Adnexal Tumors Mature Counterpart Histologic Features Clinical Significance

Trichoepithelioma Hair follicle Hair matrix, outer root sheath differentiation Multiple trichoepitheliomas, dominant inheritance

Trichofolliculoma

Sebaceous adenoma

Sebaceous gland Cytoplasmic lipid vacuoles Association with internal malignancy

Sebaceous epithelioma

Syringocystadenoma papilliferum Apocrine gland Apocrine type ("decapitation") secretion May develop in mixed epidermal-adnexal hamartomas of

face and scalp termed nevus sebaceus

Syringoma Eccrine gland Eccrine ducts lined by membranous eosinophilic

cuticles; tadpole-like epithelial structures

May be confused with basal cell carcinoma clinically

Premalignant and Malignant Epidermal Tumors

ACTINIC KERATOSIS

Before the development of overt malignancy of the epidermis, a series of progressively dysplastic changes occur, a phenomenon analogous to the atypia that precedes carcinoma of the

squamous mucosa of the uterine cervix ( Chapter 22 ). Because this dysplasia is usually the result of chronic exposure to sunlight and is associated with build-up of excess keratin, these

lesions are called actinic keratoses. As would be expected, they occur with particularly high incidence in lightly pigmented individuals. Exposure to ionizing radiation, hydrocarbons,

and arsenicals may induce similar lesions.

Actinic keratoses are usually less than 1 cm in diameter; are tan-brown, red, or skin-colored; and have a rough, sandpaper-like consistency. Some lesions may produce so much keratin

that a "cutaneous horn" develops ( Fig. 25-13A ). Such horns may become so prominent that they actually resemble the

Figure 25-12Keratoacanthoma. A, This symmetric crater-like nodule has a prominent central keratin plug. B, At low power, the crater-like architecture may be appreciated with an

elastic tissue stain where the dermis is red, epithelial elements are gray, and the central keratin plug is yellow. C, Higher power view shows keratoacanthoma to be composed of large,

glassy squamous cells and central islands of eosinophilic keratin.

Figure 25-13Actinic keratosis. A, Excessive scale formation in this lesion has produced a "cutaneous horn." B, Basal cell layer atypia is associated with marked hyperkeratosis and

parakeratosis. C, Progression to full-thickness nuclear atypia, with or without the presence of superficial epidermal maturation, heralds the development of early squamous cell

carcinoma in situ.

Figure 25-14Invasive squamous cell carcinoma. A, Lesions are often nodular and ulcerated. B, Tongues of atypical squamous epithelium have transgressed the basement membrane,

invading deeply into the dermis. C, Invasive tumor cells exhibit enlarged nuclei with angulated contours and prominent nucleoli.

Figure 25-15Basal cell carcinoma. Pearly, telangiectatic nodules (A) are composed of nests of basaloid cells within the dermis (B) that are often separated from the adjacent stroma by

thin clefts (C).

TABLE 25-3-- A Survey of Familial Cancer Syndromes with Cutaneous Manifestations[44]

Date: 2016-04-22; view: 795