SKIN TUMOURS

PROF.K.S.RAVISHANKAR M.S,F.I.C.S

SHREE BALAJI MEDICAL COLLEGE

ANATOMY OF SKIN

SKIN TUMOURS SITES

CLASSIFICATION OF SKIN TUMOURS

• BENIGN

EPIDERMAL• SEBORRHIC KERATOSIS• PAPILLOMA• TRICHILEMMAL TUMOUR• SEBACEOUS ADENOMA• SEBACEOUS EPITHELIOMA• HYDROCYSTOMA,SYRINGOMA,SPIRADENOMA

DERMAL -NEUROFIBROMA

– DERMATOFIBROMA

CLASSIFICATION OF SKIN TUMOURS

• MALIGNANT TUMOURS– SQUAMOUS CELL CARCINOMA– BASAL CELL CARCINOMA– MALIGNANT MELANOMA– MALIGNANT SKIN ADNEXAL

TUMOUR– SECONDARIES IN SKIN (eg.

sister joseph nodule)

SKIN ADNEXAL TUMOURS

• Tumours arising from accessory skin structures like sebaceous glands , sweat glands , hair follicles

•CLASSIFICATION– ECCRINE GLAND TUMOURS

•Syringoma , Hidradenoma,Syringo cystadenoma

– HAIR TUMOURS•Trichoepithelioma,Tricholemmoma

PRE MALIGNANT LESIONS• Actinic Keratosis- 5-20% will develop

Squamous/basal cell ca• Actinic Cheilitis• Paget’s disease of nipple• Xeroderma pigmentosa• Chronic Radiation Keratosis• Bowen’s Disease• Bowenoid Papulosis• Leukoplakia / Erythroplakia• Dysplastic Melanocytic Nevi (DMN)

BCC AND SCC

Risk factors:-• ACTINIC LIGHT:- 90% OF TUMORS

OCCURS IN SUN EXPOSED AREAS.

• ARSENIC:- EXPOSURE PREDISPOSE TO DEVELOPMENT OF BOWENS DISEASE,MULTIPLE SCC AND BCC.

• IRRADIATION:-FOR BENIGN CONDITIONS

• COAL TAR EXPOSURE• IMMUNOSUPPRESSION:-POST TRANSPLANT

• CHRONIC INFLAMMATION AND TRAUMA:-

CHRONIC OSTEOMYELITIS, FISTULAS,THERMAL OR ELECTRICAL BURNS.

• ATROPHIC SKIN LESIONS:-DISCOID LUPUS.

• VACCINATION SCARS.

HEREDITARY FACTORS• XERODERMA PIGMENTOSA:-AUTOSOMMAL RECESSIVE.• BASAL CELL NEVUS SYNDROME:AUTOSOMAL

DOMINANT.

INFECTIVE FACTOR;-• HUMAN PAPPILOMA VIRUS TYPES 5 AND 8:- VERRUCUS• SCC OF GENITALS:-HPV 16&18• PERIUNGUAL SCC.

Xeroderma pigmentosaActinic keratosis

Bowen’s disease of penisLeukoplakia

BASAL CELL CARCINOMA

• Most common skin cancer arising from the basal layer of epidermis and its appendages

• Low metastatic potiential• Locally invasive,

aggressive, and destructive to skin and bone.

ETIOLOGY OF BCC• Sun exposure is the most important environmental

cause of BCC.

• Ionizing radiation causes mutation of tumor suppressor genes

• UV B light: 280-320nm, UV A light 320-400nm

• Amount of UV B exposure during childhood and adolescence is directly proportional to risk for BCC

Clinical presentation

Distribution of BCC: 70% on face 25% on trunk 5% on penis, vulva, or perianal skin

Clinical subtypes (4) Nodular- most commonSuperficial- small buds of tumour massesPigmented- resembles naevus or melanomaMorpheaform- aggressive behavior, worst

prognosis

NODULAR PIGMENTED

SUPERFICIAL MORPHEA FORM

DIAGNOSIS

Initial evaluation involves

Assessment of location

Punch or excisional biopsy

Staging

SQUAMOUS CELL CA

SQUAMOUS CELL CA TYPES

• Bowen’s disease– SCCA in situ– Full thickness

dysplasia

• Bowenoid SCCA– Looks like bowen’s– Invades through BM

• Adenoid SCCA– Nodular ulcerative

lesion– Often periauricular

• Generic SCCA– Most common

– Highest rate of metastasis

• Verrucous SCCA– Verruciform lesions

– Invades by blunt, pseudopod-like growth

• Spindle SCCA– Indistinct clinically

CLINICAL FEATURES

• An ulcerative or ulceroproliferative lesion

• Raised and everted edge

• Indurated, bloody discharge from lesion +

• Regional lymph nodes commonly involved

• Variants- marjolin’s ulcer and verrucous carcinoma

Histology of SCC

• Malignant whorls of squamous cells with epithelial or keratin pearls are characteristic.

• Broder’s classification:– I-Well differentiated:75% keratin

pearls– II-Moderately differentiated: 50%

keratin pearls.– III- Poorly differentiated: 25%

keratin pearls– IV- < 25% keratin pearls

DIAGNOSIS• Although the diagnosis of SCC is often

strongly suspected based on clinical findings, a skin biopsy is required for definitive diagnosis.

• A shave biopsy, punch biopsy, incisional biopsy, or excisional biopsy, wedge biopsy may be used.

• All skin biopsy samples obtained to diagnose SCC must reach at least the depth of the mid dermis to allow for determination of the presence or absence of invasive disease.

STAGING• TX - Primary tumor cannot be assessed• T0 - No evidence of primary tumor• Tis - Carcinoma in situ• T1 - Tumor less than 2 cm in greatest

diameter• T2 - Tumor 2-5 cm in greatest diameter• T3 - Tumor greater than 5 cm in greatest

diameter• T4 - Tumor with deep invasion into

cartilage, muscle, or bone.

Regional lymph nodes[N]• NX Regional lymph nodes cannot be

assessed• NO No regional lymph node metastasis• N1 Regional lymph node metastasis,

DISTANT METASTASIS[M]• MX Presence of distant mets cannot

be assessed • M0 No distant metastasis• M1 Distant metastasis

MANAGEMENT• ACTINIC KERATOSIS:-LIQUID NITROGEN ,

ELECTRICAL CURETTAGE.

• BCC:-TRADITIONAL SURGICAL RESECTIONS, MOH’ S MICROGRAPHIC SURG

INDICATIONS FOR MOH’S SURG:-• LOCATED IN REGIONS WHERE HIGH RISK

FOR TUMOR RECURRENCE AREAS,• DIAMETER >1CM ON FACE,• PERINEURAL INVASION,• MORHEFORM,SCLEROTIC AND INFILTRATIVE

TYPE BCC.

• ELECTRO CURETTAGE, CRYOSURGERY, RADIOTHERAPHY,

EXTENSIVE RESCTION AND RECONSTRUCTION: -AMPUTATION IN CERTAIN CASES

• CHEMOTHERAPHY:- NO ADJUVANT ROLE,MAY BE OF USE N

METASTATIC SKIN LESIONS

SUPERFICIAL BRACHYTERAPY

MOH’S SURGERY

FOLLOW UP• Low-risk tumors are usually cured with

appropriate surgical therapy; recurrence may occur.

• Thus, patients with a history of SCC should be evaluated with a complete skin examination every 6-12 months.

• Patients with high-risk tumors require skin and lymph node examinations at 3- to 6-month intervals for at least 2 years after diagnosis.

Marjolin’s ulcerWell differentiated squamous cell ca that occurs in chronic scars like burn scar, scar of venous ulcer

No lymphatics in scar tissue hence no spread to regional lymph nodes.

Scar contains no nerves, hence painless.

Wide excision or amputation for larger lesions

Radiotherapy contraindicated for fear of transformation into poorly differentiated sq cell ca.

Verrucous cancer Dry, exophytic,warty growth

No lymph node spread

No blood spread

Surgery is the treatment of choice- wide excision

Examples:

1. Giant Condyloma Acuminatum (Buschke-Lowenstein tumour)- in genitalia

2. Carcinoma cuniculatum-( Verrucous ca of feet)

3. Oral florid verrucous ca

Melanoma - Outline

• General statistics and development• Risk factors and patient assessement• Pathology and prognosis• Work-up and staging• Surgical treatment• Lymph node controversy/sentinel

node • Adjuvant therapy

Melanoma - Statistics

• Mortality increase 2nd only to lung• 5th most prevalent, incidence 7%/year

increase• 5% skin cancer, 75% skin cancer death• Men common sites- front and back of

trunk• Women common sites- lower leg• Mostly arise from benign naevus or

adjacent area

Development of Nevi

• Junctional nevi– nests along dermal-epidermal junction

• Compound nevi– “invade” dermis, first as nests then cords and

single cells• Dermal nevi

– junctional component lost only in papillary and reticular dermis

Histologically, nevi are classified generally as having atypical cells, as in dysplastic nevi, or normal cytology, as in the common nevus.

Junctional Nevi

Compound Nevi

Dermal Nevi

Dysplastic Nevi

Types of Melanoma

• Acral lentiginous• Amelanotic melanoma• Superfical spreading melanoma• Lentigo maligna melanoma• Nodular melanoma

Superficial spreading

• Most common, 70% of all melanomas• 4th to 5th decade• Clinically variable

pigmentation,irregular borders, biphasic growth

• Histologically-asymmetry, poor circumscription and lack of maturation

Superficial spreading

Lentigo maligna

• 20% of cutaneous melanomas• Most benign form of melanoma• Longest radial growth phase >15

yrs• Occurs in Hutchinson’s freckle• Elderly sun exposed areas• Clinical dark, irregular ink spot

Lentigo maligna

Nodular melanoma

• 12% of all melanomas• Most malignant type• Aggressive vertical growth phase• Sun-exposed and nonexposed

areas• Usual presentation- darkly

pigmented raised nodule

Nodular melanoma

Acral lentiginous melanoma

• Occurs in palms,soles and subungual areas

• Worse prognosis than superficial spreading

• Pigment spread to the proximal or lateral nail folds is termed the Hutchinson sign, which is a hallmark for acral lentiginous melanoma.

AMELANOTIC MELANOMA

• Appear pink but close inspection reveals pigmentation

• Lack of pigmentation causes delay in diagnosis.

• Worst prognosis of all melanomas

Melanoma

• 70% of melanomas occur on a pre existing nevus.

• 30% of melanomas occur de-novo

When to suspect malignant transformation in a mole?

• Asymmetrical outline--- A• Border irregularity-------B• Colour change------------C• Diameter>6mm-----------D• Elevation------------------E

Diagnosis• Excision biopsy of suspected lesions

mainstay of diagnosis• Performed with 1-2mm margin and has to

be full thickness to ascertain the following:– Tumor thickness (Breslow depth)– Presence of ulceration– Anatomic level of invasion (Clark level)– Presence of mitoses– Presence of regression– Lymphatic/vessel invasion or vascular

involvement– Host response (tumor-infiltrating lymphocytes)

• LYMPHATIC SPREAD:-SINGLE REGIONAL LYMPHNODES[N1],

• MULTIPLE NODES{2-3 NODES}[N2A]

• SATELLITE NODULE AND INTRANSIT NODULES WITHOUT NODES

• MORE THAN FOUR NODES WITH INTRANSIT[N3].

DISTANT METASTASES:-METS TO SKIN SUBCUTANEOUS

TISSUE[DISTANT NODES]{M1A}{M1B} METS TO LUNG{M1C} ANY VISCERAL METS WITH RAISED LDH

SENTINEL LYMPH NODE BIOPSY

• Sentinel lymph node biopsy (SLNB) is indicated for pathologic staging of the regional nodal basin for primary tumors greater than or equal to 1 mm depth and when certain high-risk histologic features (eg, ulceration, extensive regression) are present in thinner melanomas < 1mm)

STAGING-CLARKE’S AND BRESLOW

Staging-Clark

• Level I - in situ at basement membrane

• Level II - through basement membrane into papillary dermis

• Level III - spread to papillary/reticular interface

• Level IV - spread to reticular dermis• Level V - sub-cutaneous invasion

Staging-Breslow

• <0.76 mm - thin• 0.76 - 1.49 - intermediate• 1.50 - 4.00 - intermediate• >4.00 mm - thick

Latest Breslow classification– <1mm- Thin melanomas– 1-4mm- Intermediate thickness

melanomas– >4mm- Thick melanomas

AJCC Staging

Work-up

• Labs and imaging– CXR , CT chest and LFT– H&N CT neck routine– If stage III(regional) or IV (distant) -

CT head, chest, abdomen, pelvis– Hpe: S-100 and homatropine

methylbromide (HMB45) stains are positive in melanoma.

Surgical Treatment

– Treatment of Primary (WLE)– Current recommendations for margins of

excision are as follows: •Lesions <1 mm in thickness - 1 cm

margin •Lesions 1-2 mm in thickness - 2 cm

margin •Lesions >2mm in thickness – 3 cm

margin• All depths to underlying muscle fascia

Management of lymph nodes

• SLN biopsy• Node dissection• Isolated limb perfusion

Adjuant chemotherapy• Cytotoxic drugs• Interferon• BCG

Metastatic disease• Bleomycin, Oncovin, Lomustin

Dacarbazin• Tamoxifen• interleukin

• Prognosis– anatomic site, ulceration, gender,

histologic type, nodal disease– head and neck, trunk and acral

regions worse prognosis– women better prognosis than men– Ulceration, angiogenesis and vascular

invasion-poor prognosis

PrognosisBreslow (thickness in millimeters) strongest predictor

Depth of tumor invasion

5 yr survival (%)

<0.5 mm 99

> 3 mm 30

Prognosis

Clark level less predictive, thin melanomas useful(<1mm)

Level

Tumor extent 5 yr Survival (%)

I Tumor is confined to epidermis (in situ) 100

II Tumor extends beyond basal lamina into papillary dermis

85

III Tumor extends into papillary dermis and abuts onto, but does not invade, the reticular dermis

65

IV Tumor extends into reticular dermis 50

V Tumor extends into subcutaneous fat 15

Prognosis• Survival according to regional

lymph node involvement

Node involvement

5 yr survival (%)

Negative nodes 75 (85% for negative SLN)

1 – 3 positive nodes 504 or more positive nodes

25

Prognosis• Survival according to metastatic spread

Stage

Extent 5 yr survival (%)

II Local recurrences within 3 cm of primary site

30

III Satellitosis <20

IV Distant metastases <10

ACANTHOSIS NIGRICANS

NECROLYTIC MIGRATORY ERYHTEMA

Thank You