Figure 3 - uploaded by Mark R Wick
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Basaloid epidermal hyperplasia over a dermatofibroma. This proliferation bears a strong resemblance to superficial-multifocal basal cell carcinoma, but it is strictly confined to the epidermis overlying the mesenchymal lesion (hematoxylin-eosin, original magnification 200).
Source publication
Pseudoneoplastic cutaneous lesions are diverse, not only morphologically but also with respect to their causes and cellular lineages. They include proliferations of epithelial, as well as mesenchymal, elements.
This review aims to consider selected lesions in the aforementioned groups, contrasting them with histologically similar neoplasms of the s...
Context in source publication
Context 1
... cells in PEH demonstrate one of 2 morphotypes: ei- ther they are keratinized polygonal cells with eosinophilic cytoplasm and distinct intercellular bridges, 14 or they are basaloid cells with compact hyperchromatic nuclei and scanty amphophilic cytoplasm 34 (Figure 3). Nucleoli and mitoses are variably seen in both PEH and carcinomas and, therefore, cannot be used in differential diagnosis. ...
Citations
... Similarly, prior studies have suggested that pseudoinvasive inverted epithelial proliferations are often linked to ischemic change. 20,22,[27][28][29] The main differential diagnosis for this phenomenon, aside from true invasion, is pseudocarcinomatous urothelial hyperplasia of the bladder. 22,28 Originally described by Baker and Young, 28 pseudocarcinomatous urothelial hyperplasia is another ischemia-related pseudoinvasive process, in which small nests of epithelial cells are present within the lamina propria and thereby mimic invasion. ...
Context.—
Retraction artifact, paradoxic maturation/differentiation, desmoplasia, and complex irregular growth are morphologic criteria of invasion in urothelial carcinoma.
Objective.—
To describe changes mimicking invasion in noninvasive papillary urothelial carcinoma (NPUC).
Design.—
We reviewed 159 consecutive in-house patients with NPUC for either the presence of pseudoinvasion (irregular carcinoma nests within dense hyalinized stroma in the absence of other criteria of invasion) or precursor findings (stromal hyalinization not yet associated with epithelial architectural alteration). We assessed the correlation of these findings with age, sex, evidence of peripheral vascular disease, tumor grade, tumor infarction, and tumor size. We then followed up the patients clinically for tumor recurrence or progression.
Results.—
We identified 233 separate NPUCs (136 high grade and 97 low grade) in 125 men and 34 women. Of the 233 tumors, 26 (11.2%) had pseudoinvasion and 24 of 233 tumors (10.3%) had precursor findings. Except for complex irregular growth, no other criteria for invasion were seen. Pseudoinvasion and precursor findings were more common in men (47 of 183 [26%] versus 3 of 50 [6%]; P = .003), larger tumors (mean size, 2.6 versus 1.2 cm; P < .001), and tumors with infarction (33 of 50 [66%] versus 29 of 183 [15.8%]; P < .001). In multivariable analysis, tumor size (odds ratio, 1.49; P =.006), male sex (odds ratio, 6.48; P = .007), and the presence of infarction (odds ratio, 6.59; P < .001) were significant variables. Recurrence rates did not differ between patients with and without pseudoinvasion (31% [5 of 16] versus 42% [45 of 107], respectively; P = .41). None of the tumors with pseudoinvasion progressed to invasive carcinoma.
Conclusions.—
Given the correlation with size and presence of infarcted papillae, we suggest the possibility of tumor ischemia/infarction as a plausible etiology of pseudoinvasion. Awareness of this phenomenon is important for the accurate diagnosis of invasion in papillary urothelial carcinoma.
... Pseudocarcinomatous epidermal hyperplasia consists of an exuberant proliferation of epithelium with downgrowth into the dermis and occurs in response to underlying infectious, inflammatory and neoplastic conditions. 1 -4 The histopathological features of pseudocarcinomatous hyperplasia may simulate welldifferentiated squamous cell carcinoma (SCC), but some features of carcinoma, including nuclear atypia; atypical mitotic figures; enlarged, hyperchromatic or pleomorphic nuclei; dyskeratosis; and vascular, lymphatic or perineural invasion are not usually seen with pseudocarcinomatous hyperplasia. 5,6 The identification of an underlying disorder is also useful in excluding SCC in difficult cases. However, an incorrect diagnosis of carcinoma may occur, especially if a small biopsy is poorly oriented and has been taken from a peripheral, superficial or inflamed area of involvement by pseudocarcinomatous hyperplasia. ...
Since the use of laminin-5 as a marker of invasiveness has been proposed by several authors, our objective was to compare the expression of this protein in pseudocarcinomatous hyperplasia and squamous cell carcinoma (SCC).
Sixty-four paraffin-embedded skin biopsy samples with diagnosis of epidermal hyperplasia (non-pseudocarcinomatous), pseudocarcinomatous hyperplasia, actinic keratosis/carcinoma in situ, microinvasive and frankly invasive SCC were obtained for immunohistochemical study.
Adjacent normal epithelium and epidermal hyperplasia (non-pseudocarcinomatous) showed no staining. In pseudocarcinomatous hyperplasia, laminin-5 was positive, at least focally, in 14 of 16 (87.5%) samples and was concentrated in peripheral cells of elongated rete pegs and in migrating cells in dermis. In samples of microinvasive carcinoma (n = 7), the expression was observed in all cases and was concentrated in the leading edge of the tumor. All cases (n = 21) of frankly invasive SCC showed cells expressing laminin-5, at least focally. Well-differentiated areas of the tumor presented a pattern of expression in peripheral cells of tumor nests while a diffuse pattern of expression was observed in less differentiated areas.
We showed that cytoplasmic laminin-5 expression should not be used as a criterion of malignancy and is not useful in distinguishing pseudocarcinomatous hyperplasia from microinvasive and well-differentiated SCC.
Clear cell acanthoma (CCA) is classically considered a benign epidermal tumor, although rare case reports have described CCA with malignant features. Here, we present a case of a patient with a biopsy proven CCA that regrew post-biopsy and was subsequently completely excised. Histologic examination of the tumor in the excision specimen revealed malignant cytologic features that were not present in the initial biopsy. A review of the literature identified five additional cases of CCA with similar malignant cytologic features. On analysis, common histopathologic characteristics included cellular pleomorphism, increased nuclear-to-cytoplasmic ratio, prominent nucleoli, and atypical mitotic figures. We support the designation of atypical clear cell acanthoma for these entities with features of both CCA and significant cytologic atypia. As none of these cases exhibited clinically aggressive behavior, further study is warranted.
Because cutaneous melanomas manifest a wide spectrum of clinical and pathologic presentations, several other lesions enter into their differential diagnosis. This review considers those entities, including melanocytic hyperplasia, cellular nodules in congenital nevi, atypical lentiginous melanocytic proliferations, “special site” nevi, epithelioid histiocytoma, neurothekeoma, cellular schwannoma, and proliferating scars.
Because cutaneous melanomas manifest a wide spectrum of clinical and pathologic presentations, several other lesions enter into their differential diagnosis. This review considers those entities, including melanocytic hyperplasia, cellular nodules in congenital nevi, atypical lentiginous melanocytic proliferations, “special site” nevi, epithelioid histiocytoma, neurothekeoma, cellular schwannoma, and proliferating scars.
