individual
 TREATMENT
SURGICAL EXCISION:
• Wide local excision with
clear margin of 2– 15 mm
depending on
macroscopic variant.
• Primary suturing/skin
graft/z plasty/rhomboidal
flap or rotational flap
• MOHS (Microscopically
Oriented Histographic
Surgery)
 SURGICAL TREATMENT
Indication:
• Rodent ulcer eroding into cartilage or bone
• BCC close to the eye
• Recurrent BCC
 MOHS

ADVANTAGES
• High cure rate
• Decreased morbidity
• Tissue conservation.

DISADVANTAGES
• need for two separate
procedures when
reconstruction is
required.
 DESTRUCTIVE TREATMENTS
• Electrodesiccation and
curettage (EDC)
• Cryosurgery
• Carbon dioxide laser
• Radiotherapy.
 ELECTRODESICCATION AND CURETTAGE (EDC)

• Effective only for very small

and superficial tumors
• Lesions less than 2 mm are
completely removed in
100%
• Lesions 2–5 mm are
removed in 85% of cases
• Tumors more than 3 cm
recur in 50% of cases.
 CRYOTHERAPY
• Treatment for small tumors.
COMPLICATIONS
• Marked edema
• Permanent hypopigmentation
• Increased morbidity.
 CARBON DIOXIDE LASER

• Useful for treatment of • Treatment of deeper

multiple tumors lesions will produce
• Useful in patients with scarring
hereditary Gorlin’s • Laser produces
syndrome superficial
• Useful only for vaporization of tissue
superficial BCCs • Usually requires 3
confined to the passes on clinically
epidermis and papillary visible tumor.
dermis
 RADIOTHERAPY
• RADIOSENSITIVE with overall cure
rate of 92%.
ADVANTAGES
• Can be used in areas which are
difficult to reconstruct
• Less traumatic than surgical
excision
• No need for hospitalization
• Wide margin of tissue can be
treated
• Radiotherapy is not given, once it
erodes cartilage or bone.
DISADVANTAGES OF RADIOTHERAPY
• Expensive facilities are necessary
• Radiation dermatitis
• Osteitis and chondritis
• Scarring
• Ulceration
• Ectropion
CAUSE OF DEATH IN BCC
• Direct intracranial extension by infiltration
• Erosion of major blood vessels.
 MALIGNANT MELANOMA
• It is a malignant tumour arising from
epidermal melanocyte
• most aggressive cutaneous malignant tumour
• It is of neural crest (ectodermal) origin.
• It is 20 times more commonly seen in whites
than blacks.
• It forms 3% of all malignancies
• It forms 5% of the cutaneous malignancy
• 7% present as occult metastasis
SITES OF MELANOMA OTHER SITES:
• Head and neck—25% • Eyes (iris, ciliary body,
• Trunk—25% choroids)
• Lower limb—25% • Mucocutaneous junction
• Upper limb·11% (anorectal region,
• Other sites·14% genitalia)
• Head and neck
(meninges, oropharynx,
nasopharynx, paranasal
sinuses).
 RISK FACTORS
• Exposure to sunlight
• Ethnic factors, socioeconomic status , lifestyle,
climate.
• Albinism.
• Xeroderma pigmentosa
• Junctional naevus.
• Familial dysplastic naevus syndrome.
• Sporadic dysplastic naevi
• Large congenital naevi (larger than 20 cm).
• Patients who are on immunosuppressive drugs or
after renal transplantation or NHL
 JUNCTIONAL MOLE

• If the movement of the melanocytes stop before

they have all migrated into the dermis, there will
be clusters of cells at various stages of maturity
in the epidermis and dermis.
• Junctional moles are immature and unstable
and can turn malignant.
• The majority of the malignant melanomas begin
in junctional moles
COMPOUND MOLE
• When intradermal and junctional features are
both present in one mole.
INTRADERMAL NAEVUS:
• Cluster of dermal melanocytes is seen without
junctional component. Common in face.
 TYPES OF MALIGNANT MELANOMA

• Superficial spreading
• Nodular
• Lentigo malignant
• Acral lentigenous
• Amelanotic.
 GROWTH PHASE
• RADIAL GROWTH PHASE: Radial growth is an
intraepidermal growth.

• VERTICAL GROWTH PHASE: The vertical

growth is the tumor growth in dermis leading
to nodule formation
 SUPERFI CIAL SPREADING
• Most common.
• 64-70%.
• It commonly arises from a pre-
existing naevus.
• Occurs in any part of the body
with variegated irregular look.
• It has more radial growth.
• better prognosis.
 NODULAR MELANOMA:
• More aggressive. It is
common in younger age
group.
• common in trunk, head and
neck
• Common in mucosa and
mucocutaneous junction;
uniform; nodular;
• It has more vertical growth
• Nodal spread is common.
• Has got poor prognosis.
 LENTIGO MALIGNA MELANOMA:

• 7-15%.
• Less common, least
malignant.
• Occurs in old age and elderly
women.
• common in face (Hutchinson’s
melanotic freckle).
• It is slow growing, variegated,
brown macule/Lentigo.
 ACRAL LENTIGINOUS MELANOMA:
• 5%.
• Occurs in palms, soles and
subungual region.
• Common in Japan.
• It has got a poor prognosis.
• It is least common.
• Usually attains large size;
nodular type with more vertical
growth phase.
• It is often flat, irregular macule.
• It mimics fungal
infection/pyogenic granuloma.
 AMELANOTIC MELANOMA:

• This is the worst type.

• Because of the
undifferentiation, tumour cells
loose their capacity to
synthesise melanin.
• It presents as rapidly progressive
pinkish fleshy tumour.
• It may mimic soft tissue
sarcoma.
• It needs markers like S100,
HMB45 for diagnosis.
 CLINICAL FEATURES
• It can stat in a pre-existing naevus
• De novo in a normal skin
• No induration is seen in melanoma.
• Pigmentation with irregular surface and
margin with rapid growth.
• Ulceration, bleeding, itching, change in the
colour.
Major signs:
Change in size (diameter more than 6 mm),
shape and colour
Other changes:
• Inflammation, crusting, bleeding, itching
• Nodularity, ulceration, halo around a mole
• Satellite lesions
 SPREAD
• Lymphatics: spreads to regional lymph nodes
either by permeation or by embolisation.
• Blood: To lungs, liver, brain, skin,bones.
Secondaries are typically black.
• Melanoma in choroid has got better
prognosis, because as there are no lymphatics,
spread is delayed.
• SATELLITE LESION:
Intra- lymphatic metastatic lesion
within 2 cm of the primary tumor.

• IN-TRANSIT METASTASIS:
Intra-lymphatic metastasis more
than 2 cm from the primary lesion
but not beyond regional lymph
node basin.
 CLARK LEVEL
• Level 1: Only in
epidermis
• Level 2: Extension into
papillary dermis
• Level 3: Filling of
papillary dermis
completely
• Level 4: Extension into
reticular dermis
• Level 5: Extension into
subcutaneous tissue
 BRESLOW’S THICKNESS
• The thickness of the
melanomatous lesion is
measured from the top
of the granular cell layer
to the base of the
tumor with the help of
ocular micrometer.
• most important
prognostic factor for
malignant melanoma.
 INVESTIGATION
• Incision biopsy
• Excision biopsy
• FNAC of lymph node.
• U/S abdomen to look for liver secondaries.
• Chest X-ray to look for secondaries in lung.
HRCT of chest is ideal.
• CT scan of head, chest, abdomen, pelvis.
• Urine for melanuria signifies advanced disease.
• Sentinel lymph node biopsy (SLNB).
Immunohistochemistry:
• HMB—45 Hydroxy Methyl Bromide
• Melan—A
• Mart 1
• S 100
• LDH
 Treatment
WIDE LOCAL EXCISION (WLE):
• wide excision with clearance of
margin as well as depth.
• Primary closure or SSG or local
fl aps are used to cover the
defect
• If primary area is wide, then
amputation with one joint
above is done.
• In fingers and toes,
disarticulation is required.
• Melanoma in anal canal--require
abdominoperineal resection.
• Enucleation in case of melanoma
in eye.
• Melanoma in pregnancy:
treated with termination of
pregnancy
specific therapy for melanoma.
Pregnancy should be postponed
for 2 years.
MANAGEMENT OF POSITIVE NODE
• Therapeutic radical lymph node dissection is
recommended
• For the lower limb ---radical ilio inguinal block
dissection
 Loco Regional Recurrent Melanoma
• Wide excision with 2 cm margin is recommended
ISOLATED LIMB PERFUSION:

• Isolating blood circuit to the extremity and administering

chemotherapeutic agent regionally at a concentration of 15–25 times
higher without side effects is called hyperthermic isolated limb perfusion.

• A small bore vascular catheter is introduced into the femoral vessel from
contralateral limb.

• A pneumatic tourniquet above the limb is applied and a small bore

vascular catheter is used for introducing the agent.
• Melphalan and Actinomycin D in 400 mL of saline
• Gives significant palliation of locoregional symptoms
• No improval in survival is noted
 FOR DISTANT SPREAD
• Chemotherapy and immunotherapy is the
main treatment.
• Isolated lung or liver metastasis can be
resected.
• Radiotherapy is useful for bone and brain
secondaries
 CHEMOTHERAPY
Indications:
• Secondaries in lungs, liver, bones.
• After surgery for melanoma.
Drugs
• DTIC: Diethyl Triamine Imino Carboxamide.
• Melphalan
• Carboplatin, vindesine.
• CVD regime—is cisplatin, vinblastine and
dacarbazine
IMMUNOTHERAPY/BIOLOGICAL THERAPY

• Interferon α
• GM2 ganglioside-based vaccine

monoclonal antibodies:
• Trametinib
• Dabrafenib.
 BAD PROGNOSIS
• Tumor thickness in mm is the most important
prognostic indicator
• LDH
• Mitotic rate
• Tumor infiltrating lymphocytes (TIL)
• Ulceration—more than 3 mm ulcer
• Vertical growth phase
• Regression.
 FOLLOWUP
• In stage I and II disease after treatment, follow
up is done at 6 months interval for 3 years. It
is done by clinical examination, LDH assay,
USG abdomen and chest X-ray.

• In stage III disease, PET scan CT of head, chest

and abdomen are indicated.
THANK YOU