MALIGNANT SKIN

TUMORS, KAPOSI’S
SARCOMA
Clinical Lecture Notes
Gregory University Medical School
Dr U Ogbonna
Anatomy & physiology
• The skin is the outermost covering of the body with varying thickness
at different parts
• It is made up of 2 layers; epidermis and dermis
Epidermis
• thickness 0.04-1.4mm
• Epithelium ; stratified sqamus keratinizing
• Cells present; keratinocytes,melanocytes, langerhans cells& merkels
cells
Dermis
• Located just underneath the epidermis, it consist of non cellular
connective tissue
Elastic fibers
Collagen
Ground substance
• Interspaced within this are nerves,blood vessels,lymphatic vessels
muscle units, pilosebaceous units, eccrine sweat unit
• 15-40 times thicker than the epidermis
• Cells here are; fibroblast, mast cells, hystiocytes, langerhans cells and
lymphocytes
• Layers;
Papillary; thin
Reticular; this has elastic & collagen fibers fibroblast and blood
vessels
Functions
• External cover to protect against minor trauma & invasion by
microorganisms
• Temp regulation / water loss
• Sensibility ;point ,temp ,pressure proprioception
• Metabolism: vit D production
Aetiology of malignant skin lesions
Host related
• Phenotype
• Syndromes
Xeroderma pigmentosum
Nevoid BC syndrome (Gorlins synd)
Albinism
porokeratosis
Predisposing lesions

Actinic keratosis 10-13%

Nevus sebaceous of Jadassohn
Cutaneous horns
• Immunologic factors
Environmental factors
• Ultraviolet radiation
• Ionizing irradiation
• Chemicals
Polycyclic aromatic HC
Dimethyl benzanthracene
Psolarens
Arsenic , HCL
• Viral infections e.g. HPV
Classification
Primary or secondary
Primary:
• Basal cell Carcinoma
• Squamous Cell Carcinoma
• Malignant Melanoma
These are epidermal in origin
dermal appendage tumours
• Sebaceous glands,
• Hair follicle,
• Sweat glands,
• Nerve ending and
• Blood vessels.
• These give rise to various forms of adenocarcinomas, sarcomas etc.
• Though rare, Kaposi's sarcoma deserves special attention
• Other connective tissues sarcomas such as liposarcoma and dermato
fibrosarcomas can present to the plastic surgeon

• Metastasis to skin
Basal Cell Carcinoma (BCC)
• Common primary malignant skin tumor
• Areas of predilection: head, face, neck, upper extremities
• Cell of origin: basal layer of epidermis
• Risk factors: age, fair skin, chronic sun exposure
• Ass with UVB keratinocyte damage
• Ass genetic syndromes: basal cell nevus syndrome(BCNS; Gorlin
syndrome), Basex syndrome, Rombo syndrome
• Presentation:
• Pink, pearly papule with overlying telangiectasia
• Borders are raised and rolled
• Erosion or ulceration- “Rodent ulcer”
• Ass genetic syndromes: basal cell nevus syndrome(BCNS; Gorlin
syndrome), Basex syndrome, Rombo syndrome
• Presentation:
• Pink, pearly papule with overlying telangiectasia
• Borders are raised and rolled
• Erosion or ulceration- “Rodent ulcer”
Clinico-pathologic types of BCC
• Nodular: Cystic, pigmented, keratotic; the most common type of BCC;
usually presents as a round, pearly, flesh-colored papule with
telangiectases

• Infiltrative: Tumor infiltrates the dermis in thin strands between

collagen fibers, making tumor margins less clinically apparent
• Micronodular: Not prone to ulceration; may appear yellow-white
when stretched, is firm to the touch, and may have a seemingly well-
defined border

• Morpheaform: Appears as a white or yellow, waxy, sclerotic plaque

that rarely ulcerates; is flat or slightly depressed, fibrotic, and firm
• Superficial: Seen mostly on the upper trunk or shoulders; appears
clinically as an erythematous, well-circumscribed patch or plaque,
often with a whitish scale
Diagnosis
• Biopsy
• Shave biopsy: Most often, the only biopsy that is required

• Punch biopsy: May be indicated in the case of a pigmented lesion if there is

difficulty distinguishing between pigmented BCC and melanoma; ensures that
the depth of the lesion can be determined if it proves to be a malignant
melanoma
• Incision biopsy
• Excision biopsy-when the lesion is small and clinical diagnosis is
almost certain. May be the final intervention and treatment.
• Histology
• Undifferentiated: When there is little or no differentiation, the carcinoma is
referred to as solid BCC; this form includes pigmented BCC, superficial BCC,
sclerosing BCC, and infiltrative BCC (a histologic subtype)

• Differentiated: Differentiated BCC often has slight differentiation toward hair

(keratotic BCC), sebaceous glands (BCC with sebaceous differentiation), and
tubular glands (adenoid BCC); noduloulcerative (nodular) BCC is usually
differentiated
Treatment
• Surgery is mainstay of treatment
• Excision
• Electrodessication and curettage
• Mohs micrographic surgery
• Cryosurgery
• Radiotherapy
• Advanced and extensive lesion
• Aggressive tumors
• Photodynamic therapy
Squamous cell carcinoma
• 2nd most common skin cancer
• Increasing incidence world wide:
• Aging population
• Improved detection
• Increased use of tanning beds
• Ozone layer depletion
• Most common site in whites is head and neck
• Lower limb and other sites in Africans
• Cell of origin: Malphigian layer of the skin
• Predisposition:
• Fair skin, albinos
• Chronic exposure to UV rays of the sun
• Long standing chronic granulomatous conditions such as syphilis, lupus
vulgaris, hydradenitis supurutiva,
• Chronic ulcers, chronic osteomyelitis, venous ulcers, burn ulcers ( Marjohlin’s
ulcer)
• Precursor (premalignant conditions)
• Squamous cell carcinoma in-situ (Bowen disease)
• Actinic keratosis
• Presentation
• Abnormal growth on the skin
• Non-healing ulcer
• Usually a shallow ulcer with heaped-up edges
• May be preceded by actinic keratosis
• Pathology
• Histologically characterized by invasive nest of cells showing variable central
keratinization and horn cell formation (cell nest)
• Histologic types
• Well differentiated - Characterized by more normal-appearing nuclei with
abundant cytoplasm and extracellular keratin pearls
• Moderately differentiated - Exhibits features intermediate between well-
differentiated and poorly differentiated lesions
• Poorly differentiated - Shows a high degree of nuclear atypia with frequent
mitoses, a greater nuclear-cytoplasmic ratio, and less keratinization
 • Highly undifferentiated - Shows epithelial cells that may be difficult to
distinguish from mesenchymal, melanoma, or lymphoma cells

• Diagnosis: History, Physical examination, histology, X-rays, CT, MRI

Management
• Surgical excision with clear margins, as verified by frozen sections
• Mohs micrographic surgery for invasive SCC in the facial region
• Radiation therapy as an adjuvant to surgery, to provide improved
locoregional control, or as primary therapy in patients who are unable
to undergo surgical excision
• Chemotherapy, such as treatment with oral 5-fluorouracil (5-FU) and
epidermal growth factor receptor (EGFR) inhibitors, as adjuvant
therapy for select highest-risk cases
• Systemic chemotherapy for metastatic cSCC
Malignant melanoma
• MALIGNANCY OF MELANOCYTES
• DERIVED FROM NEURAL CREST CELLS – SKIN, EYES, EARS, GI TRACT, LEPTOMENINGES, AND ORAL
AND GENITAL MUCOSA
• SKIN CANCER 12.7% OF MALIGNANCIES IN BLACKS; MELANOMA 2ND COMMONEST.
• COMMONEST CAUSE OF SKIN CANCER-RELATED DEATH >77%
• EARLY DETECTION BEST MEANS OF REDUCING MORTALITY
• INCIDENCE RISING AT 6%/YR (FASTER THAN ANY OTHER CANCER);
• PROTECTIVE FOOT WEAR MAY HELP PREVENTION
• LESS FREQUENT IN BLACKS(1/20 THAT OF WHITES), BUT WITH HIGHER MORTALITY RATES.
AETIOLOGY/ RISK FACTORS
• TRAUMA TO THE SOLE OF THE FOOT
• ? PRE-EXISTING MOLE ON THE FOOT.
• ATYPICAL/DYSPLASTIC NAEVI(>5-10)
• LARGE NO. OF NAEVI(>100)
• GIANT CONGENITAL NAEVI(>20CM DIAMETER)
• MELANOMA IN 1ST DEGREE RELATIVE(2.2 FOLD HIGHER RISK)
• PRIOR NONMELANOMA SKIN CANCER
• MALE SEX
• SUN SENSITIVITY/EXCESSIVE EXPOSURE TO THE SUN
AETIOLOGY/ RISK FACTORS CONTD.
• AGE OLDER THAN 50YRS.
• PRESENCE OF XERODERMA PIGMENTOSUM OR FAMILIAL ATYPICAL
MOLE MELANOMA SYNDROME(500-1000 FOLD GREATER RISK)
• A FAIR SKIN PHENOTYPE
• IMMUNOSUPPRESSIVE STATES – TRANSPLANT PATIENTS,
HAEMATOLOGICAL MALIGNANCIES
PATHOGENESIS
• IN BLACKS, PLANTAR FOOT COMMONEST SITE(93%), FOLLOWED BY SUBUNGAL,
PALMAR, ANDMUCOSAL SITES.
• PLANTAR PREDILECTION PROMPTS SPECULATION OF TRAUMA AS ETIOLOGICAL
FACTOR
• ALSO PLANTAR MELANOMA LESS IN AMERICAN BLACKS THAN THE AFRICAN ?
LATTER LESS LIKELY TO WEAR PROTECTIVE FOOTWEAR
• UVB (280-320NM) MAJOR CULPRIT IN WHITES:
• -INITIATION-PROMOTION MODEL
• -AFFECTS LANGERHAN CELLS (APCs)
• -INCREASES SUPPRESSOR T LYMPHOCYTES
• NONENVIRONMENTAL FACTORS
CLINICOPATHOLOGIC SUBTYPES
• SUPERFICIAL SPREADING MELANOMA
• NODULAR MELANOMA
• LENTIGO MALIGNA MELANOMA
• ACRAL LENTIGINOUS
• RARE VARIANTS: DESMOPLASTIC, MALIGNANT BLUE NAEVUS, CLEAR
CELL SARCOMA
SUPERFICIAL SPREADING MELANOMA
NODULAR MELANOMA
LENTIGO MALIGNA MELANOMA
ACRAL LENTIGINOUS MELANOMA
MICROSTAGING
• TWO METHODS:
• CLARK CLASSIFICATION – LEVELS I-V
• BRESLOW CLASSIFICATION – MORE PROGNOSTIC, MORE
REPRODUCIBLE, LESS SUBJECTIVE
CLINICAL STAGING
• OLD SYSTEM – STAGES I-III
• 1983 AJCC/IUCC 4 STAGING SYSTEM – INCORPORATES
MICROSTAGING; MORE PROGNOSTIC
• AJCC 2002 REVISED STAGING – CLARK’S LEVEL ONLY IN LESIONS
<1MM, ULCERATION, AND NO. OF NODES CONSIDERED
TREATMENT 1 – SURGICAL EXCISION
• LESION USUALLY > 4CM – 3CM MARGIN. PRESERVE DEEP FASCIA IF POSSIBLE
• MELANOMA IN SITU – EXCISION OF 0.5CM NORMAL SKIN
• LESIONS < 1MM THICK – 1CM MARGIN
• INTERMEDIATE-THICKNESS LESIONS (1-4MM) – 2CM MARGIN
• WIDE DEFECT – SSG
• SUBUNGUAL MELENOMA AMPUTATION AT METATARSOPHALANGEAL JOINT
• MOHS MICROGRAPHIC SURGERY: HISTOLOGIC CONTROL OF EXCISION MARGINS
TREATMENT II – REGIONAL
LYMPHADENECTOMY
• THERAPEUTIC L/N DISSECTION – CLIN. +VE NODES: 13%-35% 5YR
SURVIVAL, AVOIDS PAIN , SKIN BREAKDOWN, TUMOR NECROSIS
• ELECTIVE L/N DISSECTION – CLIN. NORMAL APPEARING NODES –
CONTROVERSIAL: 50%VS 45% 5YR SURVIVAL
• SUPERFICIAL+/- DEEP GROIN DISSECTION
ADJUVANT THERAPY
• CHEMOTHERAPY – DTIC, CISPLATIN, CAMUSTINE(BCNU) ON DAYS 1 & 8 EVERY
28DAYS FOR 3 COURSES +/- TAMOXIFEN 20MG DLY: 11% COMPLETE RESPONSE;
40% OVERALL RESPONSE
• BCG IMMUNOTHERAPY
• RADIOTHERAPY – LARGE DOSES PER FRACTION (4-8Gy)
• ISOLATED LIMB PERFUSION – MELPHALAN ACTINOMYCIN D, AND NITROGEN
MUSTARD; HYPERTHERMIA : ADV. LOCAL DZ.
• IFN alfa-2b 20 MILLION/m2 qd 5d/wk for 4wk, THEN 10million U/m2 SC 3X/wk for
48 wks
PROGNOSIS
DEPENDS ON THE FOLLOWING:
• TUMOR THICKNESS
• REGIONAL NODES
• HIGHER NO. OF +VE NODES
• DISTANT METASTASIS
• ANATOMIC SITE
• PRESENCE OF ULCERATION
• PRESENCE OF REGRESSION
• MALE SEX
• POOR PROGNOSIS IN OUR ENVIRONMENT DUE TO LATE PRESENTATION
PREVENTION
• PROTECTIVE FOOT WEAR
• PUBLIC HEALTH EDUCATION; ENCOURAGE TO TEACH OTHERS
• REPORT SUSPICIOUS LESIONS
Kaposi’s sarcoma (KS)
• Indolent angio-proliferative spindle cell tumor
• Derived from endothelial and immune cells infected with human
herpes virus type 8(HHV-8)
• HHV-8 is the causative agent of KS: it is present in 95% to 98% of all
cases
Classification of KS
• 4 types, viz:
• Epidemic (AIDS related)
• Iatrogenic (immunosuppressant therapy related)
• Classic, or sporadic
• Endemic (African)
• Nonepidemic KS- usually seen in men who have sex with men (gay); no
evidence of HIV or immune defficiency
Symptoms and signs
• Skin lesions, oral mucosa, lymph nodes and visceral organs
• Cutaneous lesions are most common
• Lower extremities, head and neck
• Macular, papular, nodular or plaquelike appearance
• Lesions may be discrete or confluent
• GIT:
• Odynophagia, dysphagia
• Nausea, vomiting, abdominal pain
• Hematemesis, hematochezia, melena
• Bowel obstruction
• Pulmonary: cough, dyspnoea, haemoptysis, chest pain
• Diagnosis: history, Physical examination
• Laboratory: CD4 lymphocyte count, HIV viral load
• Imaging: CXR, Thallium and Gallium scans to differential from infection
• Thallium- taken up by tumor
• Gallium: taken up by infection
• Procedures:
• Punch biopsy or incision biopy
• Bronchoscopy
• Oesophagoduodenoscopy or colonoscopy
Histological findings
• Histological types:
• Proliferation of spindle cells
• Prominent, slitlike vascular spaces
• Extravasated red blood cells.
Management
• Antiretroviral therapy
• Local therapy:
• Radiation, cryotherapy, laser, surgical excision, topical retinoids, topical vinca
alkaloids
• Immunomodulation- interferon- alfa on clinical trial
• Combination therapy- Actinomycin-D, Bleomycin, Vincristine
• Cytotoxic drugs (approvrd by FDA)
• Liposomal doxorubicin (Doxil)
• Liposomal daunorubicin (DaunoXome)
• Paclitaxel (Taxol) or oral etoposide (VePesid)