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Chapter7, tier2
I began this section with the impression that a discussion of vertical growth patterns would have application to an the interpretation of MDM of Spitz type (i.e., juvenile melanoma). I selected, as an introduction, the patterns of the common dysplasia-melanoma sequence (I recognize that in one system of logic - incidently, a most popular system - the continuum of “steps” has been merged to form a concrete neoplasm, “one melanoma.” Melanoma in situ, in its respective system of logic, is biologically and histologically singular; in this approach, the only concession is an “in-situ” stage). Logic, of one type or another, can be structured to contradict my impression and selection. On the other hand, the choice of another system of logic might justify my selection. In this approach to alternating systems of logic, Barnhill might find justification for his condemnation of tautology, and specifically point the finger at me.
To begin at the beginning, neoplastic melanocytes at the dermal-epidermal interface tend to fill the domain of the basal layer of the epidermis (lentiginous spread) (fig. c11t3P1); the numbers become so great that melanocytic cells begin to displace basal keratinocytes. To accommodate the enlarging crowd, some of the cells take refuge by forming colonies (i.e., nests and fascicles at the dermal-epidermal interface) (fig. c11t3P2). The colonies, in the epidermal domain at the dermal-epidermal interface, are junctional in location.
Junctional nests have a limited right of domain in the epidermis. Some nests relinquish the right, and “drop” into the dermis; the patterns then are compound (fig. c11t3P3 & 4). In the dysplasias, the junctional and dermal nests elicit a stromal and inflammatory response (fig. c11t3P3 & 4). The two qualify as host immune response. Characteristically, the stromal response early on is desmoplastic; it is often expressed in lamellar patterns (lamellar fibrosis). In the sequential delivery of junctional nests into the dermis, some of the nests come to be arranged in stacks (fig. c11t3P4); in most of these strata, cytologic features are variable; the deepest nests tend to be the least atypical; the more superficial nests are composed of the more atypical cells. In this stratification by degrees of atypia, the value to be assigned to the function, stratification, might be that each nests is its own community, and that the more atypical cells (the youngest in regard to depth in the dermis, or the most recent migrants in regard to length of time as a dermal resident) are representative of a higher grade of neoplasia (they provide a marker for neoplastic progressions with the epidermal component as the site of the initial progressions). The duration of this stage of neoplasia can be roughly measured by the number of strata, and by the thickness (vertical dimensions) of the altered papillary dermis. In this stage of neoplasia, progressions occur primarily in the junctional component of the epidermis. Progressions are marked by higher degrees of cytologic atypia, and by a tendency for neoplastic melanocytes to lose their relationship with basal keratinocytes; as a consequence, some of the cells, individually and in nests, migrate upward into the epidermis (fig. c11t3P5); in response, the epidermis undergoes hyperplasia of both the basal and superficial units. In this stage, partial regression is also common; focally, regression may be total (fig. c11t3P6). Rounded neoplastic cells are common in the epidermal and dermal components of common dysplasias. In some examples, the cells are spindle shaped, and variably pigmented (fig. c11t3P7). In spindle cell variants, the cells tend to form fascicles rather than rounded nests; not all spindle cell variants can be accommodated in the Spitz-like category.
As a variation, Spitz qualities are a feature of the atypical cells of what, by most criteria, would be a dysplasia (fig. c12t3P1 & 2). The cells tend to be spindle shaped and loosely attached to their neighbors; they cluster in junctional components to form fascicles.
Some melanocytic neoplasms are characterized by dermal dysplasia in association with a prominent lymphoid infiltrate. Some of these lesions may also show patterns of common dysplasia at the dermal-epidermal junction, but the atypical cells of the dermal dysplasia seem to be independent of phenomena at the dermal-epidermal interface (fig. c12t3P3-5). Lesions of this dermal type are usually dismissed as “halo nevus;” the atypia generally is ignored (perhaps it is dismissed as a response to the inflammation). I believe that halo nevi qualify as neoplasias arising in the setting of a common nevus. The changes, particularly in the dermal variants, usually are subtle; this type of neoplasia might be characterized as near-neoplasia. In some examples, cytologic features are more strikingly atypical; the cells are plump and rounded; they have enlarged nuclei with either dense chromatin, or marginated chromatin and a prominent nucleolus. Generally, the plump cells tend to be arranged in nevocyte-like patterns and intermixed among more common nevus cells. In some examples these plump, atypical cells form an expansile nodule; the nodule assumes the characteristics of a typical vertical growth component. Partial or complete regression is a regular feature of halo nevus-like near-neoplasia. In my experience, the areas of regression do not seem to be associated with the same degree of melanoderma as commonly seen in regression of classic melanomas.
MDM are representatives of a borderland of neoplasia in which distinctions between dysplasia and melanoma are difficult to define using common histologic criteria; MDM are representatives of intermediate neoplasia in which features do not predict behavior with the same rate of success as in common melanomas.
Many melanocytic neoplasms which arise in preexisting dysplasias show both a high degree of atypia, and particular responses in the epidermis (fig. c13t3P1). In the concept of MDM, these qualities were characterized as those of the common final pathway; the implication of this characterization was that a neoplasm showing such responses has progressed to a high stage of dysplasia in the epidermal component; any further progressions require the acquisition of new attributes; in these new progressions, cells acquire the right of domain in the dermis; progressions would no longer the exclusive priviledge of cells of the epidermal domain. The representation of the pattern of the common final pathway in the epidermis in association with a vertical growth component would qualify the neoplasm as a melanoma of superficial spreading type in the classical approach to terminology (fig. c13t3P2). In fig. c13t3P2, the pattern in the dermis is that of arrested variant vertical growth. The implication of this characterization is that the nests of cells in the dermis have been delivered to this site by incremental release of nests of cells from the epidermal component; the progression in the dermal component is dependent on the degree of dysplasia in the epidermal component and the rate in which nests of cells move from the epidermis into the dermis. In fig. c13t3P3, the vertical growth component to the left qualifies as typical type; the implication of this characterization is that the dermal component is independent of phenomena at the dermal-epidermal interface; the cells of the dermal component have attained the capacity to induce a vascularized stroma that is supportive of the continued growth of cells of the dermal component. For lesions measuring less than 1mm in vertical dimensions, the patterns in the dermis often are borderline in providing distinctions between patterns of dysplasia, and patterns of early vertical growth (fig. c13t3P4-6). In the concept of minimal deviation melanoma, a lesion show the qualities of the common final pathway, and a vertical growth component, but measuring less than 1 mm in vertical dimensions (Breslow’s criteria), would be a variant of minimal deviation melanoma; physicalities would impact on the characterization of such a lesion; the lesion would also qualify as borderline neoplasia of indeterminate malignant potential. Even a lesion showing the patterns of the common final pathway and high grade dysplasia in the epidermal as well as the dermal component qualifies as MDM, if the vertical dimensions of the vertical growth component is less than 1 mm (figs. c17t3P1-3). Some melanomas retain nevus cell-like qualities (figs. c13t3P7 & 8, figs. c14t3P1, figs. c15t3P1-6, and figs. c16t3P1-3). These nevoid variants qualify as nevoid melanomas. In the concept of MDM, these variants are given recognition by selecting designations that relate the variant MDM to variants of “nevi.;” In this approach, a lesion in which Spitz-like features are represented is a MDM of Spitz-like type. A lesion in which the process is mostly dermal is a dermal variant of MDM.
The reader might refer to the contribution by Barnhill, et al (Hum Pathol 1999, 30: 513-520) in a search for patterns of typical vertical growth. He might also search out LeBoit’s contribution on Spitz nevus with halo nevus phenomena in a search for patterns of typical vertical growth. I would also caution the reader to be wary of lesions in the literature that have been characterized as “spitzoid melanomas.” For the most part, these are nevoid pigmented spindle cell melanomas.
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