Epidermal Tumors

Tumors of the surface epidermis

• Seborrheic keratosis

• Keratoacanthoma

• Epidermal nevi

• Cutaneous cysts

• Warty dyskeratoma

• Clear cell acanthoma

• Solar keratosis

Precancerous leukoplakia

Oral florid papillomatosis

• Bowen’s dis.

• Erythroplasia of Queyrat

(Bowen’s dis. of glans penis)

Paget’s dis.

SCC

C) CarcinomasB) Precancerous (in situ)A) Benign

20%

6-17%

10%

5-11%

30%

Seborrheic keratosis

One or more sharply defined, light brown to black,

slightly raised lesions (as if stuck on surface) with soft

velvety or finely verrucous surface. It occurs on trunk,

face or extremities.

Treatment

1. Removal with a small sharp curette.

2. Freezing.

3. TCA.

4. Cauterization.

Seborrheic Keratosis (Cont’d)

Keratoacanthoma (KA): rapidly growing, self healing, epidermal tumor

that has a striking resemblance, both clinically & histologically to SCC.

• Solitary KA: firm, skin-colored to pink, dome-shaped nodule with a

horn filled crater in its center. It usually involutes spontaneously in less

than 6 ms with slightly depressed scar.

Seborrheic Keratosis (Cont’d)

• Multiple KAs:

Multiple self-healing epitheliomas

(Ferguson-Smith).

Eruptive keratoacanthoma

(Crzybowzki).

Treatment of KA

• Excision biopsy to exclude SCC.

• Curettage and cauterization of small lesions.

• 5-fluorouracil intralesionally.

• Radiotherapy.

• Multiple KAs: methotrexate or oral retinoids.

Epidermal nevi

They are circumscribed hamartomatous lesions composed only of

keratinocytes. They present usually at birth or shortly later.

I) Localized type “Nevus Unius Lateris”

II) Systematized type “Ichthyosis hystrix”

Epidermal nevi

• Epidermal nevus is a general term referring to birthmarks which

originate from skin structures

• “Nevus verrucous” is keratinocytes

• “Nevus sebaceous” from sebaceous glands

• “Nevus comedomicus” from hair follicles

• “Nevus syringocystadenoma” from sweat glands

Cutaneous cysts

Epidermal cysts (the most common type)

• Spontaneously.

• Traumatic implantation of epidermis into the dermis.

• The wall of the cyst is composed of true epidermis, i.e. squamous,

granular & horn cells. The cyst is filled with horny material arranged in

laminated layers.

Milia

• Primary milia: arise spontaneously on face.

• Secondary milia: arise

In association with many dermatoses, e.g. BP, DEB,

PCT, LSA.

After trauma, e.g. dermabrasion.

Steatocystoma multiplex

Sites

• Sternal region, axillae and

scrotal area.

Actinic keratosis (AK) “Solar keratosis”

• Most common premalignant skin lesion in elderly

persons (≥40 yrs), fair complexion, with excessive sun

exposure, > in men.

• Sun-exposed areas as face, dorsa of hands & bald

portions of the scalp in men.

• Multiple erythematous, ill-defined macules or papules,

often covered by adherent scales with little or no

infiltration. Marked hyperkeratosis may be seen.

Actinic keratosis (Cont’d)

• SCC may develop in one or more of the lesions of AK

in about 20% of the patients, usually after a long latent

period, e.g. 10 years.

• SCC arising in AK or de-novo in sun-damaged skin

very rarely metastasize (0.5%), but in actinic cheilitis,

the incidence is 11%.

Actinic keratosis (Cont’d)

Histopathology

• SCC in situ.

• Morphologically, anaplastic cells are present.

However, biologically, the lesions are still benign.

Invasion into the dermis, if present at all, is limited to

the most superficial portion.

Actinic keratosis (Cont’d)

Radiotherapy is contraindicated.

• Sun avoidance.

• Electrodessication & curettage.

• Cryosurgery with liquid nitrogen.

• Topical chemotherapy: 5-fluorouracil, 0.1-5% (5-FU) –

Efudex cream®.

• Chemical peel with TCA 35%.

• Retinoids: oral or topical.

Treatment

Leukoplakia

White patch or plaque on the mucosa that can’t be rubbed-off.

Types:

• Homogeneous leukoplakia: low malignant potential.

• Verrucous leukoplakia.

• Speckled leukoplakia: white nodules on an erythematous

background. Increased risk of malignant change.

• Smokers keratosis.

• Oral hairy leukoplakia.

All cases of leukoplakia should be examined

histologically.

Leukoplakia (Cont’d)

Etiology • Chemical irritation, tobacco smoking.

• Mechanical irritation through dental stumps.

• HPV: HPV-11 & HPV-16.

• Candidal infection.

• Syphilis (usually on the dorsum of the tongue).

Leukoplakia (Cont’d)

• The overall transformation rates of leukoplakia to SCC

range from 6-17%.

• The site is important: leukoplakias on the buccal

mucosa are usually benign, whereas leukoplakias of

the floor of the mouth have higher transformation

rates.

Leukoplakia (Cont’d)

• Benign

• 17%

• 3%

In situ anaplasia

(precancerous

leukoplakia)

Infiltrating SCC

20%

80%

Bowen’s disease

• On exposed skin (predisposed by

chronic exposure to sun).

• Unexposed skin (caused by the

ingestion of arsenic).

• On lesions of EV (caused by HPV-5).

• On lesions of porokeratosis.

• No etiological factors.

5

Bowen’s disease (Cont’d)

• Slowly enlarging erythematous patch of

sharp but irregular outline, showing

little or no infiltration.

• In 5-11% of cases of Bowen’s disease,

SCC develops.

Squamous cell carcinoma (SCC)

• Malignant tumor of epidermal

keratinocytes with an average

metastatic rate of 2-3% of all

patients.

Squamous cell carcinoma (SCC)

Etiology

I) Extrinsic factors:• Ultraviolet radiation: the major factor for the development of

non-melanoma skin cancer (NMSC). PUVA therapy also

increases the risk for development of SCC.

• Exposure to carcinogenic cpds, e.g. coal, arsenic, tobacco.

• Ionizing radiations from X-rays.

• HPVs, e.g. HPV-16 (cervical & penile SCCs), HPV-5 & -8

(oncogenic in EV) & HPV-6 & -11 (verrucous carcinoma of

anogenital areas).

SCC – Etiology (Cont’d)

II) Intrinsic factors (Cont’d)

• Genodermatoses: e.g. xeroderma pig., albinism, porokeratosis &

dysk. congenita have a high incidence of SCC & other cut.

malignancies.

• Immunosuppression: 2ry to immunosuppressive drugs, HIV inf.,

lymphomas or organ transplants.

SCC (Cont’d)

Clinically

• Solitary, firm, slowly enlarging nodule with indurated base.• Shallow ulcer with raised everted edge, indurated base.• Verrucous or fungoid lesions.

Histopathology

• The more malignant the tumor, the greater is the number of

atypical squamous cells & the less the number of differentiated

cells (horn pearls).

SCC (Cont’d)

Grading system

• Grade 1 (less malignant): more than 75% of the cells are differentiated, i.e. several horn pearls with relatively slight atypicality.

• Grade 2, more than 50%.• Grade 3, more than 25%.• Grade 4, less than 25% are differentiated (more

malignant).

The degree of atypicality of the tumor cells & the

depth of penetration are important factors in

grading.

Treatment

• Local destruction:

• Radiotherapy.

• Excisional: with a safety margin.

Curettage & electrodessication. Cryosurgery.

CO2 laser ablation.

Intralesional & topical 5-fluorouracil.

Paget’s disease of the breast

• Exclusively in women.

• Age: 55 years.

• It occurs unilaterally on the areola & nipple as a

sharply defined, slightly infiltrated area of erythema

showing scaling, oozing & crusting. Ulceration or

retraction of the nipple may be found.

• It is commonly associated with intraductal carcinoma

of the breast.

Paget’s disease of the breast (Cont’d)

Origin of Paget cells

• The glandular origin was supported by immuno-

histochemical studies, e.g. carcinoembryogenic

antigen is found in Paget cells which is found also

in normal apocrine & eccrine glands but not in

keratinocytes or melanocytes.

Treatment • Modified radical mastectomy.

Extramammary Paget’s disease

• Occurs commonly in the anogenital region, e.g. vulva, perianal area,

scrotum or axillae, i.e. areas in which apocrine glands occur.

• In 20% of cases, it is 2ry to extension of an adenocarcinoma, either of the

rectum to the perianal region, of the cervix to the vulva, or of the urinary

bladder to the urethra & glans penis.

Extramammary Paget’s disease (Cont’d)

Clinically• There is slowly enlarging, erythematous patch with oozing & crusting,

with sharp but irregular border & in contrast to mammary type, itching is

common.

Treatment • Surgical excision.

Tumors of epidermal appendages

Trichoepithelioma

Autosomal dominant.

Numerous, rounded, skin-colored, firm nodules located mainly in the

nasolabial folds, forehead & upper lip.

• Solitary: non-hereditary.

• Multiple:

Tumors of epidermal appendages (Cont’d)

Nevus sebaceous of Jadassohn (Organoid nevus)

• At or soon after birth, solitary, linear or round

yellow-brown, hairless, slightly elevated plaque

usually located on the scalp or face.

• In puberty, verrucous or nodular.

• Later in life, some lesions may develop various

types of appendage tumors, e.g.

syringocystadenoma papilliferum, BCC.

3Stage

s

Three phases of N. sebaceus

Infant phaseFlat, smoothDecreased hair

Pubertal phaseGrows when oil glands expand – papularOrange peel surface

Tumor phaseAdults usuallyExact % unknownProbably <5%

Syringoma

• An adenoma of intraepidermal eccrine ducts.

• More in females.

• In lower lids, cheeks, axillae, abdomen and vulva.

• Small, skin-colored or slightly yellow, soft papules.

• Eruptive hidradenoma or syringoma: the lesions arise in large numbers

in successive crops on the anterior trunk of young persons.

Basal cell carcinoma “BCC”

• BCC is the most common malignancy in

humans.

• Although rarely metastatic, it is capable of

significant local destruction & disfigurement.

BCC (Cont’d)

Predisposing factors• UV light.

• Chronic intake of inorganic arsenic.

• Predisposing skin conditions: dermatofibromas,

nevus sebaceous of Jahadsson, burn scars.

• Predisposing syndromes: nevoid basal cell

carcinoma syndrome, Basex syndrome, Rombo’s

syndrome & xeroderma pigmentosum.

• Immunsuppression & X-ray irradiations.

However, BCC may arise without apparent cause.

BCC (Cont’d)

Clinical features

• It occurs almost exclusively on hair-bearing skin, especially on the face.

Clinical types

• Nodulo-ulcerative.• Pigmented.• Superficial.• Morphea-like.• Fibroepithelioma of Pinkus.

BCC (Cont’d)

Histologically: 2 types of BCC are known • Undifferentiated (solid) BCC: composed of basaloid cells. The

peripheral cell layer of tumor masses show a palisade arrangement of

nuclei.

• Differentiated: either toward hair structure (keratotic BCC), toward

glandular structures (adenoid BCC) or toward sebaceous structures.

BCC (Cont’d)

Treatment

• Excision: with safety margin ½ inch for small tumors.

• Radiotherapy.

• Curettage & electrosurgery.

• Cryosurgery.

• Mohs micrographic surgery (MMS).

• Cytotoxic agents: e.g. 5-fluorouracil topically.

• Intralesional injection of -2b interferon (IntronA®).

• Photodynamic therapy.