Skin Tumors

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Figure 3.1 Seborrheic keratosis with mild pigmentation in the skin of a senior pathologist. Pseudohorny cysts are evident

Figure 3.2 Actinic Keratosis. Note the hyperparakeratosis, moderate malpighian atypia, and dermal inflammatory infiltrate

Figure 3.3 Clinical Appearance of Bowen Disease. A slightly elevated red patch of irregular contours is seen. This clinical appearance conforms to the syndrome originally described by Bowen

Figure 3.4 Microscopic Appearance of Bowen Disease. The atypia involves the full thickness of the epithelium. This example also has focal clear cell change

Figure 3.5 Squamous Cell Carcinoma. A, Tumor of the face with rolled edges and depressed center. B, Tumor of the leg with exophytic appearance

Figure 3.6 Deeply invasive, well-differentiated squamous cell carcinoma

Figure 3.7 Squamous cell carcinoma with spindle metaplastic features

Figure 3.8 Adenoid (acantholytic) squamous cell carcinoma, resulting in a pseudoglandular appearance

Figure 3.9 Verrucous Carcinoma of Skin. A, Typical appearance of lesion located in sole of foot. B, Papillomatous growth associated with hyperkeratosis and pushing type of invasion into the underlying dermis. (Courtesy Dr Daniel Santa Cruz, St. Louis.)

Figure 3.10 Pseudoepitheliomatous hyperplasia following removal of a benign nevus

Figure 3.11 Gross appearance of basal cell carcinoma of forehead. The lesion is nodular and pigmented

Figure 3.12 Multiple basal cell carcinomas in the skin of the back of an elderly patient

Figure 3.13 Typical nodular appearance with peripheral palisading of cutaneous basal cell carcinoma

Figure 3.14 A and B, Clinical and microscopic appearance of pigmented basal cell carcinoma. Melanin is largely present in macrophages located in the stroma between tumor lobules

Figure 3.15 Highly organoid appearance of fibroepithelioma of Pinkus

Figure 3.16 A and B, Low- and high-power views of lymphoepithelioma-like carcinoma

Figure 3.17 Eccrine Poroma. The tumor characteristically grows in the form of cords and nests of small tumor cells attached to the epidermis

Figure 3.18 Hidradenoma. The lesion is lobulated and shows a prominent clear cell component

Figure 3.19 Syringoma. Small glandular structures with little "tails" are typical of this entity

Figure 3.20 Myoepithelioma of skin consistent with sweat gland origin. The tumor cells have a typical hyaline cytoplasm. (Courtesy Dr Fabio Facchetti, Brescia, Italy.)

Figure 3.21 Clinical appearance of multiple dermal eccrine cylindroma extensively involving the scalp and other sites of the head and neck. This is sometimes referred to as turban tumor

Figure 3.22 Eccrine Dermal Cylindroma. Compact nests of tumor cells surrounded by thick basement membrane

Figure 3.23 Eccrine Spiradenoma. The lesion is highly cellular and infiltrated by lymphocytes

Figure 3.24 Clinical appearance of eccrine spiradenoma of the knee associated with a prominent vascular component that resulted in a hemangioma-like appearance clinically

Figure 3.25 Aggressive Digital Papillary Adenocarcinoma. A, Primary tumor with areas of back to back glands as well as papillary areas. B, Metastatic tumor involving a lymph node

Figure 3.26 Gross appearance of resected specimen of sweat gland carcinoma of the axilla. The tumor grows in a multinodular fashion and shows several areas of ulceration

Figure 3.27 Typical branching configuration of sweat gland carcinoma

Figure 3.28 A and B, Sweat gland carcinoma of myoepithelial type located in the toe

Figure 3.29 A and B, Microcystic adnexal carcinoma composed of nests of keratinocytes in a whorling

pattern. This tumor was located in skin of upper lip in a 28-year-old woman

Figure 3.30 Microcystic adnexal carcinoma

Figure 3.31 Extramammary Paget Disease of the Skin. A, The tumor consists of intraepidermal collections of neoplastic cells with small hyperchromatic nuclei and relatively abundant cytoplasm. The tumor cells typically spare the basal layer. B, Extramammary Paget disease immunostained for epithelial membrane antigen

Figure 3.32 Clear Cell Papulosis of Skin. Large clear cells arranged singly or in small clusters are seen in the basal portions of the epidermis. (Slide contributed by Dr TT Kuo, Taipei, Taiwan.)

Figure 3.33 Nevus Sebaceus of Jadassohn. A, Gross appearance. B, Microscopic appearance, showing epidermal papillomatous hyperplasia and increased number of sebaceous glands

Figure 3.34 Sebaceous Adenoma. The tumor has a distinctly lobular architecture. The light and dark areas correspond to well-differentiated sebaceous cells and generative cells, respectively

Figure 3.35 Sebaceous Carcinoma. The tumor is composed of an increased number of atypical basaloid cells with some cells exhibiting evident sebaceous differentiation

Figure 3.36 Inverted Follicular Keratosis. There are numerous "keratotic eddies."

Figure 3.37 Organoid pattern in trichoepithelioma with islands of basaloid cells surrounded by a fibroblastic stroma. Focal papillary mesenchymal bodies are present

Figure 3.38 Desmoplastic Trichoepithelioma. This benign tumor is not to be confused with basal cell carcinoma

Figure 3.39 Trichoblastoma. This tumor is morphologically similar to trichoepithelioma and is composed of islands of basaloid epithelium surrounded by a fibroblastic stroma

Figure 3.40 Trichilemmoma. The tumor presents as an endophytic lobular growth of glycogen-rich clear cells. (Courtesy Dr D Santa Cruz, St Louis.)

Figure 3.41 Highly organoid pattern of trichofolliculoma

Figure 3.42 Clinical appearance of keratoacanthoma

Figure 3.43 Low-power appearance of keratoacanthoma

 Figure 3.44 Keratinous cyst of epidermal type with secondary inflammation

Figure 3.45 Gross appearance of keratinous cyst of trichilemmal type. Grumous material composed of pilar-type keratin occupies the lumen

Figure 3.46 Keratinous cyst of pilar type showing trichilemmal pattern of keratinization

Figure 3.47 Warty Dyskeratoma. There is an inverted proliferation of keratinocytes with prominent acantholysis

Figure 3.48 Cut surface of a proliferating pilar tumor. It has a multinodular appearance, with both an exophytic and an endophytic component

Figure 3.49 Low-power appearance of proliferating pilar tumor. The lobulated contour is characteristic

Figure 3.50 Gross appearance of pilomatrixoma

Figure 3.51 Microscopic Appearance of Pilomatrixoma. The basal cells keratinize as does cortex of hair (without granular layer) and produce "ghost" cells

Figure 3.52 Typical Junctional Nevus. Two large theques of melanocytes expand the basal layer of the epidermis

Figure 3.53 Blue Nevus of the Ordinary Type. The cells are spindle- shaped and heavily pigmented

Figure 3.54 Large Cellular Blue Nevus. A, A distinct nesting pattern is present, with most of the melanin being located in macrophages situated in the intervening stroma. B, Numerous oval to spindle tumor cells with indistinct nucleoli. There is no mitotic activity

Figure 3.55 Spitz Nevus of Spindle Cell Type. This example is pre- dominantly junctional in location

Figure 3.56 A and B, Spitz nevus of epithelioid type. The tumor cells feature large size, polygonal shape, occasional multinucleation, and a strongly eosinophilic cytoplasm

Figure 3.57 Reed Nevus. The tumor is heavily pigmented, in contrast to the usual type of Spitz nevus

Figure 3.58 Spitz nevus of the spindle cell type that is predominantly intradermal

Figure 3.59 Congenital nevus with central hyperpigmented area. This corresponded microscopically to a pagetoid intraepidermal proliferation of melanocytes

Figure 3.60 Vascular involvement in congenital nevus. This is not a sign of malignancy

Figure 3.61 A and B, Clinical appearance of dysplastic nevi in patient with the dysplastic nevus syndrome. These nevi are large, have an irregular outline, and feature a variegated appearance. (Courtesy Dr D Santa Cruz, St Louis.)

Figure 3.62 A and B, So-called dysplastic nevus. There is dermal fibrosis, inflammation, and a proliferation of melanocytes at the dermoepidermal junction, with bridging of rete ridges

 Figure 3.63 Typical Clinical Appearance of Halo Nevus. Heavily pigmented center is surrounded by sharply defined oval area of depig- mentation. Pigmented nevus may be situated in center, as here, or be eccentric. (Courtesy Dr AW Kopf, New York.)

Figure 3.64 Halo Nevus. The low-power view is that of an inflammatory dermal nodule

 Figure 3.65 Halo Nevus. High-power view showing residual melanocytes amid a heavy inflammatory infiltrate

Figure 3.66 Balloon Cell Nevus. The tumor cells are arranged in nests and have a voluminous pale cytoplasm

Figure 3.67 Recurrent Nevus Following Shave Excision. There is an irregular proliferation of melanocytes along the dermoepidermal junction, associated with some dermal fibrosis and clusters of melanin-laden macrophages. This lesion should not be overdiagnosed as malignant melanoma

Figure 3.68 So-Called Lentigo Maligna. The atypical melanocytes are present along the basal layer individually and in theques

Figure 3.69 Clinical appearance of melanoma of superficially spreading type. The nodular light area corresponds to a focus of amelanotic malignant melanoma featuring deep dermal invasion

Figure 3.70 A, Pagetoid appearance of melanocytes in superficially spreading malignant melanoma. B, Malignant melanoma showing transepidermal migration. There is also individual necrosis of neoplastic melanocytes. Some of the melanin has reached the horny layer (so-called pigmented parakeratosis)

Figure 3.71 Malignant melanoma in the region of the Achilles tendon showing prominent spindling. This is a common finding in tumors at this site

Figure 3.72 Melanoma containing highly anaplastic tumor cells

Figure 3.73 Prominent trabecular pattern of growth in melanoma

Figure 3.74 Malignant Melanoma With Nevoid Pattern of Growth. A, Low-power view showing a polypoid configuration suggestive of a benign intradermal nevus. B, High-power view showing only minimal atypicality of the tumor cells. This tumor recurred locally and eventually metastasized to regional lymph nodes. (Slide contributed by Dr Paul Duray, Bethesda, MD.)

Figure 3.75 Myxoid Changes in Malignant Melanoma. This secondary alteration is more common at metastatic sites but can also be seen in the primary lesion

Figure 3.76 Desmoplastic Malignant Melanoma. The spindle cells have a deceptively bland appearance. The collections of lymphocytes are a characteristic feature

Figure 3.77 Malignant melanoma of skin immunostained for S-100 protein. Strong nuclear and cytoplasmic reactivity is present

Figure 3.78 HMB-45 immunoreactivity in melanoma

Figure 3.79 Stage 2 and stage 3 melanosomes with characteristic lattice arrangement in malignant melanoma of skin metastatic to lung (x81,000)

Figure 3.80 Targeted Therapies in Melanoma. Advances in our understanding of the genetics of melanoma have led to the development of targeted therapeutic agents that are directed at commonly observed molecular aberrations in melanoma involved in tumor proliferation and resistance to chemotherapy. MITF, Microphthalmia transcription factor. (Adapted from Singh M, Lin J, Hocker TL, Tsao H. Genetics of melanoma tumorigenesis. Br J Dermatol. 2008;158(1):15-21.)

Figure 3.81 Area of Regression in Malignant Melanoma. There is extensive dermal fibrosis, epidermal atrophy, numerous dermal melano- phages, and dyskeratotic cells in the dermoepidermal junction. Viable tumor was present in other areas

Figure 3.82 Metastatic malignant melanoma with secondary epidermal involvement

Figure 3.83 Isolated melanoma cells in sentinel lymph node, demonstrated with HMB-45 immunostain

Figure 3.84 Microscopic Appearance of Solar Lentigo. There is elongation of rete ridges associated with hyperpigmentation of the basal layer

Figure 3.85 Merkel Cell Carcinoma. This unfortunate patient had involvement of almost the entire face by an extensively ulcerated neoplasm that failed to respond with chemotherapy after an initial diagnosis of malignant lymphoma

Figure 3.86 Merkel Cell Carcinoma Involving the Hand. This particular lesion was associated with Bowen disease of the overlying epidermis

Figure 3.87 Medium-power view of Merkel cell carcinoma

Figure 3.88 High-power view of the same tumor shown in Fig. 4.135. Note the finely granular, dusty quality of the chromatin and the small nucleoli

Figure 3.89 Merkel cell carcinoma showing marked degree of epider- motropism. (Slide contributed by Dr Philip LeBoit, San Francisco.)

Figure 3.90 Same Tumor Shown in Figs. 3.87 and 3.88. Ultrastructurally, neurosecretory-type granules are seen in periphery of cytoplasm beneath cell membrane (x4400; inset x41,100)

Figure 3.91 Dot-like immunoreactivity for keratin in Merkel cell carcinoma

Figure 3.92 Gross appearance of keloid of ear. The lesion has a polypoid shape

Figure 3.93 Microscopic appearance of keloid, with characteristic wide bands of hyalinized collagen

Figure 3.94 Pleomorphic Fibroma. A large triangular cell with hyperchromatic nuclei is encased within dense fibrous tissue

Figure 3.95 Benign Fibrous Histiocytoma of Skin. The tumor depicted in A is predominantly fibrous,

whereas that shown in B is mainly composed of hemosiderin-laden macrophages

Figure 3.96 Benign Fibrous Histiocytoma. This lesion is associated with basaloid proliferation of the overlying skin. This change does not represent a basal cell carcinoma

Figure 3.97 Aneurysmal Fibrous Histiocytoma. A, Low-power appear- ance. The empty space in the center of the lesion was occupied by blood. B, Higher-power view, showing recent and old hemorrhage

Figure 3.98 Epithelioid fibrous histiocytoma

Figure 3.99 Clinical appearance of atypical fibroxanthoma. The lesion is characteristically elevated, reddish, and ulcerated

Figure 3.100 Low-power view of atypical fibroxanthoma. The lesion is typically polypoid and ulcerated

 Figure 3.122 Clinical appearance of typical pyogenic granuloma

Figure 3.123 Low-power microscopic view of typical pyogenic granuloma