Basal cell carcinoma (BCC) is the most common malignant neoplasm of humans. Rising dramatically in incidence in North America, as likely reflects changing habits of the population and a move from more northerly climes to the sunbelt of the Southern and Southwestern United States, the incidence is surely to rise even higher in the future. The last decade has seen significant advances in our understanding of BCC biology and novel approaches to therapy, which hinge upon accurate diagnosis and subclassification by pathologists. The purpose of this review article is to summate the research advances in our understanding of BCC biology and to acquaint pathologists and clinicians to the practical issues in BCC diagnosis and subclassification which flow there from.

A potential diagnostic pitfall in the histologic assessment of melanoma is the inability to recognize unusual melanoma variants. Of these, the more treacherous examples include the desmoplastic melanoma, the nevoid melanoma, the so-called 'minimal-deviation melanoma,' melanoma with prominent pigment synthesis or 'animal-type melanoma,' and the malignant blue nevus. Also problematic are the unusual phenotypic profiles seen in vertical growth phase melanomas; these include those tumors whose morphological peculiarities mimic cancers of nonmelanocytic lineage and those melanomas that express aberrant antigenic profiles not commonly associated with a melanocytic histogenesis. Metaplastic change in melanoma, balloon cell melanoma, signet-ring cell melanoma, myxoid melanoma, small cell melanoma and rhabdoid melanoma all have the potential to mimic metastatic and primary neoplasms of different lineage derivations. Abnormal immunohistochemical expression of CD 34, cytokeratins, epithelial membrane antigen, and smooth muscle markers as well as the deficient expression of S100 protein and melanocyte lineage-specific markers such as GP100 protein (ie HMB-45 antibody) and A103 (ie Melan-A) also present confusing diagnostic challenges. In this review, we will discuss in some detail certain of these novel clinicopathologic types of melanoma, as well as the abnormal phenotypic expressions seen in vertical growth phase melanoma. Modern Pathology (2006) 19, S41-S70. doi:10.1038/modpathol.3800516Keywords: melanoma; variants; phenotype; immunohistochemistry; morphology Desmoplastic melanoma Introduction and Clinical FeaturesDemoplastic melanoma is a rare variant of malignant melanoma first recognized in 1971.1 Desmoplastic and neurotropic melanoma may be mistaken clinically for a scar, a fibroma, a basal cell carcinoma, or a fibromatosis. Sometimes there is pronounced mucin deposition that imparts a boggy quality to the lesion. 2,3 The clinical clue to the diagnosis, when present, is cutaneous or mucosal pigmentation overlying a palpable dermal or submucosal nodule. That said, only half of desmoplastic melanomas are clinically pigmented. 3 Desmoplastic melanomas tend to occur in the head and neck area and the upper back [4][5][6][7] but are also seen in mucosal sites such as the vulva or gingiva 8 and in acral locations. Typically, they occur in older patients, with mean ages in the larger series falling into the sixth to eighth decades of life. 4,6,[9][10][11][12][13][14][15] Larger series show a male preponderance of 1.75 to 1. 15 Although any given desmoplastic melanoma can be deeply invasive, when matched for depth of invasion, they are associated with a lesser risk of metastatic disease than conventional melanomas of similar depth. The classical clinical finding is that of a pale or fleshy firm nodule reminiscent of a scar, which tends to delay clinical diagnosis and biopsy. Carlson et al,6 who reported an equal distribution in men and women, found most tumors to be located in the head and neck area (75%) and to be nonpigment...

Since its first description in 1930, the pathogenesis of pyoderma gangrenosum (PG) has remained obscure even as an ever-widening array of systemic diseases has been described in association with it. The histopathologic distinction of PG from other ulcerative processes with dermal neutrophilia is challenging and at times impossible. In consequence, when confronted with a biopsy from such a lesion, the pathologist has an obligation to obtain a full and detailed clinical history. In short, as a diagnosis of PG does not hinge exclusively upon the biopsy findings in isolation from other studies, a solid knowledge of the clinical features, the systemic disease associations and the differential diagnosis will help the pathologist to avoid diagnostic pitfalls or the generation of a report which is non-contributory to patient care. In this review, we describe in detail the different clinicopathologic forms of PG, summarize the diseases associated with this process in the literature and in our experience, and briefly review the treatment options.